If a bird were to ingest parts of the oleander plant, are there any treatment options? The answer is yes, but of course the more promptly treatment can be provided, the better the potential outcome. Treatment for any animal with oleander toxicosis includes supportive care (such as intravenous fluids), GI decontamination methods, and treatment of cardiac arrythmias, if present. GI decontamination methods comprise removal of the material from the GI tract – if a bird has ingested the oleander very recently (within minutes to an hour), crop lavage may allow removal of some of the material -- as well as oral administration of activated charcoal. Activated charcoal adsorbs many different types of toxins, including the toxic compounds important in oleander ingestion (oleandrin and oleandrigenin), meaning that it essentially binds to the toxicants so they can be passed in the feces. Cathartics (psyllium fiber being one example) can promote passage of the charcoal and its adsorbed toxicants.

In the case of the 6-month-old domestic goose I mentioned in the last post, the bird received IV fluids, antibiotic and anti-inflammatory therapy, activated charcoal, and a special form of treatment called intravenous lipid emulsion (ILE) therapy. Lipid emulsions are solutions containing 20% of some type of lipid (fat) such as soybean oil, among a few other ingredients. The lipid is thought to capture toxicants and carry them away from sensitive organs and to organs that can detoxify or eliminate them. ILEs are mainly used to treat overdoses of various lipid-soluble drugs and poisons. Oleander toxicants are lipid-soluble and ILE therapy in this goose was an innovative approach to treatment. The bird’s condition began to improve within 2 hours, it was discharged after 3 days in the hospital, and made a complete recovery. Within 10 days, bloodwork abnormalities had resolved. Note: These treatment options should only be administered by a veterinarian.

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Oleander (Nerium oleander) is a well-known toxic plant that has caused poisonings in many different animal species and humans. But is it a concern for birds?  

Oleander is cardiotoxic owing to its cardiac glycosides, which by disrupting electrical activity in the heart, can cause arrhythmia or cardiac arrest. Symptoms may include sudden death, lethargy and weakness, incoordination and collapse, rapid and weak pulse, vomiting, diarrhea, hypersalivation (drooling), and abdominal pain. All parts of the plant are toxic; horses and cattle grazing on oleander leaves can die after eating as little as 0.005% of their body weight, or put another way, 40-50 milligrams per kilogram of body weight. 

There has been some investigation into the toxic effects of oleander in birds. Feeding 0.12 - 0.7 g of pulverized, freeze-dried leaves to canaries resulted in sudden death. Illness was also induced in budgerigars in a similar experiment. In another study, oleander leaves were fed to broiler chickens at a dose of 500 milligrams per kilogram of body weight. Within an hour of administration, clinical signs of sudden death, depression, vomiting, diarrhea, and hypersalivation were seen. Electrocardiograms (ECGs) were performed and showed various types of arrhythmia, bradycardia (slow heart rate) being the most common abnormality. When the birds were necropsied, researchers found congestion and hemorrhage within many organs, especially the heart, lungs, liver, and kidneys. In addition, cell necrosis had occurred in the heart, liver, and kidneys. The walls of the stomach and intestine were also damaged. 

A case report described a 6-month-old domestic goose that was presented after eating oleander leaves. The bird showed signs of depression, weakness and incoordination to the extent that it was unable to stand on its own, and loss of appetite. There were no apparent cardiovascular abnormalities on physical examination, but bloodwork showed evidence of heart muscle damage. 

Unlike the other reports, this one had a happy ending – the goose was successfully treated and recovered!  

Certainly the moral of the story is to prevent birds access to any parts of the oleander plant. But in the next post, we will discuss what treatment options exist if ingestion does occur. 

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What about treatment? Unfortunately, there is no established treatment for avocado poisoning. If a patient can be seen by a veterinarian very soon after avocado ingestion, it may be possible to remove some of the material from the crop before it passes further into the GI tract and gets digested. Beyond this, we are at a disadvantage because we don’t fully understand the mechanisms by which avocado exerts its destructive effects on the body. However, if we consider the speculative causes of illness and death – heart damage, congestive heart failure, and elevated blood pressure – we can theorize on a treatment approach that might help in some cases. Treatment steps could include oxygen supplementation, diuretics and other drugs used to eliminate excess fluid and stabilize congestive heart failure patients, and anti-inflammatories to combat the inflammatory process. The hope would be that if heart and other organ damage isn’t too severe, the patient could be supported until the organs recover. The fact that some animals with avocado poisoning recover on their own suggests that perhaps some levels of organ damage are reversible and recovery can be assisted in sick patients with the right medical intervention.  

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Toxic effects of avocado ingestion include fluid buildup beneath the skin and in the lungs (called edema) and around the heart (called pericardial effusion), inflammation and destruction of the heart muscle, kidney injury, and congestion and hemorrhage within the lungs. It has been speculated that edema, congestion, and hemorrhage are the result of a hypertensive crisis (a large increase in blood pressure) and/or the result of heart failure. The ostriches mentioned above suffered damage to their hearts and lungs, congestive heart failure, and severe edema. Symptoms reported in cockatiels were respiratory distress occurring between 12 – 24 hours after eating avocado fruit, whereas a pet canary passed away suddenly 36 hours after he was fed avocado.  

These incidents led researches to question what the heck was going on here—how is avocado toxic and how much is needed to cause illness and death in birds? In order to answer these questions, experimental poisonings (sadly) were carried out in ostriches, chickens, budgies, and canaries. A number of New Hampshire hens were tube fed mixtures of Hass and Fuerte avocado leaves or unripe fruit, dosed between 5 and 25 grams per kilogram of body weight. The researchers found that the hens all continued to behave normally, with no recognizable symptoms, but the birds that had received higher doses had sustained damage to their heart muscle. Very likely, the birds would have suffered more severe illness or death had the dose of avocado been higher. 

In a similar experiment, ostriches were fed Hass leaves, unripe Hass fruit, Fuerte leaves, or unripe Fuerte fruit, dosed between 30 and 100 grams per kilogram of body weight. The birds died between 3 and 5 days after these feedings. Similar to what happened in the natural poisoning, the birds had edema in their body tissues, pericardial effusion, and damage to their hearts, lungs, and kidneys. Findings of the study suggested that Hass leaves were more toxic than the fruit and that the Hass fruit was equally toxic to Fuerte leaves and fruit. The conclusion was that a lethal dose for ostriches ranged between 80 to 100 grams per kilogram of body weight. 

In another study, several canaries and budgerigars were tube fed either low or high doses of either ripe Hass or Fuerte fruit. One canary and nearly all the budgerigars died within 24-48 hours of receiving 100 grams avocado per kilogram of body weight (approximately 2.2 grams per canary and 3.6 grams per budgerigar). The birds became lethargic with fluffed feathers, stopped eating, and exhibited labored breathing. Post-mortem findings were similar to those seen in natural poisonings. Conclusions were that higher doses were more toxic and that budgerigars were more susceptible.  

What we can conclude from these sad tales is that all parts of the avocado plant and fruit can be toxic to birds, and that the larger the amount ingested, the greater the toxic effect and risk of death. Hass and Fuerte varieties may be more toxic, but it should be assumed that any variety poses a danger and thus all parts of the plant and fruits should be kept away from our birds.  

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Thanks to everyone who submitted topic ideas for household hazards we bird parents should be aware of. We received some great suggestions, including toxic plants, vegetables, or fruits, aflatoxins, and the fungal infection known as aspergillosis. In the coming posts we will discuss each of these topics, as well as any others you’d like to hear about. 

In the next 3 posts we’re going to take a deep dive into the details about a toxic plant that most of us have heard about: the avocado. The avocado tree (Persea americana) is native to Mexico and Central America. It produces avocado fruits, which are technically large berries containing a single seed. What is it about this tree and its fruits that is so toxic anyway? 

Persin is the toxic compound in avocados. Some varieties (or cultivars) of avocado are more toxic than others. Fuerte and Hass varieties, frequently found in our grocery stores, are both considered toxic. Other parts of the plant are toxic as well, including its leaves and bark. Avocado toxicity affects a number of other animals, not just birds. Livestock (cattle, goats, sheep), horses, rabbits, and rodents can be sickened or killed by ingesting parts of the plant or fruit.

Naturally-occurring poisonings with avocado have been reported in a few groups of birds, including psittacines (parrots), passerines (songbirds, e.g. canaries), and ratites (e.g. ostriches). The first such report, made in the 1940s, told the story of canaries dying in an aviary after avocado was added to their diet. In another report, a group of ostriches allowed to graze in an avocado orchard containing Hass and Fuerte cultivars died within 96 hours of ingesting leaves and immature fruits from the plants. Deaths have also been recorded in pet canaries, cockatiels, and grey parrots. 

So what are the toxic effects of avocado ingestion, what do the symptoms look like, how much is deadly, and is there any treatment? We will address these questions in the next posts. Please stay tuned, and in the meantime, please keep the suggestions and ideas coming!

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A key factor that differentiates the treatment of zinc toxicosis from lead toxicosis is that, unlike lead, zinc doesn’t stick around once it’s removed from the GI tract. If the source of zinc can be removed, zinc levels in the body’s tissues will rapidly drop. Sometimes this happens on its own: the patient may poop out the ingested zinc when the pieces and particles are small enough. Sometimes they need a little help, though, because GI motility can slow or stop as a result of zinc toxicosis. GI motility and passage of the material can be assisted by supportive care measures including fluid therapy, tube feeding of easily-digestible formula and bulking agents (like psyllium fiber), and pain management. As with lead poisoning, GI protectants and antibiotic therapy to control secondary bacterial infection from a damaged GI tract are also important supportive care steps. 

If particulates and small objects remain within the stomach and gizzard and aren’t moving forward, they can sometimes be flushed out via a procedure called gastric lavage. Larger objects, such as a penny sitting in a duck’s gizzard, may need to be physically removed, either endoscopically or surgically (see photo). In the case of zinc-galvanized objects, such as a wing nut ingested by a curious and ill-advised chicken, removal of the item may not be necessary; once the zinc coating has worn off, the object is no longer a threat. It is not uncommon to find old washers, nuts, bolts, and the like in poultry gizzards on an X-ray; when too large to pass, they might remain there and participate in the grinding and pulverizing of food. However, sharp objects (like nails, wood screws, and wires) are a different matter – their danger goes beyond a zinc coating because they may perforate the stomach, gizzard, or intestine.

So what about chelation therapy? We talked about how important this type of treatment is for lead toxicosis. Indeed, it has its place in treating zinc toxicosis too. In some cases, when symptoms are very severe and zinc cannot be rapidly eliminated from the GI tract (as in the case of a zinc-galvanized object), chelation is indicated. The first-line chelator of choice, as for lead poisoning, is CaEDTA. It has a high affinity for zinc and when given by injection, binds to zinc ions and allows them to be excreted by the body. Fortunately, once the source of zinc has been removed from the GI tract, chelation therapy can be stopped. 

Thanks to everyone who tuned in to our discussion of lead and zinc poisoning. There are many other household hazards birds can get into – for the next series of posts, I’d like to poll the audience for their suggestions:

What would YOU like to learn about next??

Let’s go back to the little caique patient I introduced in the last post. An avian veterinarian presented with a patient with those symptoms may indeed have zinc toxicosis among her list of top suspects. But in order to treat him effectively, she has to be reasonably sure she’s narrowed it down and has the right suspect in her sights. 

As in any case, putting the pieces together requires asking the right questions, both when talking to the bird’s owners and when selecting the most helpful diagnostic tests. Details in the patient’s history might hint at the relative likelihood of zinc (or other heavy metal or toxin) exposure; the symptoms might be compatible; findings of routine tests might be consistent and suggestive of zinc toxicosis.

In the case of the little caique, his Mom told me that he had been chewing on the edge of a decorative metal picture frame only a few hours before his symptoms began. Bloodwork can show regenerative anemia and elevated kidney values, as they did in his case, but the same can be said for lead toxicosis and other types of conditions. Another clue might be the discovery of ingested metal in the GI tract using X-ray imaging, but the tricky part is that the type of metal cannot be determined this way. All kinds of metal look the same on X-rays and sometimes inert or non-toxic metals can hang around in the GI tract for a long time and have nothing to do with the current illness. Further, metallic particles may be too small to see, may have been recently passed (but left organ damage behind), or the bird may have ingested some other zinc-containing substance that isn’t metallic at all – like the zinc oxide in diaper rash cream. 

The picture frame-nibbling caique was found to have several particles of metal in his GI tract (see photo). Fluoroscopy, a type of real-time, video X-ray imaging, was used to discover the particles and determine that his GI tract motility had ground to a halt. These findings were consistent with zinc toxicosis, but not definitive proof.

In most cases, all these clues, combined with a positive response to treatment, come together to build a pretty persuasive circumstantial case. Corroborating evidence could come from sending ingested material (like the picture frame) for analysis to determine what metals it contains, but this would take time, and the source is not always known. What about blood testing for zinc? This type of analysis can be done, but the problem is that, unlike lead, zinc belongs in the body and will be present at some level in the bloodstream of healthy birds. Interpreting zinc levels as normal or abnormal is challenging because normal amounts are undefined in many species AND zinc levels naturally vary throughout the day. It’s fair to say that if a patient has sky-high levels of zinc in his bloodstream and tests negative for lead, the case against zinc becomes even stronger. 

If a patient were to pass away, a conclusive diagnosis can be made postmortem through visible and microscopic findings as well as levels of zinc measured in certain key organs.

When a veterinarian is presented with a patient with a history of potential exposure, compatible clinical signs, and diagnostic findings consistent with zinc toxicosis, beginning treatment is the logical next step, even if the diagnosis is unconfirmed. In the next post, we will take a look at the veterinarian’s arsenal in treating this condition. 

So what does zinc toxicosis look like, and how does it differ from lead toxicosis? There are both similarities and differences to unpack here. Like lead, zinc is absorbed into body tissues after ingestion. Zinc accumulates most in the liver, pancreas, kidneys, lining of the intestine, and the brain. However, unlike lead, it does not get stored in the bones long-term just to rear its ugly head later. Once removed from the GI tract, levels will quickly drop. Lead and zinc share some toxic effects, including damage and destruction of red blood cells leading to anemia and kidney damage that can potentially cause failure. Although zinc toxicosis can cause neurologic problems, this is not a prominent feature as it is in lead toxicosis. The most profound toxic effects of zinc center on the liver and GI tract. These can include severe liver damage and failure, severe damage and destruction of the pancreas, and destruction of the linings of the stomach, gizzard, and intestine. The parrot mentioned previously who ingested zinc oxide diaper rash cream came to the clinic passing tubular blood clots due to sloughing of the intestinal lining. Birds with severe damage to their GI tracts can develop sepsis (a systemic bacterial infection) when GI flora migrates through the damaged GI lining and into the bloodstream.

Symptoms of zinc toxicosis usually begin rapidly after ingestion, and unfortunately sometimes the first sign is sudden death. Besides vague and generic symptoms like lethargy, weakness, and weight loss, the most common and notable symptoms are gastrointestinal in nature: loss of appetite, GI motility that has slowed or completely stopped, regurgitation, and passage digested or frank blood in the feces. Other key signs are drinking large amounts of water (called polydipsia) and passing large volumes of urine (called polyuria), and passing urine that is blood-tinged (see photo). Neurologic manifestations include incoordination and weakness or paralysis of the legs. If the patient is anemic due to red blood cell damage and blood loss, the veterinarian may notice pale mucous membranes. The caique shown in the photo developed lethargy, loss of appetite, regurgitation, polydipsia, polyuria, and red-tinged urine after he nibbled zinc-containing metal off a decorative picture frame.

You may have noticed that many of these symptoms bear similarities to those of lead toxicosis. So how does a veterinarian determine the difference? Please stay tuned for the next post to learn more.

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So what’s the deal with zinc galvanized metal? Zinc galvanization is a process by which a protective coating of zinc is applied to steel or iron in order to prevent rusting. This is used for wire, wire mesh, screws, nails, bolts, nuts, washers, and the like. The zinc coating can be applied different ways, like dipping in molten zinc or electroplating. Depending on the technique, galvanized objects or material may appear dull, matte grey (not that shiny) and have a slightly rough texture, may appear shiny and smooth, or fall somewhere in between.

Rougher-textured objects may have little bits (or “blebs”) of zinc that can be popped off by a curious beak. Zinc coatings can also be worn or chipped away by strong and/or persistent beaks, or the whole object swallowed depending on the size of the bird. For example, it’s not uncommon for backyard poultry to ingest wires, nuts, bolts, nails, screws, or washers unearthed by digging and scratching in the soil. The objects themselves can damage the GI tract, but if they’re also zinc coated, toxic effects become part of the problem.

Further, newly galvanized materials are vulnerable to corrosion by exposure to moisture. Oxidation results in the formation of “white rust” composed of zinc hydroxide. I got to see this process in action when I washed some of my birds’ perches. A little while after the washers and wing nuts got wet, a whitish powder appeared on their surfaces and some wiped off onto my fingertips (see photos). This material was zinc hydroxide and could potentially be nibbled or licked off by my birds. By contrast, zinc galvanized materials that are allowed to weather naturally through cycles of wet and dry in the environment can develop a “patina” of the more stable compound zinc carbonate. This acts as its own protective layer, preventing further corrosion of the zinc beneath.

Probably the safest bet is to use stainless steel hardware and construction materials whenever possible, but it may not be necessary to banish all zinc-galvanized materials from a bird’s environment. An individual birds’ behavior must be taken into account—careful observation can tell you whether a pet bird has a tendency to mouth, lick, chew, or pick at metal components, fasteners, or cage bars in their environment. And even if he or she engages in these kinds of behaviors, it doesn’t mean that they will ingest enough zinc to cause illness. It’s just important to be aware that zinc is out there -- it is a component of numerous metal alloys and is used in galvanization and plating – and if a sufficient amount is ingested at one time, it can make birds sick. In the posts to follow, we will talk about what signs and symptoms to watch out for and what can be done to diagnose and treat zinc toxicosis.

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As if lead wasn’t bad enough, there are other forms of heavy metal toxicosis. The most common of these is caused by lead’s ugly cousin: zinc. While the two share a lot in common, there are some key differences -- sources, effects on the body, symptoms, diagnostic challenges, and treatment approaches --that set them apart. Today we embark on a deep dive into the similarities and differences between the members of this shady family.

First, let’s talk sources. Lead and zinc can be picked up through ingestion of some similar items we’ve talked about, like bits of metal from jewelry, ornamented clothing items and accessories, and home décor items. Any number of metals can contain some zinc because it is a component of many metal alloys. I once treated a parrot who became very ill with zinc toxicosis after nibbling on the edge of a decorative metal picture frame. 

Believe it or not, United States pennies minted after 1982 are composed of mostly zinc. Prior to that time, they were made of 95% copper and 5% zinc, but when copper became more costly, the composition was changed to a zinc core coated with a thin layer of copper. Ingestion of pennies is a common cause of zinc toxicosis in pet poultry like chickens and ducks, and also occurs in wild birds and in zoo collections when people toss coins into lakes and ponds.

A source of zinc you may never have thought of is medication containing zinc oxide, like sunscreen and some diaper rash creams. Under the “anything is possible in this crazy world” category, I once saw a parrot who developed severe zinc toxicosis after he decided that chewing up a tube of diaper rash cream was a super fun idea. He ultimately recovered and did great, but it was worrisome there for a bit.

Besides these sources, there is a whole other category of items containing zinc that we need to consider: zinc galvanized metals, including wire, hardware, and fasteners. In the right circumstances, these materials can pose a threat to curious birds. Please stay tuned for the next post to find out how.  

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So we’ve talked about the rather scary scenario of lead toxicosis – how it can happen, the harm it can do, and the challenges in diagnosing it. Now let’s move on to the solution: what can be done to treat this serious illness?

Treatment is a multifaceted affair, but the cornerstone of treatment is something called chelation therapy. Chelators are drugs that bind to heavy metal ions (like lead), forming a stable, water-soluble complex that can be excreted by the body in the urine. The first-line chelator of choice is called calcium disodium ethylenediaminetetraacetic acid, which is one heck of a mouthful, so we use the acronym CaEDTA for short.

CaEDTA is an excellent chelator of lead and is best at removing lead from the bones. It must be given by injection because it is not absorbed into the body when given orally. In many cases, this is just as well, because patients may be regurgitating and unable to keep down oral medications. Because CaEDTA is given by injection 2 to 3 times daily during the course of treatment, patients most often stay in the hospital until they are stabilized and CaEDTA treatment can be discontinued. The duration of treatment depends on when the ingested lead is eliminated from the GI tract, resolution of symptoms, and results of follow-up blood lead testing.

Another treatment consideration is removal of lead from the GI tract, because as long as it remains there, more lead will continue to be absorbed into the body. This absorption can even be increased when a patient is receiving CaEDTA. As we’ve discussed, sometimes lead-containing material has already been passed in the feces by the time a patient is presented to the hospital. If not, it needs to be removed or helped to pass. Finer particulate material is likely to pass more readily, and this can be helped along with supportive care steps and treatment with bulking agents (like psyllium fiber) and/or laxatives. Particulates and small objects remaining within the stomach and gizzard can sometimes be flushed out via a procedure called gastric lavage. Larger objects, such as a large chunk of metal, may need to be physically removed, either endoscopically or surgically.

Supportive care measures include fluid therapy (to keep the patient hydrated, help improve GI motility, and support kidney function while chelated metal is being excreted) and nutritional support (tube feeding easily-digestible formula) until the patient is eating well on their own. In some cases, pain management, GI protectants to heal GI mucosal ulceration, antibiotic therapy to control secondary bacterial infection from a damaged GI tract, and anticonvulsant medications to control  seizures are needed also.

Chelation therapy with CaEDTA may be continued for up to 10 days at a time, followed by a 3- to 5-day rest period to allow any remaining lead in the body’s tissues to redistribute and appear in the blood. Blood lead concentration is then retested to determine if further courses of chelation are needed. Many patients with lead toxicosis recover fully, but prognosis depends on how quickly the condition is diagnosed and treated; patients who are severely debilitated or have chronic disease resulting in permanent neurologic and organ damage have a poorer prognosis. 

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When a patient presents with symptoms consistent with lead poisoning, as described in the last post, an avian veterinarian must determine whether lead is really the culprit, or if something else entirely is going on. The first step in the investigation is taking a good history – in other words, asking lots of questions to determine the likelihood of lead exposure. Important pieces of information are how long the symptoms have been going, how suddenly they developed, and whether there’s anything new in the home environment (including things the bird has been chewing on) that could be a source of exposure.

Here are some examples of exposures I’ve encountered in practice: chewing on painted walls/windowsills/baseboards in an old home where there are layers of lead-based paint under more recent paint; chewing up old vinyl mini blinds; ingesting bits of “bling” – glass or crystal embellishments, rhinestones, beads; eating bits of solder from stained glass lamps or picture frames; and in poultry, ingesting lead paint chips peeling off an old barn or lead fishing weights scratched out of the soil or dredged from a pond bottom. In one unusual instance, a small parrot became ill when he picked off and ate the tiny glass spheres applied to a decorative plastic fruit arrangement.

Sometimes lead exposure is known or at least a strong possibility, but there are many cases in which lead ingestion was never on the radar. Birds have a real knack for getting into things without anyone realizing it. Whether lead exposure is a prime suspect or not, the investigation must continue with collection of more diagnostic clues. Bloodwork may show increases in kidney values and tissue enzymes, as well as a regenerative anemia. But these findings aren’t specific for lead poisoning. Changes in the appearance of red blood cells can provide more support for the hypothesis, but blood lead testing is needed to provide a more definitive answer. Lead is not something normally found in the body, so the presence of even small amounts (≥0.2 parts per million) is a significant finding. Indeed the amount detected in the blood stream may only represent a fraction of the total amount of lead in the body’s tissues.

Analysis of a blood sample for lead is specialized testing that is only available through certain laboratories, so the veterinarian usually doesn’t have the results in hand for at least a day or two. In the meantime, he or she must gather additional evidence, including X-ray imaging.

In cases of lead toxicosis, X-rays may show an enlarged spleen and signs of reduced GI motility. But one of the most important revelations that X-rays can provide is the presence of metallic material in a bird’s GI tract. Metal is readily visible on an X-ray because it is so dense that it appears brilliant white on the image. While an exciting lead, this discovery really only amounts to circumstantial evidence. Why? Because even though you can see metal on an X-ray, you cannot necessarily tell what kind of metal it is or how long it’s been there. Birds pick up and ingest all sorts of strange things, often without anyone knowing about it. Many types of metals are non-toxic and metal fragments or objects can become trapped in the ventriculus (gizzard) for long periods of time (even years)--see photos. So the presence of metal in the GI tract, instead of a smoking gun, could be nothing more than a red herring.

Still, as the saying goes, if it looks like a duck, and quacks like a duck, it’s likely a duck. Compatible symptoms and lab results, combined with the presence of metal in the GI tract can add up to a pretty strong circumstantial case of lead toxicosis. Even if results of blood lead testing are still pending, the veterinarian has enough cause to start treatment.

Finding metal in the GI tract can be a lucky break, but here’s another tricky twist that can make diagnosis difficult: some lead-containing materials (like paint chips, fragments of mini blind, and bits of crystal) are NOT visible on an X-ray because they’re not dense enough to stand out from the soft tissues of the GI tract. Or, the ingested particulates are so fine and tiny that they cannot be distinguished from the food and tissues that surround them. In some circumstances, the ingested material has already been passed by the time the X-rays are taken – even though lead has already been absorbed into the body, the X-ray evidence of its ingestion is already gone.

Due to these challenges, the veterinarian needs to consider starting treatment for lead poisoning even if the diagnosis is unconfirmed. Indeed, sometimes the patient’s positive response to treatment is huge clue in its own right. Birds with acute lead toxicosis, including those with profound neurologic abnormalities, may improve very quickly once treatment is initiated. 

Stay tuned for the next post, where we will describe what is involved in treating lead toxicosis.

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So you may be wondering, if my bird were to get lead poisoning, what would the symptoms be like? Well, lead can affect the body in multiple ways. Once ingested, much of the lead is passed undigested in the feces. But some will be rapidly absorbed through the small intestine. Lead paint dust can even be inhaled, in which case absorption happens through the lungs. Lead likes to attach itself to red blood cells and thereby gets delivered to all body tissues. Over time, its distribution in the body changes so that most of it gets stored in the bones and only a small amount (about 2-4%) stays in the bloodstream and organs. The bones can store lead for many years and it can be released, even years after exposure, under certain circumstances. For example, when female birds begin laying eggs they mobilize calcium from the bones to make egg shells; if they’ve been exposed to lead in the past, stored lead can be released from the bones during this process.

Lead exerts many toxic effects on the body’s tissues: it damages red blood cells and blood vessels and can result in anemia, it injures and interferes with the function of the central nervous system and peripheral nerves, and it causes kidney damage. Symptoms can be quite variable and depend on how much lead is ingested and how quickly it is absorbed into the body. In the acute stages, lead poisoning can cause neurologic abnormalities, including seizures, blindness, coma, head tilt or circling, incoordination, and weakness. Birds may begin drinking more water and passing more urine or they may have blood-tinged or very green urine or urates. Other symptoms are more vague, like lethargy, loss of appetite, and regurgitation of food. With chronic lead poisoning, weight loss, muscle atrophy, and poor GI motility can be seen.

In truth, there are many other possible causes of symptoms like these. So how does a veterinarian determine that lead toxicosis is to blame? In the next post, we will discuss how avian veterinarians tackle this diagnostic challenge.

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Lead is among the so-called “heavy metals” which can have toxic effects when absorbed and accumulated in body tissues. Most of us are familiar with lead poisoning occurring in humans, but may not have thought about the potential for it causing illness in pet birds. Unfortunately, lead toxicosis is a condition that avian veterinarians must grapple with periodically. It can be successfully treated in many cases, but since an ounce of prevention is worth a pound of cure, we want our pet bird parents to be aware of potential sources of lead in the home environment and to be in the know about what lead poisoning does and looks like in birds. 

Lead can lurk in many types of materials a bird might ingest. Some are more obvious, like metal fragments containing lead, which might come from inexpensive or costume jewelry, accessories, or home décor items, or from leaded solder used in stained glass or electronic components. Less obvious sources of lead are lead-based paint chips or dust that birds might chew or accidentally ingest, as well as bits of leaded glass and crystal as might be found in glass beads or rhinestones. Some additional sources of lead might surprise you: glazed pottery (especially when the glaze is damaged or corroded) and even older vinyl miniblinds! The United States Consumer Product Safety Commission has found that older (pre-1997) vinyl miniblinds imported from China, Indonesia, Taiwan, and Mexico can contain high levels of lead. I have seen a few cases of lead toxicosis in parrots that chewed on these blinds.

What other kinds of materials can you think of that might contain lead?

In the next posts we will discuss what happens if a bird ingests a toxic amount of lead, as well as how the problem is diagnosed and the condition treated. Please stay tuned!

In keeping with the theme of “birds behaving badly” by ingesting all manner of inappropriate things, let’s move on to another category of foreign body hazards: BLING. By bling, I mean all the glittery, sparkly, shiny things that irresistibly draw the eye and beak. The attraction of shiny things seems to be nearly universal among birds of all kinds, and while fascinating and fun to play with and explore, these objects and materials can cause serious problems when ingested.

For our indoor companion birds, including parrots, the most common types of objects ingested are bits of metal, gems, rhinestones, and beads from jewelry and bedazzled clothing items and accessories. All of us bird parents know how much our birds like to pick at our earrings, facial jewelry, rings, necklaces, bracelets, and the like. They will also pick at the shiny objects (like sequins, rhinestones, and beads) that are sometimes applied to shirts, sweaters and sweatshirts, dresses, scarves, hats, sunglasses, reading glasses…you name it. Cell phone cases, purses, and wallets may also be adorned with these kinds of decorative objects. Even the teeth from metal zippers can be irresistible to a parrot and hazardous if swallowed.

Another, less obvious source of materials like these are home décor items like candleholders, ornamental picture frames, stained glass art and lamps, bedazzled pillows, and other decorative items. I saw one sad case in which a small parrot had picked tiny, translucent, rhinestone-like gems off a candle holder, eaten several, and passed away as a result.

So why can ingestion of items like these be dangerous and even deadly? The problem is not only the irritation, damage, and obstruction of the GI tract that can result from the physical presence and passage of these objects, but also their toxic effects. Bits of metal, fake gems, and beads from costume or inexpensive jewelry, clothing, accessories, and home décor items often contain heavy metals like lead and zinc which can cause serious illness.

In the next series of posts, we will delve into the details of how these types of materials and objects cause illness and how it can be recognized and treated. We will also explore some other potential sources of heavy metals in the home environment and discover what shiny and sinister things can pose a threat to our outdoor birds.

#AAVBirdTales

So, you might ask, what happens when birds ingest too much gritty, gravelly, grouty, sandy bits of mineral-density material? Well, not only can this material fill up the GI tract and partially obstruct the passage of food, it can also “sand blast” the lining of the GI tract, causing damage as it moves along or sits in one location, like in the gizzard. The majority of the GI tract is lined with a delicate layer of mucosal cells, and the gizzard sports an extra layer on top of this called “koilin.” Koilin is made up of a carbohydrate-protein complex and basically acts as a protective “liner” within the gizzard (think rubber all-weather mats over your car’s carpet floor mats, or pads on a football player). As the muscular gizzard contracts to grind up and pulverize hard bits of food, the koilin layer takes most of the abuse and protects the more delicate mucosa underneath. Large quantities of mineral-density particulates can tear up the koilin and underlying mucosa within the gizzard as well as the mucosal lining throughout the rest of the GI tract. These “wounds” in the mucosal lining are termed erosions, or when deeper and more severe, ulcerations. Erosions and ulcerations result in bleeding and pain, and provide a site for opportunistic infection by microorganisms in the GI tract. These can cause local infection at the site of injury, penetrate into deeper tissue, or even make their way into the bloodstream or into the liver via the bile ducts. The physical presence of all those bits of mineral foreign material, in addition to pain and injury to the GI tract, can result in reduced motility and impaired passage and digestion of food.

Symptoms range in severity and can include lethargy (loss of energy and reduced activity level), reduced appetite, weight loss, regurgitation or vomiting, and changes in feces (like scant, dark brown, or black feces or undigested seed in the feces). Birds with GI upset and pain may sit fluffed with eyes closed, sometimes with a hunched or even horizontal posture. Small parrots may be seen grinding their beaks or may act as if they’re eating (picking up foods and breaking them up or husking seeds), but then dropping the food rather than actually ingesting it. On physical examination, a veterinarian may note lethargy, dehydration, reduced pectoral muscle mass, active regurgitation or plastering of food material on the head and facial feathers (evidence of past regurgitation), scant or absent feces being passed, whole seeds being passed in the feces, digested blood in the feces (which appears black and is called melena), enlargement of the crop with food, distention of the abdomen, and abdominal pain. On occasion, they may discover that there is gritty material in the feces. Melena is a very concerning symptom because it indicates that there is bleeding in the upper portions of the GI tract. A life-threatening amount of blood can be lost this way, especially in small birds. 

A key diagnostic step needed to identify the problem is taking radiographs (X-rays) and/or X-ray “video” using a fluoroscope (a special piece of equipment that is essentially an X-ray video camera). Unlike regular X-rays, a fluoroscope shows the motility of the GI tract (and movement of mineral-density material within it) in real-time. In either case, mineral-density particulates stand out very distinctly on the images because they are as dense as the bones. Take a look at these two X-rays of an Amazon parrot. Two different views were taken of his body, one from the front and one from the side. In both views, you can see (inside the red circle) lots of little white bits of mineral-density material. They are bright and obvious because they are denser than the surrounding soft tissues. The material fills the stomach (called the proventriculus) and is also present in the gizzard (called the ventriculus). It’s very common to see small numbers of mineral-density particulates in the stomach and/or gizzard of healthy birds, but when large quantities of these particulates are consumed at once, GI disturbances and illness can result. This parrot had chewed up and eaten pieces from a concrete, textured perch and came to us with symptoms of lethargy, reduced appetite, scant feces, and abdominal pain. 

Treatment in cases like this is largely supportive and is best provided in-hospital until the patient has been stabilized. Goals are to keep the patient as comfortable as possible, protect the lining of the GI tract and help it to heal, control secondary infection, and facilitate passage of the material through and out of the GI tract. Fortunately, small particulates can be passed and almost never require surgical removal. Some of them are likely to stay behind (trapped in the gizzard) long-term, but are unlikely to cause any further problems. Passage of the particulates can be assisted by keeping the patient well-hydrated with subcutaneous fluids, giving laxatives and psyllium fiber, and feeding easily digestible foods (including tube-feedings with formula until appetite has returned). Pain management, broad-spectrum antibiotic therapy, and a GI protectant called sucralfate are all important components of the treatment plan. Sucralfate is a liquid medication that adheres to damaged areas of GI mucosa, stops bleeding from these areas, and helps them to heal.

Most birds will fully recover if they receive timely treatment, but preventative measures must be taken to avoid similar incidents from happening again. The environment must be carefully inspected in an effort to identify the source of the ingested material. Those items should be removed from the cage and larger environment and the bird should be prevented from accessing areas in the home (like brick mantels and fireplaces, or tiled floors) where they can pick up bits of mortar or grout. They should ideally be prevented from “foraging” in the carpet, or if that isn’t possible, the carpeting should be vacuumed regularly. Pet parrots do not need to be supplied with grit or gravel. Other species that are more exclusively granivorous, like canaries, pigeons, doves, and chickens, can be provided grit or oyster shell but in moderation, and should be prevented from gorging on large amounts at once.

Thank you to everyone who tuned into the discussion about polyester (“fleece”) GI foreign bodies and Gogy the caique’s story of survival 😊  I would like to move on to share more examples of household hazards for pet bird parents to be aware of.  For now, we are going to stay in the category of foreign material ingestion and its effects on the GI tract. It never ceases to amaze me what birds will consume and why some individuals seem to make poor choices (sometimes repeatedly) while others do not. It is entirely normal for our parrots to chew up various materials in their environment, but usually not appropriate for them to ingest it. And yet, sometimes they do. It is normal for some species of birds, whose diet is largely composed of seeds and grains, to pick up and ingest small bits of grit, gravel, or stones. The theory is that this type of material aids in digestion by helping to pulverize these food items within the ventriculus (the “grinding” portion of the stomach, also called the gizzard). Seed-eating birds are termed “granivorous” and include small parrot species (for example, budgerigars and cockatiels), song birds (for example, canaries and finches), chickens and other game birds, pigeons, and doves. For most of our pet parrots, even those eating some or all seed, it isn’t necessary to provide grit/gravel for them to have normal digestion. Even though grit products are sold at pet stores for this purpose, it is not my or my colleague’s standard recommendation for parrot parents to buy and provide these to their birds. It isn’t really necessary and in fact over-ingestion of this type of material can cause illness. That is the subject of today’s post. 

Even though pet parrots don’t require grit/gravel for digestion, that doesn’t mean that they won’t ingest material like it – they will sometimes seek out mineral-density particulates in the environment and eat them. Consuming small numbers of these particulates isn’t harmful; some will pass through the GI tract and come out in the feces and some will stay “trapped” in the gizzard where they contribute to the pulverization of food. The trouble comes when large quantities of these particulates are consumed at once or very frequently. This can cause the GI tract to become packed with this material and partially obstructed and the particulates can traumatize the lining of the GI tract, causing pain and bleeding. Needless to say, this can greatly disrupt normal digestion rather than assist it.

Here is a list of materials that pet birds can find in their home environments and some of the most common causes we see of GI upset when ingested frequently or in large amounts:

• Mortar picked from between bricks (for example, a brick fireplace or interior wall)
• Grout picked from between tiles
• Bits bitten off lava rocks or oyster shells (these are sometimes incorporated into bird toys),  mineral blocks with coarse particulates, textured (or sandy) perches, or the hard backing of cuttle bones
• Bits of sand, grit, gravel picked up from the floor or out of carpeting (this kind of material can be tracked in on our shoes)

In the next post, we’ll talk about the symptoms that can be seen when birds ingest harmful amounts of these sorts of materials. We’ll also talk about what treatment is needed in most cases to get them well again, as well as preventative steps to avoid a repeat offense. 

#AAVBirdTales

Gogy had been a total Rockstar in surgery and was recovering well. But for the next few days we would need to keep watching her like a hawk. We needed to make sure her GI tract would get moving again and function properly, considering that it had been insulted both by the presence of the foreign body and also by an invasive procedure. We also needed to monitor very closely for any signs of serious complications – most importantly, dehiscence (or opening up) of the gizzard incision. Even though we had carefully sutured it closed, there remained a chance that the gizzard wall wouldn’t heal properly. That can happen when the tissue has been stretched and irritated for a long period of time. If dehiscence occurs and GI contents leak out, this causes peritonitis, which is infection within the body cavity that can quickly become life-threatening. If such a complication is to occur, it usually will do so within the first few days to a week after surgery. So we watched for any suspicious symptoms such as lethargy, poor appetite, regurgitation, failure to pass feces, or abdominal pain or distention. We literally watched every bite she ate and inspected every dropping she passed -- she must have thought we were pretty weird to be so fascinated with her ins and outs!

Thankfully she passed all of our tests with flying colors! She continued to feel great after surgery, ate everything in sight, and passed lots of wonderful poops. It’s funny how veterinarians get so excited about feces, but it’s true, we do! A few days after surgery it was time for her to go home and her family and flockmates were delighted to have her back.

Our experience with foreign material ingestion is that birds don’t necessarily learn from their mistakes. We knew that if Gogy had access to a fleece sleeping hut again, there was a good chance that over time she would end up with another wad of fibers in her GI tract. We discussed this with her family and they agreed that it was a good idea to remove the hut. Ultimately Gogy didn’t really mind and adjusted well to roosting on a perch to sleep like any other self-respecting parrot would in the wild. 😉

That was 4 years ago, and since then Gogy has moved on to getting into other forms of mischief! Her Mom was nice enough to send me several photos documenting her daily shenanigans, posted here. She wrote, “She’s a constant trouble maker… in fact, most (of the photos) are of her getting into trouble, or getting caught in things. She’s definitely our most independent bird… She loves to do her own thing and explore.”

We are beyond grateful that Gogy is back to living her best life. Sure, she could get herself into some trouble again, but that’s true for any bird at any time. We are always standing by if help is needed.

Much thanks to Gogy and her wonderful human and avian family for permission to share her story.

Once Gogy had awakened from anesthesia and appeared stable, we examined the foreign body more closely (see photo #7). It was covered with some food and barium, but underneath that was a tightly compressed wad of tiny synthetic fibers. After pulling the wad apart, we could see that the deeper fibers had retained their original green color.

We discussed the discovery with Gogy’s family and asked if they had any ideas about where this material had come from. They did – the fibers matched those of a green, fleece sleeping hut she had used for many years. While she enjoyed spending time in this hut, she had not appeared to chew on it, at least not enough to visibly damage the fabric. I mentioned in a previous post how even birds who don’t seem to be chewing on fleece fabric can still develop a GI foreign body composed of its polyester fibers. This was true for Gogy. The evidence pointed to ingestion and gradual accumulation of these fine fibers over a long period of time. Only once the wad of fibers had become large enough to partially obstruct her GI tract did she develop clear symptoms of illness.
Everyone was excited and relieved that the surgery had been successful and Gogy had begun her recovery, but there would still be several days of in-patient care in the hospital to ensure she was healing well.

In the next post we will conclude Gogy’s story and check in with her to see what she’s up to now, 4 years later.

Fluoroscope images are a little different than X-ray images in that black and white are reversed, rather like a photo negative. For example, on an Xray the bones of a bird will appear white. The same is true for barium. But on the fluoroscope, the bones and barium appear black. Take a look at photo #1: this is an image taken from the fluoroscope video of another bird (not Gogy) with a normal GI tract. It shows the bird standing facing the left of the image. At the base of its neck is the crop, which is basically a sac that holds the food right after it’s swallowed. You can see that it is full of barium, and that some of the barium has moved into the stomach, gizzard, and intestine. When we watch the video of the barium moving through, we can see that it empties out of the crop a little bit at a time, slides through the thoracic esophagus, and drops into the stomach. From there, it passes through a narrow channel into the gizzard. The gizzard functions much like a rock tumbler – it has regular contractions, turning over and over to grind up the food inside. Barium then leaves the gizzard and moves through the many loops of intestine before being passed in the droppings. The intestine has its own regular movement, called peristalsis, in which the muscle in the intestinal wall contracts and moves the contents in the right direction. In most parrots, barium moves through the whole GI tract pretty quickly – usually within a couple hours.

Photo 1

We performed Gogy’s barium study using the fluoroscope. We hoped it would answer the following questions: WHY did her stomach and gizzard appear so large on her Xrays? Were they just filled with food and not working properly? Were they filled with some sort of foreign body with the same density as food? Was there a blockage further along the GI tract preventing food from emptying out? Or was there a mass taking up space inside, like a tumor growing from the wall of the stomach?

Take a look at video #1. It shows the beginning of the barium study.

Video 1

We could see that barium was leaving the crop, going through the thoracic esophagus, and entering the stomach pretty normally. The stomach looked relatively normal at first…but once it had filled more fully with barium (video #2), we could see that it was hugely enlarged.

Video 2

The same was true for the gizzard. The gizzard was working hard to contract and churn, but its movements were a little sluggish and strained. It was having difficulty making its revolutions smoothly. The intestine looked and functioned normally. Photo #2 is a still image taken from the video. It shows how enlarged the stomach and gizzard were.

Photo 2

Even though the barium was able to make its way through the GI tract, it did so very slowly. Barium remained in the stomach and gizzard several hours after the study began. At this point, we knew that there wasn’t a complete obstruction and that there wasn’t a mass growing from the wall of the stomach or gizzard. We also knew that the GI tract was doing its best to function normally. What we didn’t know was whether the contents of the stomach and gizzard were merely food mixed with barium or whether there was something else lurking inside that blended in with the rest. We needed to pick up with the study the next morning and see if any barium was left, and if so, where.

Fabric or fiber foreign bodies can blend in amongst food (and even barium) very well. For this reason, it is difficult, and sometimes impossible, to find them using non-invasive imaging techniques like these. Sometimes the best opportunity to identify them is AFTER most of the barium and food have emptied out of the GI tract. If the barium coats the foreign body and sticks to its surface, those traces of barium can be seen the following day.

Sure enough, we could see the next day that although nearly all the barium had left the GI tract, there was an area where barium lingered in the gizzard. It appeared that the barium was highlighting a distinct shape. Video #3 shows what appears to be a barium-coated object moving within the gizzard. This was highly suspicious of a foreign body, but it was also possible that some barium had become trapped amongst food material.

There was only one way to know for sure – have a look inside. 

Video 3

Now that Gogy had been admitted to the hospital, we had a lot of detective work ahead of us to figure out what was going on. She hadn’t given us many clues so far – our best lead to follow was her distended abdomen and abdominal pain. We had an area of interest, but we still had to keep our minds open to any possibility because these symptoms can have many possible causes. Our diagnostic investigation would need to include be made up of a series of tests, each giving us one or two pieces of the larger puzzle.

First, Gogy patiently allowed us to collect a blood sample. Bloodwork would allow us to evaluate her liver and kidney function, blood sugar, blood protein levels, red blood cell count, and white blood cell counts. We learned that her blood uric acid was slightly elevated. Uric acid is the major waste product of avian kidneys and is in fact the white part of the dropping. The level of uric acid can increase in the blood stream with dehydration, reduced kidney function, or blockage of uric acid flow out of the kidneys and into the dropping. Since Gogy had not been eating and drinking normally, dehydration was considered the most likely cause of this mild uric acid increase. Subcutaneous fluids would be an important part of her supportive care by improving her hydration and helping the kidneys excrete this waste.

Bloodwork results also showed very low levels of blood proteins. A bird’s blood, just like ours, is composed of red and white blood cells, but also a number of different proteins. These protein levels can decrease for a number of different reasons, including blood loss, liver disease, chronic malnutrition, or gastrointestinal disease that disrupts digestion and absorption of protein from food. There wasn’t any evidence of blood loss or liver disease, and we knew that Gogy had been provided a good-quality diet her whole life. Even though she hadn’t been feeling well and had lost weight, her appetite at home was relatively normal. These clues led us to wonder if there could be a problem with her digestion and ability to absorb the nutrients she consumed.

The final bloodwork abnormality was her white blood cell count – she had elevated numbers of circulating white blood cells, especially of a type of white blood cell involved in acute inflammation. This told us that, at minimum, there was something going on in her body that was causing significant inflammation. Whether an infection was the cause of that inflammation wasn’t clear, but we started a broad-spectrum antibiotic to address that possibility.  

Now that blood work had been completed, the next step was Xray and ultrasound imaging to get an idea of what might be going on in her abdomen. She received a mild sedative (similar to Valium) to relax her so she would calmly allow us to position her for the images. We took two different X-ray views of her body, one from the front and one from the side. On the side view, we could see that the gizzard (the grinding part of the stomach, also called the ventriculus) was very large. The borders of the stomach (also called the proventriculus), which lies between the heart and the gizzard, were not very distinct on this view. But when we looked at the view from the front of her body, the stomach was more clearly visible, and we could see that both it and the gizzard were very enlarged. This was clearly the cause of her distended belly.

What the Xrays couldn’t tell us was WHY the stomach and gizzard appeared so large. Were they just filled with food and not working properly? Were they filled with some sort of foreign body with the same density as food? Was there a blockage further along the GI tract preventing food from emptying out? Or was there a mass taking up space inside, like a tumor growing from the wall of the stomach?

An ultrasound of her abdomen gave us another look at her gizzard. We could see that it was functioning well – it had good motility, so it was contracting regularly and turning over and over like a rock tumbler, like it’s supposed to do. It was hard to tell what was inside; the contents essentially looked like food. Some portions of the intestine were visible and appeared to be contracting normally. Her heart and liver looked normal.

Each of these tests had given us a useful piece of information. Collectively, they had narrowed things down to one system -- the GI tract. But there were still some unanswered questions: was the problem confined to the stomach or gizzard or was there something going on further downstream that we couldn’t see with X-rays and ultrasound? What exactly was inside the stomach and gizzard? Was there an obstruction, somewhere along the line, slowing down passage of food through the GI tract?

Gogy had had a big day and needed to rest. But the following day, to answer these lingering questions, there was another step we would need to take: a barium study.

Gogy is a sassy, rambunctious force of nature otherwise known as a white-bellied caique. 😊  She was 13 years old when she started to show some signs of illness and her family brought her into the clinic. Birds with GI foreign bodies can show a variety of different symptoms, ranging from mild to severe. These symptoms can include lethargy (loss of energy and reduced activity level), changes in appetite (usually a decrease or loss of appetite, but sometimes increased appetite), weight loss, regurgitation or vomiting, changes in feces (like loose, smelly, discolored, or scant feces), and sometimes increases in water intake and urine output. The trouble is, these symptoms are somewhat generic – they can be seen with all sorts of different illnesses, not just GI foreign bodies. Indeed, Gogy’s symptoms were relatively vague: she had not been feeling herself lately and had become less active and more withdrawn. Her appetite seemed okay, but she had lost weight. 

In birds with GI foreign bodies, these are some of the abnormalities we might see on a physical examination: lethargy, weakness, dehydration, reduced pectoral muscle mass, active regurgitation or plastering of food material on the head and facial feathers (evidence of past regurgitation), scant or absent feces being passed, whole seeds being passed in the feces, diarrhea, digested or fresh blood in the feces, enlargement of the crop with food (or sometimes foreign material), distention of the abdomen, and abdominal pain (reacting painfully  when the abdomen is touched or standing with a hunched or horizontal posture). On her physical exam, Gogy was a little quiet and we noticed that her pectoral muscle mass was low. Her abdomen was slightly distended and she was uncomfortable when her abdomen was palpated. There wasn’t anything unusual felt in her crop. Her droppings looked normal for the most part, but the amount of feces being passed was scanty. 

These symptoms and physical exam findings weren’t specific to any one illness, so a thorough and step-wise diagnostic workup was going to be needed to figure out what was going on. We recommended this to Gogy’s family and asked that she be admitted to the hospital for supportive care, including pain management, broad-spectrum antibiotic therapy, and subcutaneous fluids. A diagnostic workup was initiated with complete blood work, radiographs (Xrays), and an abdominal ultrasound. 

Please stay tuned for the next post when we share Gogy’s test results and the next steps taken to diagnose her GI foreign body.

#AAVBirdTales

In the next series of posts, I’ll be sharing some specific cases of foreign material ingestion and describing how our patients were diagnosed and treated.

But be aware that ingestion of the material is not the only potential hazard posed by these types of products. My colleagues and I have seen many instances of birds becoming trapped in holes in the material or in the strings, loops, and fasteners that attach these huts and toys to the cage bars. Patients have gotten a toe, foot, leg, wing, head, or neck trapped and entangled, resulting in cuts and abrasions, constriction injuries and disruption of blood supply, self-mutilation or self-amputation of the extremity in an attempt to escape, and even strangulation. Some of these incidents prove fatal or result in severe injury requiring hospitalization and extensive treatment.

Yet another consideration is the influence of sleeping huts and snuggle toys on the reproductive behavior of our pet birds. Whether it seems that way or not, sleeping huts are perceived as nesting sites because the enclosed space mimics a nest cavity. The presence of a nest, as well as cuddling and other courtship behaviors with a mate (or surrogate object) are powerful reproductive stimuli. As a result, birds provided with these tents and cuddle toys are more likely to exhibit reproductive behavior (including egg laying) and aggression in defense of the perceived nest or mate.

Many of us bird parents find ourselves drawn to these types of products because we want to offer our birds a comfortable place to sleep. Fortunately, there are ways to provide a secure, comfortable, and attractive roosting site without them. You’ve probably observed that your birds like to roost high in the cage – my birds seem to prefer a top rear corner. I like to provide a perch in that location (with adequate head and tail clearance), and to make it feel more secure, place some toys and chewing materials (some woven through the cage bars) surrounding it to provide some concealment without enclosing the space too much.

We would love to hear readers’ ideas about their cage setups and how you create a comfortable, secure roosting spot for your birds.

#AAVBirdTales

As we’ve talked about, these types of fabrics are commonly used in the construction of sleeping huts or hammocks, snuggle toys, and toys intended for chewing or preening. They are sometimes used as a soft substrate or a cage cover. In practice I see enough cases of polyester fiber GI foreign bodies, many with devastating consequences, that I don’t think using these fabrics is worth the risk.

So, what types of materials are safer alternatives to fleece polyester fabrics?

I recommend natural fabrics sourced from plants -- cotton (like the patterned flannel shown in the photo) being the most common example. Other natural materials that can be used are cardboard, paper, wood (including cork), seagrass mats, coconut fiber/husks, bamboo, yucca, and dried corn husks, palm leaves, and banana leaves. These materials are often sold for pet birds to chew, either incorporated into toys or woven into mats, baskets, and other shapes.

Disclaimer: Even with natural materials, there remains some risk of ingestion of fibers/particulates and formation of a partially or completely obstructive lump of material. We DO see this from time to time in practice, but it's much less common (or at least much less likely to produce clinical illness) than foreign bodies composed of artificial fibers. Interestingly, we have noticed that these types of materials more commonly collect into a cohesive foreign body in the crop, where they are much easier to diagnose and remove.

Aside from the materials they’re made from, there are other hazards posed by sleeping huts and cuddle toys. These will be discussed in the next post.

#AAVBirdTales

So why, you might ask, are gastrointestinal foreign bodies such a concern with fleece huts?? Sure, it makes sense that if birds are chewing the material they could be ingesting it, but what about birds who DON’T seem to be actively chewing the fabric – are they at risk too? The answer, unfortunately, is YES.

Here’s why:

Synthetic “fleece” fabrics are composed of very fine polyester fibers that will come off when the fabric is damaged but also will shed off during normal use or when mouthed by a bird. Try rubbing and pinching this material between your fingertips—if you look closely, you may see that very tiny, fine fibers have come off on your fingertips. These fibers can come off onto a bird’s body and be unknowingly ingested when preening, or they can enter the mouth and be ingested just by mouthing the fabric.

These fibers have a tendency to collect in the gastrointestinal tract to form a wad that grows in size over time. This process can happen gradually over a long period of time or proceed more quickly if a bird mouths or chews the material more actively. In this way, fibers can be ingested and foreign bodies can form even if a bird hasn’t caused obvious damage to the fabric. This is the scenario we suspect in one of our more puzzling foreign body cases: a white-bellied caique used the same fleece hut for 8 years without causing any visible damage, but became obstructed with a wad of polyester fibers matching in color with the fleece of the hut.

Now when we consider that many pet birds use fleece huts or similar products and never become obstructed, we have to wonder how commonplace this problem really is. Undoubtedly some, perhaps even most, of ingested fibers will be passed in the feces. It’s unclear why some birds build up wads of fibers in the GI tract and others do not. It’s possible that some fabrics “exfoliate” fibers differently than others, or that their microfibers have different characteristics that make them more or less likely to become trapped in the GI tract or to collect together. The individual behavior of the bird likely plays a role as well – some birds may ingest fibers more purposefully, for example by “grooming” the material. The reality is that these types of foreign bodies are probably more common than anyone realizes. There have been several instances in our practice when we discovered wads of fibers at necropsy in the GI tracts of birds who had passed away for an unrelated reason. Very likely many of these foreign bodies stay under the radar because their size or location causes few if any symptoms, at least initially.

The next question you might be asking is, “Ok, if these fleece fabrics are dangerous, are there any safer alternatives?” I believe there are, and this will be the subject of the next post.

You know, those little tents sold for birds to hang out and sleep in? They’re often referred to as fleece huts but are marketed and sold under many different names. There are also similar products, usually attached to the side of the cage, intended for birds to snuggle against. Different materials are used in the construction of these huts and related products, but they are most often made of synthetic, polyester fabric that most people call “fleece.”
 
These types of products are desirable to bird parents because they’re soft and cuddly and seem to offer our birds comfort. Indeed, birds generally like them a lot and spend quite a bit of time nestled inside. They often mouth or chew the material, sometimes tearing holes in the fabric. Although it may seem that these products are a great way to provide fun, enrichment, and a sense of safety and comfort, great danger lurks here. There are significant risks posed by these products, including gastrointestinal foreign bodies, entrapment in the material or attachments, and reproductive issues related to perception of the hut as a nest.
 
Let’s begin by discussing the issue of gastrointestinal foreign bodies. We will take a deep dive into this in the coming posts, to include presentation of a real-life case example.
 
Please stay tuned!

Photo credit: "File:Blue-crowned Parakeet - pet in parrot tent.jpg" by The_Gut is licensed with CC BY 2.0. To view a copy of this license, visit https://creativecommons.org/licenses/by/2.0

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Dr. Fitzgerald has been a member of AAV since 2007 and is currently a Member-at-Large on the AAV Advisory Council. She has lectured extensively at AAV's annual conferences, ExoticsCon and other veterinary conferences, and is an avian veterinarian at the avian-exclusive Medical Center For Birds in Oakley, California. She is a 2007 graduate of Texas A&M University College of Veterinary Medicine and received her ABVP board certification in avian practice in 2012. Dr. Fitzgerald has had a lifetime love affair with animals of all kinds, but particularly enjoys working with birds. She has always considered veterinary medicine her true calling and has focused her career on caring for companion birds and their people. In the Bird Tales series, Dr. Fitzgerald looks forward to sharing her experience in avian practice, including spotlights on special patients and cases, tips to avoid household dangers, information about common illnesses and how to spot them, and more.
 

A Note from Dr. Fitzgerald About this Series: 

“As an associate veterinarian in an avian-exclusive practice, I encounter many situations in which household hazards have caused great harm or death to pet birds. I would like to bring about awareness of these hazards because as the saying goes “to be forewarned is to be forearmed.”  Many bird parents will already be familiar with many of these dangers, but there may be some that are unfamiliar and unexpected. To best safeguard our birds we must keep learning as much as we can and stay ever-vigilant. My goal is to get the word out and provide insights about important hazards from a veterinary perspective.”

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