Many commercial pet diet manufacturers follow these nutritional recommendations when formulating pet diets. However, unconventional diets such as unbalanced foods, raw foods and homemade diets are not nutritionally adequate to meet the dietary thiamine recommendations, which in turn increases the risk of developing thiamine malnutrition.

Sweet Potato Diet on a Maltese Terrier

An owner fed a diet of boiled sweet potato for 4 weeks on his 5‐year‐old neutered male Maltese Terrier dog and this nutritionally incomplete diet eventually led to the suboptimal thiamine status of the body. The sweet potatoes fed to the dog were well‐boiled before feeding, and this heating procedure for cooking would have led to a sufficient amount of thiamine loss in sweet potatoes. Because of the low thiamine content in boiled sweet potato (0.09 mg per 100 g of boiled sweet potato), a large quantity of sweet potatoes is needed to be significant to supply adequate amounts of thiamine. Furthermore, intake of dietary carbohydrates has been known to increase the dietary requirements for thiamine based on data from previous human studies. Boiled sweet potatoes are not only low in thiamine, but rich in carbohydrates (approximately 80% of the dry matter in sweet potatoes). Given this background, the consumption of boiled sweet potatoes may further increase the metabolic demand for thiamine and may precipitate thiamine deficiency in a short period.

Symptoms

The Maltese Terrier dog was presented to a referring veterinarian with a 3‐day history of:

• Depression
• Anorexia
• Vomiting
• Seizure clustering
• Generalized ataxia

The owner noticed a progressive deterioration of the neurologic signs over the preceding 3 days. Symptomatic treatment before the presentation with phenobarbital (2 mg/kg twice a day orally) failed to alleviate the seizures.

The dog had been generally healthy until the occurrence of acute seizure episodes. He had been fully vaccinated and dewormed, with no history of trauma or exposure to toxins. Further medical enquiry with the owner revealed that the dog had been fed an almost exclusive diet of boiled sweet potato (Ipomoea batatas) as a primary diet source for 4 weeks with an average consumption of approximately 100–150 g (about one to one and a half small whole sweet potatoes) per day due to his picky eating behaviours (chronic food refusal). Furthermore, this food refusal had gradually worsened over time.

Neurological examination identified generalized ataxia with dysmetric movement and an inability to bear full weight on the hind limbs.

There was no cytological CSF evidence of relatively well‐recognized CNS disorders (e.g. inflammatory, neoplastic and infectious causes). Therefore, based on the inadequate diet history, the hyperlactatemic condition (Type B hyperlactatemia) and the abnormalities seen on MRI, a presumptive diagnosis of thiamine deficiency was established in this patient.

To confirm the presumptive diagnosis of thiamine deficiency, the whole blood sample was submitted to evaluate the blood thiamine concentration. Thiamine content was measured by the high‐pressure liquid chromatography (HPLC) method with the assistance of a commercial laboratory (Neodin Vetlab, Seoul, Korea). The HPLC is a preferable and reliable method of thiamine analysis in humans and animal studies, which helps by directly measuring the phosphorylated form of thiamine (thiamine pyrophosphate, TPP) within RBCs.

Treatment

Following the MRI scan and the blood sampling, a therapeutic trial using thiamine supplementation with dietary intervention was performed on the same day to evaluate the associated response and to rapidly recover the clinical signs.

Sweet potato supplementation was immediately stopped prior to starting the treatment.

Thiamine supplementation was started with oral vitamin B complex  at a total thiamine dose of 45 mg once a day for a month.

Furthermore, the dog’s diet was temporarily changed to a good‐quality prescribed dog food containing high levels of protein and fat.

Recovery

A rapid improvement in neurological signs was seen with the initiation of thiamine supplementation and diet change. There were no additional seizures after being discharged from the hospital. Furthermore, the symptoms of anorexia improved along with the normalization of previous metabolic derangement with the treatment, which consequently accelerated the recovery rate of the remaining neurological abnormalities. Finally, no residual neurological deficits were observed at 3 days after continuous management.

Two weeks after starting thiamine supplementation and dietary intervention, there were no abnormalities on physical and neurological examination. Repeated blood examination showed that the previously observed biochemical abnormalities had entirely normalized.

Conclusion

Thiamine deficiency causes metabolic encephalopathy that can be reversed with early diagnosis and appropriate treatment. Obtaining a comprehensive dietary history is extremely important in suspected cases of thiamine deficiency or in sick animals and urges prompt intervention for nutrition. Measuring blood TPP concentration by HPLC is the most reliable and intuitive method to confirm the diagnosis of thiamine deficiency. MR imaging and blood lactate levels can also provide clinically meaningful insights into the thiamine status. Clinicians should be aware that diet composition can markedly influence the thiamine requirements of dogs. Dietary changes based on dietary composition as well as a complete and well‐balanced diet might be helpful in the rapid recovery of thiamine deficiency.

Source – Veterinary Medicine and Science | First published: 23 September 2020

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What is Enteroviruses EV-D68

Acute flaccid myelitis (AFM) is a syndrome characterized by acute flaccid paralysis (AFP) and gray matter spinal cord lesions on magnetic resonance imaging (MRI). After the introduction of the term AFM in 2014, more than 500 patients, predominantly children, have been recognized both in- and outside Europe

AFM 2020 Outbreak

In August 2020 the USA the CDC has issued a warning about Acute flaccid myelitis (AFM) is an uncommon, but life-threatening neurologic condition that affects mostly children and can lead to permanent paralysis.

Enteroviruses, particularly EV-D68, are likely responsible for the increase in cases every two years since 2014.

Source

AFM Symptoms

• AFM typically presents with sudden limb weakness. Most patients had respiratory illness or fever before AFM onset.
• Patient health can decline quickly, resulting in paralysis or the need for a ventilator. AFM can lead to permanent disability.
• Patients who tested positive for EV-D68 typically had more severe AFM illness, requiring hospitalized intensive care and ventilation.
• Most cases occur between August and November.

Checklist for Possible AFM

• Muscle strength in all four limbs (What is their strength? Can they move the limb against gravity with resistance?)
• Muscle tone (Is it loose/floppy?)
• Reflexes (Are they hypo-, hyper-, or absent?)
• Cranial nerve assessment (Are there any cranial nerve deficits?)

First identified in California in 1962, enterovirus D68 (EV-D68) is one of more than 100 non-polio enteroviruses.

Where does Enteroviruses EV-D68 come from?

While they have found the infection to be highly contagious studies done into the origin is still largely unknown “In this series of patients identified in California from June 2012 through July 2015, clinical manifestations indicated a rare but distinct syndrome of acute flaccid paralysis with evidence of spinal motor neuron involvement. The etiology remains undetermined, most patients were children and young adults, and motor weakness was prolonged.” ¹

AFM Infection rates

A Study on recovery notes with AFM patients. ²

• 5–39% of patients with AFM recover partially to completely
• 78% – Most patients with AFM were hospitalized.
• 18% – Admitted to the ICU

Large EV-D68 Outbreak happened in 2014. How many people got sick?

In summer and fall 2014, the United States experienced a nationwide outbreak of EV-D68 associated with severe respiratory illness. From mid-August 2014 to January 15, 2015, CDC or state public health laboratories confirmed 1,395 people in 49 states and the District of Columbia with respiratory illness caused by EV-D68. Almost all of the confirmed cases were among children, many whom had asthma or a history of wheezing. Additionally, there were likely many thousands of mild EV-D68 infections for which people did not seek medical treatment and/or get tested. This was the first documented nationwide outbreak of EV-D68. Although illness associated with EV-D68 is not notifiable, circulation of this virus occurs most often in late summer and fall, which is the typical enterovirus season.

CDC received about 2,600 specimens for enterovirus testing during 2014, which was substantially more than usual. About 39% of those tested positive for EV-D68. 

Enterovirus infections and type 1 diabetes

In 1979 they found an association between enterovirus infections and type 1 diabetes. In 2009 they found in experimental models, like enterovirus-infected mice or in vitro-cultured beta cells, have provided important information about possible mechanisms, but still it is not known how beta cells are destroyed in human beings. The ongoing prospective studies will answer many open questions, and should the association still hold true, intervention trials will be needed to confirm causality. Even if enterovirus infections were not associated with all diabetes cases but rather with a subgroup of them, this would offer attractive possibilities to prevent the disease or part of it, for example, by an enterovirus vaccine. – ³

Alternative cause EV-D68

As we have already established the source of the infection still have not been found, what is this mystery illness relates to a thiamine induced deficiency let me explain.

Thiamine Deficiency and EV-D68 common symptoms

• Limb weakness.
• Loss of muscle function in the legs.
• muscle paralysis
• Neurological symptoms 
• Mental confusion
• Rapid heart rate
• Chest pain

Sulfur possible cause EV-D68 thiamine deficiency increasing

This unidentified enterovirus ( respiratory illness ) is the first step to full blown acute flaccid myelitis ( paralysis ). These very same symptoms, from outbreaks of respiratory illness to paralysis to death, have been observed in cattle for many years.

In veterinarian medicine it is know as Polioencephalomalacia ⁴ ( PEM ), which causes polio like symptoms and has been on the rise recently.

“Polioencephalomalacia (PEM) is an important neurologic disease of ruminants that is seen worldwide. Cattle, sheep, goats, deer, and camelids are affected. The term PEM denotes a lesion with certain gross and microscopic features that are not specific for a particular etiology or pathogenesis. Historically, PEM has been associated with altered thiamine status, but more recently an association with high sulfur intake has been observed. “ ⁵

The altered thiamine status is called thiaminase-induced diseases which means the food is acting to block absorption of thiamine or destroying it in the gut before it can be taken up.

Sulfur is added to the corn mash in the production of ethanol.
The corn mash known as distillers grain, which is known to be high in sulfur, is then fed to cattle ( dairy products and meat ), pigs and chickens ( eggs ) which are consumed by humans.

Children consume more of these products then adults in the way of milk and meats as fast foods and school lunches and at home as “lean” ground meat.

North Carolina dairy farmer lost half his cattle

In an article in 2014 one farmer on one North Carolina dairy farm is finding his cows are getting sick with “cows had neurologic signs,” while others had “severe foot problems” and “bleeding from the nose.” he has lost 325 of his 500 cattle in a 4 year period, he believes it was the sulfur added into the grain he feeds his cows. ⁶

I do find it interesting when it was so bad for that farmer in 2014 is the time the outbreak of AFM was first seen.

Australia Study on PEM by sulphur poisoning

In Australia they pointed out that PEM caused by sulphur poisoning has not been proven in WA yet, but is becoming common elsewhere in the world. It may occur when dietary sulphur exceeds 0.4% of total diet. For example, this might occur when gypsum or ammonium sulphate is included in a feedlot ration, especially when stock has access to water with high sulphur content. And sadly Thiamine injections treat the thiamine deficiency, but will not fix the problem of thiaminase-producing bacteria in the rumen, meaning there is the potential for relapse. Providing the animal with a high-quality hay diet and an oral supplement of thiamine will help significantly in returning thiamine availability in the rumen to normal. ⁷

High Sulphur in Pet Foods causing brain damage

In 2014 Dr Anne Fawcett treated a thiamine deficient cat fed exclusively on supermarket bought kangaroo meat packaged for pets. The food was tested and found to have concentrations of sulphur dioxide almost double that allowed for human consumption. Sulphur dioxide is a known cause of thiamine deficiency in humans and animals.

Some pet food suppliers treat products with high levels of sulfur dioxide to preserve the meat and to disguise signs of petrification.

“A one-off meal won’t hurt but over time these levels of sulphur dioxide cause vitamin b deficiency which causes brain damage.”
Dr Anne Fawcett

“I thought I was doing the right thing and feeding her nice ‘roo meat and it nearly killed her. My dog and cat are like children to me, so it was horrific.

“I am angry beyond imagination to find I had done this to my cat,” she said. ⁸

Conclusion

While the manifestation of AFM is infectious the origins of AFM is unknown, I propose that it may be bacteria infection run out of control from a thiamine imbalance which may be caused by an imbalance in our food supply not seen in the USA until 2014, coupled with a child’s low immunity to enteroviruses and today’s forms of processed foods which all require thiamine to process may be getting worse with imbalances of minerals found in food sources today.

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