Dogs and cats largely depend on the dietary intake of thiamine to achieve thiamine requirements that the body needs to function normally.
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.
The Maltese Terrier dog was presented to a referring veterinarian with a 3‐day history of:
- 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.
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.
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.
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.