Pyruvate Kinase Deficiency in Dogs
Bioguard Corporation Pyruvate kinase deficiency (PKD) is a hereditary genetic disorder that impairs the ability of red blood cells to metabolize properly. This defect leads to the destruction of red blood cells, resulting in severe hemolytic anemia. Affected animals can die from complications such as severe anemia and liver failure. The condition typically manifests between 4 months and 4 years of age, with common clinical signs including weakness, increased heart rate, and heart murmurs. Pathogenesis In mammals, mature red blood cells lack mitochondria, which means they cannot produce energy through oxidative phosphorylation. Instead, they rely on glycolysis to generate ATP, which is essential for maintaining cell shape and active transport across cell membranes. Pyruvate kinase (PK) plays a key role in the final step of glycolysis, where it catalyzes the conversion of phosphoenolpyruvate into pyruvate, producing ATP in the process (as shown in the diagram below). When PK is deficient, red blood cells cannot synthesize sufficient ATP, leading to impaired cell metabolism. This energy deficit causes premature red blood cell death and results in hemolytic anemia. PKD is an autosomal recessive disorder caused by mutations in the PK-LR gene, which affects the activity of pyruvate kinase. Clinical Symptoms Pyruvate kinase deficiency (PKD) typically presents between 4 months and 4 years of age, causing severe chronic hemolytic anemia. Affected dogs may display symptoms such as exercise intolerance, severe limb weakness, easy fatigue, lethargy, underweight, pale gums, weight loss, emaciation, stunted growth, poor posture, and an increased heart rate. Ultrasound exams may reveal an enlarged liver and spleen, with common findings like bone sclerosis and hemosiderosis/hemochromatosis. Treatment and Prevention Currently, there is no effective drug treatment or way to slow the progression of PKD. The only treatment option is bone marrow transplantation, which may allow dogs to live a normal lifespan. However, this treatment is costly and carries a risk of death. Without treatment, affected dogs typically succumb to severe hemolytic anemia and liver failure. Genetic testing can identify PKD defects early in dogs and cats, enabling timely intervention and care. Affected Breeds Research indicates that certain dog breeds are more predisposed to inheriting PKD, including: Basenjis, Labrador Retrievers, Pugs, West Highland White Terriers, Cairn Terriers, Dachshunds, Terriers, Miniature Poodles, Chihuahuas, and American Huskies. Among cat breeds, Somali and Abyssinian cats are commonly affected, along with Egyptian Maus, LaPerms, American Shorthairs, Bengals, Maine Coons, Norwegian Forest Cats, Siberians, and Singapuras. Genetic Detection Genetic testing can determine whether dogs and cats carry PKD defects. Carriers may pass the gene on to offspring, so they should not be bred. If an animal tests positive for PKD, early monitoring and care are essential to manage the disease. References Chapman, B.L., & Giger, U. (1990). Inherited erythrocyte pyruvate kinase deficiency in the West Highland White Terrier. Journal of Small Animal Practice, 31, 610-616. Schaer, M., Harvey, J.W., Calderwood-Mays, M., & Giger, U. (1992). Pyruvate kinase deficiency causing hemolytic anemia with secondary hemochromatosis in a Cairn Terrier. Journal of the American Animal Hospital Association, 28(3), 233-239. Gultekin, G.I., Raj, K., Foureman, P., Lehman, S., Manhart, K., Abdulmalik, O., & Giger, U. (2012). Erythrocytic pyruvate kinase mutations causing hemolytic anemia, osteosclerosis, and secondary hemochromatosis in dogs. Journal of Veterinary Internal Medicine, 26(4), 935-944.
Juvenile Hereditary Cataracts in Dogs
Bioguard Corporation Canine juvenile cataract (JHC) is a hereditary form of cataract characterized by cloudiness and degeneration of the lens in the eye. This condition prevents light and images from passing through the lens to the retina, impairing the dog’s vision and eventually leading to blindness. Affected dogs may exhibit symptoms such as bumping into furniture, losing direction, and moving slowly. JHC can also lead to intraocular complications, including uveitis, glaucoma, and lens luxation. Dogs are more prone to cataracts than any other species, and while cataracts can develop at any age, juvenile cataracts typically occur in dogs under 7 years old. Genetic mutaion related to JHC JHC is caused by a mutation in the heat shock transcription factor 4 (HSF4) gene, leading to an autosomal recessive inheritance pattern. Assuming that “A” represents a normal allele and “a” a mutated allele, an individual will exhibit symptoms of the disease only if both alleles are mutated (aa). Diagnosis A comprehensive ophthalmological examination is essential to assess the severity of cataracts and identify any associated complications. This examination typically includes tests for vision, pupillary light reflex, cataract severity and grading, and checks for any concurrent eye diseases or complications. Additional tests may include intraocular pressure measurement, tear production evaluation, corneal health assessment, fundus reflex and retinal examination, and ocular ultrasound. Genetic testing can further confirm the presence of genetic defects and is valuable as a pre-breeding health check to prevent the transmission of hereditary cataracts to offspring. Affected Breeds Breeds that are particularly prone to hereditary cataracts include Poodles, Cocker Spaniels, Boston Terriers, Siberian Huskies, Karelian Bears, Wire-haired Fox Terriers, Old English Sheepdogs, Golden Retrievers, and Labradors. It is recommended to conduct genetic testing before breeding these dogs to reduce the risk of producing affected offspring. Stages Cataracts can be classified into four stages based on the degree of lens opacity: Initial Stage: A distinct opaque white spot appears in the center of the pupil, but vision remains unaffected. Immature Stage: The lens begins to thicken both in the front and back, showing partial cloudiness. Vision becomes blurry, especially in low-light conditions, although some vision is still retained. Mature Stage: The entire lens becomes fully opaque and thickened, resulting in complete vision loss. Hypermature Stage: The clouded lens begins to shrink and clear up, making this stage prone to additional complications such as uveitis, glaucoma, and severe intraocular inflammation. This stage may also involve lens dislocation or fibrosis of the posterior capsule. Impacts and Complications The most noticeable early sign of cataracts is a change in eye color, where the lens begins to appear cloudy and white. It’s important to distinguish this from nuclear sclerosis, a common condition in older dogs. As the lens becomes cloudier, a dog’s vision deteriorates, leading to unintentional collisions with objects and increased sensitivity to the environment, often giving the dog a distant or blank stare. Cataracts typically worsen over time, resulting in a range of eye-related complications. These can include increased sensitivity, lens-induced uveitis (LIU), glaucoma, and the rupture of zonular fibers around the lens, which may cause lens dislocation or subluxation, as well as opacification of the posterior capsule. As cataracts progress to the hypermature stage, additional complications such as intraocular bleeding, retinal detachment, and further instances of glaucoma may arise. Early diagnosis and treatment are essential for managing these complications effectively and improving the overall prognosis. Diagnosis A comprehensive ophthalmological examination is essential to assess the severity of cataracts and identify any associated complications. This examination typically includes tests for vision, pupillary light reflex, cataract severity and grading, and checks for any concurrent eye diseases or complications. Additional tests may include intraocular pressure measurement, tear production evaluation, corneal health assessment, fundus reflex and retinal examination, and ocular ultrasound. Genetic testing can further confirm the presence of genetic defects and is valuable as a pre-breeding health check to prevent the transmission of hereditary cataracts to offspring. References Mellersh CS, McLaughlin B, Ahonen S, Pettitt L, Lohi H, Barnett KC. Mutation in HSF4 is associated with hereditary cataract in the Australian Shepherd. Vet Ophthalmol. 2009 Nov-Dec; 12(6):372-8. Mellersh CS, Pettitt L, Forman OP, Vaudin M, Barnett KC. Identification of mutations in HSF4 in dogs of three different breeds with hereditary cataracts. Vet Ophthalmol. 2006 Sep-Oct; 9(5):369-78.
Spinal Muscular Atrophy in Cats
Bioguard Corporation Spinal muscular atrophy (SMA) an autosomally recessive inherited neurodegenerative disorder seen in Maine Coon cats. The disease is characterized by weakness and atrophy in muscles due to loss of motor neurons that control muscle movement. Affected cats first show signs of disease around 3–4 months of age. Clinical signs include tremors, abnormal posture, and weakness in muscle. Pathogenesis SMA in Maine Coon cat is caused by the deletion of a 140 kb LIX1 gene on the A1q chromosome. Although the function of LIX1 is not yet clear, it is presumed to be related to RNA metabolism. The LIX1 is highly expressed in the central nervous system, primarily in spinal motor neurons, thus offering explanation of the restriction of their function in case of feline SMA. The disease is inherited as an autosomal recessive. Clinical signs In the earliest stages of SMA, a vet or other professional will be able to notice a slight weakness in the affected kittens. Subtle tremors in a kitten’s hind legs can also be an early symptom of SMA. Within 1 to 2 months after the symptoms appear, the muscles will gradually atrophy. After that, the symptoms will gradually become serious, the movements will become clumsy, the agility will be lost in jumping, and even breathing symptoms will appear. Muscle atrophy affects only the hind legs, and some severely affected cats move by crawling on the front legs, although mental status is not affected. The condition slowly stabilizes after up to 8 months, and some cats with SMA have more or less severe symptoms for up to 9 years. Diagnosis The first step is a general physical exam. Your doctor will look for muscle weakness and any other signs of SMA. Serum creatine kinase (creatine) elevations and electrical findings in cats are very similar to mild spinal muscular atrophy in humans. Examination of the muscles reveals neurogenic atrophy, and examination of the central and peripheral nervous systems will reveal loss of anterior horn cells. To ascertain if a cat has SMA, the diagnostic approach encompasses a physical examination, electromyography, muscle biopsy, testing for serum creatine kinase levels, and genetic testing, all aimed at facilitating early identification and intervention. Since SMA is common in Maine Coons, it is recommended that Maine Coons with similar symptoms or those intended for breeding undergo this test. References Fyfe JC, Menotti-Raymond M, David VA, et al. An approximately 140-kb deletion associated with feline spinal muscular atrophy implies an essential LIX1 function for motor neuron survival. Genome Res. 2006 Sep;16(9):1084-90.
Polycystic Kidney Disease in Cats
Bioguard Corporation Polycystic kidney disease (PKD) is a chromosomally dominant genetic disorder; it can occur in humans, cats, dogs, and other animals. In the renal cortex and medulla, there are cysts of various sizes and fluid-filled, so it is commonly known as the bubble kidney. Cysts increase in size and number over time, replacing kidney tissue and affecting their ability to filter waste from the blood, leading to chronic kidney failure. Pathogenesis Polycystic kidney disease is primarily caused by point mutations in the PKD1 gene, which is inherited as a dominant genetic disorder. The PKD1 gene plays a crucial role in regulating polycystin, a protein found on the cell membrane. A deficiency in PKD1 leads to underdevelopment of the renal tubules and collecting ducts in the renal cortex and medulla, preventing proper drainage of urine filtered by the renal glomeruli, which results in the formation of cysts characteristic of polycystic kidney disease. In the liver, this condition can also cause significant enlargement of bile ducts near the portal vein and may lead to bile duct fibrosis. Clinical symptoms Cats with polycystic kidney disease (PKD) are born with abnormal kidneys, though symptoms typically do not manifest until they are between 3 and 10 years old, with an average onset around 7 years. While the disease is present from birth, there are no noticeable symptoms in its early stages. Symptoms appear only when the disease progresses to a point where kidney tissue necrosis and kidney failure occur. As renal cysts enlarge over time, they compress the renal parenchyma, leading to irreversible kidney failure. Affected cats may experience a decreased appetite, weight loss, depression, and lack of energy. Clinical symptoms include increased thirst (polydipsia), frequent urination (polyuria), anorexia, vomiting, lethargy, and muscle twitching in the abdominal area. In severe cases, movement disorders (ataxia) or neurological issues may arise. Blood tests may reveal elevated blood urea nitrogen (BUN) and creatinine (CRE) levels, anemia, and high blood pressure. Early detection At present, it is possible to know whether cats have polycystic kidney disease through ultrasound testing and genetic testing. At 16 weeks of age, about 75% of cats with this problem had cyst-like structures on ultrasound scans, and by 36 weeks of age, 91% of cats had cysts. The accuracy of such a structure increases with age; generally speaking, when cats are over 10 weeks old, when using ultrasonic scanning, the accuracy can reach 90~95%. Genetic testing, which refers to the detection of its genotype, will be 100% accurate and can be performed at any age Breed predisposition Polycystic kidney disease mainly occurs in long-haired cats, and studies have shown that up to 38% of Persian cats have an abnormal PKD1 gene. Mainly affects cats of Persian and Persian-related breeds, such as Chinchillas, but other breeds such as Ragdolls, Scottish Folds, or other shorthair breeds such as Himalayans and Exotics have also been reported It is possible to have this genetic disorder. In addition, Meeks’s condition is relatively rare. References Schirrer L, Marín-García PJ, Llobat L. Feline Polycystic Kidney Disease: An Update. Vet Sci. 2021 Nov 8;8(11):269.
Feline Hypertrophic Cardiomyopathy
Bioguard Corporation Hypertrophic cardiomyopathy (HCM) is a primary, familial, and hereditary heart condition, and it is the most common heart disease in cats. Its key characteristic is primary concentric left ventricular hypertrophy (thickening of the heart wall), which occurs without pressure overload (such as from aortic stenosis), hormone stimulation (like in hyperthyroidism or acromegaly), myocardial involvement (such as from lymphoma), or other non-cardiac diseases. The heart consists of four chambers: the left atrium and ventricle, and the right atrium and ventricle. The right side of the heart pumps deoxygenated blood to the lungs, while the left side pumps oxygenated blood to the rest of the body. In hypertrophic cardiomyopathy (HCM), some cardiomyocytes are unable to function properly, causing the normal ones to enlarge in an attempt to maintain the heart’s output. However, this excessive thickening of the myocardium leads to a thickened left ventricle that encroaches on the ventricular space. As a result, the ventricle’s capacity to hold a normal amount of blood is reduced, and the myocardium becomes stiffer with decreased contractility. This alters the pressure within the left side of the heart, eventually causing the left atrium to enlarge. An enlarged left atrium increases the risk of congestive heart failure (CHF) in cats, which is marked by fluid accumulation in the lungs (pulmonary edema) or around the lungs (pleural effusion). HCM can occur at any age, but it is most common in adult cats around six years or older. Breeds such as Maine Coon, Ragdoll, and Domestic Shorthair are most frequently affected, while Persian, British Shorthair, and American Shorthair cats are also at higher risk. The exact cause of HCM in cats is not fully understood. Research suggests that mutations in the myosin binding protein C gene (MYBPC3) are linked to HCM in Maine Coon and Ragdoll cats. Specifically, the mutations A31P and R820W in the MYBPC3 gene are associated with this condition in these two breeds. The MYBPC3 mutation exhibits incomplete penetrance, meaning it is not a purely dominant trait. Cats with one copy of the mutated gene have a relative risk of HCM that is about 1.8 times higher than normal cats. However, cats with two copies of the mutation have a significantly higher relative risk, about 18 times greater. Despite this, some Maine Coon cats without the MYBPC3 mutation have also been diagnosed with HCM. In studies, the incidence of HCM in cats without the original mutant gene was approximately 5.4%. This indicates that while the MYBPC3 mutation is a significant factor, it is not the sole cause of HCM in Maine Coon cats, and other contributing factors remain unclear. Clinical Symptoms Most cats with HCM show no clinical symptoms, especially those with mild to moderate disease, making early detection challenging. Even severely affected cats may initially be asymptomatic but typically progress to left heart failure, systemic thromboembolism, or sudden death. Cats with heart failure exhibit signs such as shortness of breath and dyspnea due to pulmonary edema or pleural effusion. Systemic thromboembolism commonly presents as hind limb paresis or paralysis, accompanied by acute pain, lack of pulse, and fever. Genetic Testing This test is recommended for purebred cats with a genetic predisposition, especially Maine Coon and Ragdoll breeds.
Dog Frostbite: Canine Degenerative Spinal Neuropathy
Bioguard Corporation Degenerative Myelopathy, DM is a progressive chronic degenerative disease of the central nervous system, which is a recessive genetic disease that mainly occurs in the spinal nerve, similar to human amyotrophic lateral sclerosis. It is known as lou gehrig’s disease. The age of onset of dogs is between 9 and 11 years old, and the common diseased breeds will be explained later. Pathogenesis Current research points out that the cause of DM is highly correlated with the mutation of superoxide dismutase-1 (SOD 1) gene. SOD mainly plays the role of scavenging free radicals in the body. It is an important antioxidant enzyme system in the body. It can convert the more active superoxide (Superoxide, O2–) into the less active hydrogen peroxide ( H2O2) reduces excessive peroxide production in the body; however, when the SOD 1 in the dog’s body is genetically defective, free radicals cannot be eliminated. The accumulation of excessive free radicals will cause the death of motor neuron cells and produce a lot of degeneration disease. Clinical symptoms The progression of the disease can be divided into four stages based on its severity: First Stage: From complete proprioceptive dysfunction to upper motor neuron spastic paresis. Second Stage: From difficulty in standing and walking to complete paralysis of the hind limbs. Third Stage: From neuronal paralysis of the lower body to paraplegia affecting the forelimbs. Fourth Stage: From neuronal paralysis of the lower limbs to loss of brainstem function. Based on previous cases, the transition from stage 1 to stage 4 typically occurs within 6 to 9 months. The cause of the disease remains unknown, and there is currently no medication available for treatment. However, physical therapy and rehabilitation can help slow the progression of spinal cord degeneration and reduce limb atrophy. Early detection In the early stages, monitor your dog for any clinical symptoms and schedule an outpatient examination at a veterinary hospital. To diagnose degenerative myelopathy (DM), further testing may include assessing the dog’s breed, conducting neurological examinations, analyzing cerebrospinal fluid, performing X-rays, MRI scans, CT scans, and genetic testing. Early detection and treatment are crucial. Research on DM has identified degenerative spinal neuropathy in 115 dog breeds, with 48 breeds showing a high risk of SOD1 genetic defects. Note According to statistics from the American Orthopaedic Association, Corgis have the highest rate of abnormalities among all breeds. Since genetic testing began in 2008, a total of 4,428 Corgis have been tested, with the following results: 13.1% were normal, 33.6% were carriers, and 53.3% showed mutations.
GM1 Gangliosidosis in Cats
Bioguard Corporation GM1 gangliosidosis is a lysosomal storage disorder caused by deficiency of the enzyme β-galactosidase. Mutations in the GLB1 gene, encoding β-galactosidase, cause the progressive, neurosomatic, lysosomal storage disorder. Cats affected with gangliosidosis have progressive neurologic dysfunction around 3 months of age and premature death around one year old. Pathogenesis Gangliosides, normally hydrolyzed by β-galactosidase, are the main glycolipids of neuronal plasma membranes. Absent or reduced β-galactosidase activity leads to the accumulation of β-linked galactose-containing glycoconjugates including the glycosphingolipid (GSL) GM1-ganglioside in neuronal tissue. Instead of being broken down and recycled, this excess material is stored in membrane bound sacs (vacuoles) in cells. As the number of vacuoles increase, there are less available space and resources for normal cell function so that neuronal cell death and degeneration occurs, damaging the central nervous system and other organs. Clinical signs Kittens with GM1 gangliosidosis appear normal at birth and successfully achieve all developmental milestones. However, the accumulation of gangliosides in neuronal cells causes central nervous system damage. Clinical signs are apparent in cats at 2-3 months of age. Gangliosidosis is clinically characterized by discrete head and limb tremors and lack of coordination of movement. Other clinical signs include ataxia; tremor; visual disorder, which may have been due to cortical blindness; and seizures. The progressive accumulation of GM1 ganglioside in the central nervous system and cerebrospinal fluid ultimately proves fatal for cats at a young age. Diagnosis To rule other diseases causing symptoms similar to GM1 in cats, the diagnosis of gangliosidosis is carried out based on comprehensive findings using various types of specimens for histological, ultrastructural, biochemical and genetic analyses. A diagnosis of GM1 gangliosidosis requires biochemical identification of the storage product and enzyme deficiency. Affected animals had lower β-galactosidase activity in the liver and increased levels of GM1 gangliosides in the brain. In addition, DNA testing can be used to detect the mutation causing GM1 gangliosidosis in Korat cats; it can identify affected cats, carriers and normal cats, without the genetic mutation. Breeds such as the Siamese, Korat, Oriental Shorthair, Balinese, Havana Brown, Birman, Burmese, and Singapore Cat are more suscep-tible. It is recommended to conduct this test before breeding.
Bird Sexing
Bioguard Corporation Many mammals are sexually dimorphic, which means that their sex can be identified based on their appearance. However, it is not the case for most birds. Many birds are sexually monomorphic although males and females may differ markedly in size, color, and appearance in some birds, such as peacocks (Fig. 1). Knowledge of a bird’s gender is important for veterinary practitioners, ornithologists and aviculturists. Gender identification in birds is beneficial for proper pairing of birds, and preparing owners for the eventual changes their bird will experience as it matures. Furthermore, knowing the gender of a bird allows veterinarians to diagnose gender-specific diseases. Traditional sexing The traditional methods used to identify a bird’s gender include behavioral observation, morphological differences, acoustic analysis, laparoscopic examination, laparotomy, vent sexing (cloacal examination), steroid sexing, and chromosome inspection (karyotyping). These methods can be inaccurate, invasive, or costly. As an alternative to these methods, molecular DNA-based sexing methods provide fast, accurate and non-harmful to the bird. DNA sexing The XY sex-determination system is used to classify many mammals, some insects (Drosophila), and some plants (Ginkgo tree). In this system, most females have two of the same kind of sex chromosome (XX), while most males have two distinct sex chromosomes (XY). The sex of birds is determined by the ZW sex determination system. Females have the heterogametic sex chromosomes ZW, whereas males have the homogametic ZZ. The standard method of molecular sexing in birds relies on PCR amplification of non-coding sequences (introns) located in the sex-chromosome-specific gene encoding the Chromo-Helicase-DNA binding protein (CHD1), and mapping on the sexual W (CHD-W) and Z chromosomes (CHD-Z). The length polymorphisms between CHD-W and CHD-Z alleles allows for sex discrimination. Amplification of the CHD gene leads to a single amplicon in males and two distinct amplicons in females. In addition to PCR, other PCR-based technologies have been applied to avian sexing, including Single Strand Conformation Polymorphism (SSCP), Restriction Fragment Length Polymorphism (RFLP), and Amplified Fragment Length Polymorphism (AFLP). These methods, however, are not viable for commercial use. Conclusion DNA sexing provides over 99.99% accuracy in determining a bird’s gender. This testing allows bird owners to quickly and accurately identify their birds’ gender, thereby enhancing the efficiency of pairing for breeding and conservation efforts.
Polyomavirus in Birds
Long Pham Avian polyomavirus in birds poses a significant concern for caged birds, leading to substantial economic losses for pet retailers and bird enthusiasts. Initially identified in budgerigars during the early 1980s in Ontario, Canada and in the southern regions of the United States, it was initially termed Budgerigar Fledgling Disease Virus. This nonenveloped DNA virus belongs to a single genus Polyomavirus in the family Polyomaviridae. Further research revealed its ability to infect various species of psittacine birds, leading to its designation as avian polyomavirus. Avian polyomavirus is widespread, affecting psittacine birds in numerous countries, making it a notable concern in aviculture. Transmission Polyomavirus is typically transmitted through direct contact with infected birds. Additionally, transmission can occur through contact with contaminated feces, dander, air, nest boxes, incubators, feather dust, or from infected parent birds passing it to their chicks. Clinical signs Young birds, ranging from newborns to juveniles (14-56 days), are particularly vulnerable to polyomavirus infection, which is often fatal. Following infection, it typically takes 10-14 days for birds to display symptoms. However, some birds may remain asymptomatic. If symptoms do appear, the bird’s death may be imminent, often occurring within one or two days. The virus compromises the bird’s immune system, making it susceptible to other pathogens such as viruses, bacteria, fungi, and parasites, leading to secondary infections and eventual demise. Common symptoms of polyomavirus infection in birds include lethargy, regurgitation, cutaneous hemorrhage, abdominal distention, excessive urination, diarrhea, tremors, and feather abnormalities. Diagnosis The typical antemortem diagnosis involves using PCR on cloacal swabs, blood samples, and affected feather samples. It also includes conducting virus-neutralizing antibody tests on blood samples to identify birds that have previously been exposed to the virus. In a flock setting, diagnosis is commonly based on clinical observations, the characteristics of the affected birds, and findings from necropsies. Treatment and Prevention Aviary management strategies include avoiding housing budgerigars or lovebirds with other species, maintaining strict hygiene protocols, restricting access to the nursery, and enforcing a 90-day quarantine with testing before introducing new birds. Removing Avian Polyomavirus (APV) from an infected budgerigar aviary is complex and involves stopping breeding for six months. During this period, infected neonates, fledglings, and adult birds must be isolated while the aviary undergoes thorough disinfection. Nest boxes should be disinfected or replaced. After six months, breeding can resume in a sanitized environment. Preventive measures for pet stores include separating neonates from different sources, sourcing birds from facilities conducting polyomavirus testing and vaccination, and ideally avoiding transactions involving unweaned birds. References Bernier, G., M. Morin, and G. Marsolais. 1981. A generalized inclusion body disease in the Budgerigar (melopsittacus undulatus) caused by a papovavirus-like agent. Avian Diseases 25:1083-1092. Latimer, K. S., F. D. Niagro, R. P. Campagnoli, B. W. Ritchie, D. A. Pesti, and W. L. Steffens. 1993. Diagnosis of concurrent avian polyomavirus and psittacine beak and feather disease virus infections using DNA probes. Journal of the Association of Avian Veterinarians 7:141–146. Samanta, I., and S. Bandyopadhyay. 2017. Infectious diseases. Pet bird diseases and care 13–166.
Severe Fever with Thrombocytopenia Syndrome
Bioguard Corporation Severe Fever with Thrombocytopenia Syndrome (SFTS) is an emerging infectious disease that was first reported in China in 2011. It is caused by the Severe Fever with Thrombocytopenia Syndrome virus (SFTSV) and is transmitted to humans and animals through the bite of an infected tick. The main clinical symptoms of SFTS include fever, vomiting, diarrhea, multiple organ failure, thrombocytopenia, leucopenia, and elevated liver enzyme levels. SFTSV has been detected in both domestic and wild animals, although most vertebrate animals were found to be sub-clinically infected with SFTSV. Pathogen SFTSV is a tick-borne virus belonging to the Genus Bandavirus (former Huaiyangshan Banyangvirus), Family Phenuiviridae. Vector and Disease Transmission The exact lifecycle and transmission mechanisms of SFTSV are not fully understood. However, ticks, particularly the Asian longhorned tick (Haemaphysalis longicornis), are believed to be the primary route of transmission. Other ticks, including Rhipicephalus sanguineus and Haemaphysalis concinna, have also been found to carry SFTSV. This suggests that ticks play a significant role in the transmission of SFTSV, similar to other members of the Phenuiviridae family, which are also known to be vector-borne. SFTSV Transmission Ticks are believed to be the primary vectors for SFTSV transmission, mainly through their bites. However, the virus can also be transmitted by infected animals or humans. Transmission of SFTSV from infected companion animals, such as cats and dogs, to humans has been reported through various routes. Pathogenesis Cytokine storm is thought to play a crucial role in the pathophysiology of SFTS. During the acute phase of the disease, the release of cytokines triggers a systemic inflammatory response. Histopathological examination of lymph nodes reveals necrosis and hemophagocytosis. The virus can be detected in the liver, spleen, adrenal glands, bone marrow, and lymph nodes. Thrombocytopenia may occur due to viral attachment to platelets, which are subsequently cleared by the spleen. SFTSV and Animal SFTSV has been detected in both domestic and wild animals; however, most vertebrate animals appear to be sub-clinically infected. Previous research indicates that antibodies (IgG/IgM) against SFTSV were found in goats and sheep (45.70%), cattle (36.70%), dogs (27.00%), chickens (9.60%), pigs (3.20%), and rodents (3.20%). A survey conducted in Taiwan identified SFTSV in Rhipicephalus microplus ticks collected from cows and goats, and antibodies against SFTSV were also detected in goats. In experimental studies, four out of six cats infected with SFTSV died, displaying symptoms as severe or more severe than those observed in human patients (Scientific Reports, 2019). Additionally, two captive cheetahs in a Japanese zoo died of SFTS in 2017, and there have been reports of fatal SFTSV cases in cats in Japan. References Casel MA, Park SJ, Choi YK. Severe fever with thrombocytopenia syndrome virus: emerging novel phlebovirus and their control strategy. Exp Mol Med. 2021 May;53(5):713-722. Seo JW, Kim D, Yun N, et al. Clinical Update of Severe Fever with Thrombocytopenia Syndrome. Viruses. 2021 Jun 23;13(7):1213. Sharma D, Kamthania M. A new emerging pandemic of severe fever with thrombocytopenia syndrome (SFTS). Virusdisease. 2021 Jun;32(2):220-227.
