Understanding Antibiotic Classifications: A Comprehensive Guide
Antibiotics are essential tools in modern medicine, used to combat bacterial infections that could otherwise lead to severe health issues or even death. To use these powerful drugs effectively, it’s crucial to understand the different classifications of antibiotics, which are based on their chemical structure, mechanism of action, and spectrum of activity. This article explores the main classifications of antibiotics, providing an overview of their uses and how they work. Beta-Lactam Antibiotics Examples: Penicillins, Cephalosporins, Carbapenems, Monobactams Mechanism of Action: Beta-lactam antibiotics work by inhibiting the synthesis of bacterial cell walls. They target the penicillin-binding proteins (PBPs) that are crucial for forming peptidoglycan, a key component of the bacterial cell wall. By disrupting this process, beta-lactams weaken the bacterial cell wall, leading to cell lysis and death. Uses: These antibiotics are widely used to treat a variety of infections, including respiratory tract infections, urinary tract infections, skin infections, and more. Penicillins are often the first line of defense against many common bacterial infections. Macrolides Examples: Erythromycin, Azithromycin, Clarithromycin Mechanism of Action: Macrolides inhibit bacterial protein synthesis by binding to the 50S ribosomal subunit, preventing the translocation of peptides. This action effectively stops the bacteria from growing and multiplying. Uses: Macrolides are particularly useful for treating respiratory infections, such as pneumonia and bronchitis, as well as skin infections. They are also an alternative for patients allergic to penicillin. Tetracyclines Examples: Tetracycline, Doxycycline, Minocycline Mechanism of Action: Tetracyclines inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit. This prevents the attachment of aminoacyl-tRNA to the mRNA-ribosome complex, thereby halting protein synthesis and bacterial growth. Uses: Tetracyclines are used to treat a variety of infections, including skin infections, respiratory tract infections, and urinary tract infections. Aminoglycosides Examples: Gentamicin, Amikacin, Tobramycin Mechanism of Action: Aminoglycosides bind to the 30S subunit of bacterial ribosomes, leading to the misreading of mRNA. This causes the bacteria to produce faulty proteins, ultimately leading to cell death. Uses: These antibiotics are often used to treat serious infections caused by Gram-negative bacteria, such as sepsis, endocarditis, and complicated urinary tract infections. Due to their potential for toxicity, they are usually reserved for severe infections. Fluoroquinolones Examples: Ciprofloxacin, Levofloxacin. Mechanism of Action: Fluoroquinolones inhibit bacterial DNA gyrase and topoisomerase IV, enzymes critical for DNA replication and transcription. By disrupting these processes, fluoroquinolones prevent bacterial cell division and lead to cell death. Uses: Fluoroquinolones are used to treat a variety of infections, including respiratory tract infections, urinary tract infections, gastrointestinal infections, and skin infections. Sulfonamides Examples: Sulfamethoxazole, Sulfadiazine Mechanism of Action: Sulfonamides inhibit dihydropteroate synthase, an enzyme involved in folate synthesis in bacteria. Folate is necessary for DNA synthesis and cell division, so its inhibition leads to bacterial growth arrest. Uses: Sulfonamides are commonly used in combination with trimethoprim (e.g., as co-trimoxazole) to treat urinary tract infections, respiratory infections, and some types of diarrheas. Glycopeptides Examples: Vancomycin Mechanism of Action: Glycopeptides inhibit bacterial cell wall synthesis by binding to the D-alanyl-D-alanine termini of cell wall precursor units. This prevents the cross-linking of peptidoglycan chains, which is essential for bacterial cell wall strength and rigidity. Uses: Glycopeptides are used primarily to treat serious Gram-positive infections, especially those caused by methicillin-resistant Staphylococcus aureus (MRSA) and other resistant organisms. Oxazolidinones Examples: Linezolid, Tedizolid Mechanism of Action: Oxazolidinones inhibit protein synthesis by binding to the 50S subunit of the bacterial ribosome, preventing the formation of a functional initiation complex for protein translation. Uses: Oxazolidinones are used to treat serious infections caused by Gram-positive bacteria, including MRSA and vancomycin-resistant enterococci (VRE).
Fowl Pox
Bioguard Corporation Fowl pox is a slow-spreading viral disease affecting chickens, turkeys, and various other birds. It is characterized by proliferative skin lesions that develop into thick scabs (cutaneous form) and lesions in the upper respiratory and digestive tracts (diphtheritic form). A presumptive diagnosis can be made in the field based on distinctive skin lesions, but confirmation requires detecting cytoplasmic inclusion bodies in affected cells. Etiology Fowl pox has a world-wide distribution and is caused by a DNA virus of the genus Avipoxvirus of the family Poxviridae. Virions are somewhat pleomorphic, generally brick-shaped (220–450 nm long×140–260 nm wide×140–260 nm thick) with a lipoprotein surface membrane displaying tubular or globular units (10–40 nm). The large DNA virus is resistant and may survive in the environment for extended periods in dried scabs. Avipoxvirus affecting more than 230 species in 23 orders of wild and domesticated birds. Within the Avipoxvirus genus there are currently 10 recognized species: : Fowlpox virus, Canarypox virus, Juncopox virus, Mynahpox virus, Psittacinepox virus, Sparrowpox virus, Starlingpox virus, Pigeonpox virus, Turkeypox virus, and Quailpox virus, according to the International Committee on Taxonomy of Viruses. Transmission The fowl pox virus is abundant in lesions and typically spreads through contact with skin abrasions. Scabs shed from recovering birds in poultry houses can become airborne, leading to infection. Mosquitoes and other biting insects can also act as mechanical vectors, rapidly spreading the virus when mosquitoes are prevalent. The virus is highly resistant in dry scabs, making it easy to transmit to uninfected birds. Fowl pox can affect birds of any age and may occur year-round. Clinical signs Clinical signs are somewhat variable depending on the host species, virulence of the virus strain, distribution of lesions, and other complicating factors. In chickens and turkeys, signs may vary with two overlapping forms of the disease: Cutaneous (dry pox): The dry form begins with a pimple or scab on non-feathered areas of the skin such as the comb, wattles, eyelids, feet, and legs. Eventually, the infection may spread to other feathered areas of the body. Infected birds often have difficulty eating and reduced feed intake and weight loss is common. Cutaneous lesions on the eyelids may cause complete closure of one or both eyes. Diphtheritic (wet pox): The wet form produces diphtheritic, yellow canker lesions on oral mucous membranes, tongue, esophagus, or trachea. Lesions in the upper digestive and respiratory tract may result in inappetence and dyspnea, respectively. Other mild to severe respiratory signs may also occur. Lesions in the eye and nasal cavity lead to ocular or nasal discharges. Diagnosis: A presumptive diagnosis can be made in the field based on characteristic skin lesions. The diagnosis should be confirmed by laboratory testing. Microscopic examination of affected tissue sections stained with H&E reveals eosinophilic cytoplasmic inclusion bodies. Inclusions are also detected by fluorescent antibody and immunoperoxidase methods. Viral particles, with typical poxvirus morphology, can be detected by electron microscopy. The virus can be isolated in the chorioallantoic membrane (CAM) of chicken embryos, susceptible birds, or avian cell cultures. Field viruses can be detected in the laboratory by polymerase chain reaction (PCR). Prevention and Control Fowl pox and pigeon pox live virus vaccines are commonly used for immunization of chickens. Vaccination effectively prevents the disease and may limit spread within actively infected flocks. No treatment exists for birds infected with avian pox viruses. References Giotis ES, Skinner MA. Spotlight on avian pathology: fowlpox virus. Avian Pathol. 2019 Apr;48(2):87-90. Molini U, Mutjavikua V, de Villiers M et al. Molecular characterization of avipoxviruses circulating in Windhoek district, Namibia 2021. J Vet Med Sci. 2022 May 25;84(5):707-711.
Factor VII Deficiency in Dogs
Bioguard Corporation Canine Factor VII (FVII) deficiency is an autosomal recessive genetic disorder that leads to a mild to moderate blood clotting problem in affected dogs. Puppies with the condition may exhibit symptoms such as nosebleeds (epistaxis) and gum bleeding, while adult dogs are more prone to bruising and skin issues like dermatitis. Though bleeding episodes tend to decrease in severity as the dog matures, the disorder still causes ongoing issues throughout the animal’s life. FVII deficiency was first identified in the Migluo breed. Most dogs are diagnosed when they visit a veterinarian due to accidental injury, spontaneous bleeding, genetic screening, or blood tests. Pathogenesis Hemostasis is achieved through a series of events known as the coagulation cascade, which involves two interconnected pathways: the intrinsic and extrinsic pathways. The intrinsic pathway is triggered by spontaneous internal damage to the blood vessel lining, while the extrinsic pathway is activated in response to external trauma. Factor VII (FVII) is a vitamin K-dependent glycoprotein produced in the liver and released into the bloodstream as a single-chain zymogen. Once activated, FVII plays a crucial role in initiating coagulation. Following vascular injury, FVII, along with tissue factor (TF) and calcium, activates factors IX and X, leading to thrombin production. A deficiency in FVII impairs blood clotting, resulting in excessive bleeding during injuries or surgeries. Diagnosis The Buccal Mucosal Bleeding Time (BMBT) is the most commonly used test for measuring bleeding time in small animals. To perform the BMBT, the upper lip is folded back and secured with a gauze strip around the maxilla or both the maxilla and mandible. A small incision is made in the mucosa above the premolars, avoiding areas with visibly engorged vessels. Blood from the incision is gently blotted using filter paper placed near the incision without touching it. A stopwatch starts when the incision is made and stops when no blood crescent forms on the filter paper. To reduce variability, the same person should perform the BMBT whenever possible. Activated Partial Thromboplastin Time (APTT) measures the overall speed of blood clot formation through the intrinsic and common coagulation pathways. It assesses the activity of factors XII, XI, IX, VIII, X, V, II, I, as well as prekallikrein (PK) and high molecular weight kininogen (HK). Prothrombin Time (PT) is used to evaluate the extrinsic and common pathways of coagulation by measuring factors VII, X, V, II, and I. Factor VII deficiency is suspected when a dog presents with a prolonged PT and normal BMBT and APTT. Genetic testing can also identify affected dogs or carriers, especially in certain breeds. Breeds at Risk Canine Factor VII deficiency has been documented in several breeds, including the Beagle, Airedale, Alaskan Klee Kai, American Foxhound, Finnish Hound, German Wirehaired Pointer, Giant Schnauzer, Irish Water Spaniel, Japanese Spitz, Miniature Schnauzer, Papillon/Phalene, Sealyham Terrier, Scottish Deerhound, and Welsh Springer Spaniel. Management There is currently no cure for Factor VII deficiency. However, clinical symptoms can be managed through transfusions with fresh plasma or blood, or by administering recombinant activated human FVII. These treatments provide only temporary relief. Fortunately, dogs with mild to moderate FVII deficiency typically lead normal lives. References Callan MB, Aljamali MN, Margaritis P, Griot-Wenk ME, Pollak ES, Werner P, Giger U, High KA. A novel missense mutation responsible for factor VII deficiency in research Beagle colonies. J Thromb Haemost. 2006 Dec; 4(12):2616-22. Carlstrom LP, Jens JK, Dobyns ME, Passage M, Dickson PI, Ellinwood NM. Inadvertent propagation of factor VII deficiency in a canine mucopolysaccharidosis type I research breeding colony. Comp Med. 2009 Aug;59(4):378-82. Donner J, Kaukonen M, Anderson H, Moller F, Kyostila K, Sankari S, Hytonen M, Giger U, Lohi H. Genetic Panel Screening of Nearly 100 Mutations Reveals New Insights into the Breed Distribution of Risk Variants for Canine Hereditary Disorders. PLoS One. 2016 Aug 15;11(8):e0161005. Kaae JA, Callan MB, Brooks MB. Hereditary factor VII deficiency in the Alaskan Klee Kai dog. J Vet Intern Med. 2007 Sep-Oct;21(5):976-81.
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.
