Pancreatitis in Dogs
Dr. Sushant Sadotra Canine Pancreatitis is one of the most common endocrine diseases occurring in dogs. However, it is more prevalent in dog breeds such as Miniature Schnauzers, Yorkshire Terriers, Cocker Spaniels, Dachshunds, Poodles, and sled dogs. Pancreatitis, a severe inflammatory condition of the pancreas, can be short-term or long-term, based on the level of pancreatic tissue damage. It can be of acute or chronic type. It can be related to various clinical or subclinical signs and potentially life-threatening. Causes: Pathogenesis In the initial stages of Pancreatitis, the pancreatic juice is secreted in lesser amounts. Inside the pancreas, a series of steps lead to the activation of pancreatic enzymes. Co-localization of zymogen granules and lysosomes activates trypsinogen to trypsin, which further activates other zymogens. Premature activation of these digestive enzymes causes local damage such as edema, bleeding, inflammation, and necrosis of the pancreas. The inflammation process invites WBCs to the site and increases cytokine production. Altogether, this will cause further damage to pancreases and other distant complications such as generalized inflammation, disseminated intravascular coagulation, disseminated lipodystrophy, hypotension, renal failure, pulmonary failure, myocarditis, etc. Clinical Findings: Some of the most common symptoms in dogs are: The milder form of Pancreatitis can be related to subclinical or may have minor or nonspecific signs of anorexia, lethargy, or diarrhea. Diagnosis: Among all the methods discussed, histopathology is the gold standard for the diagnosis of canine Pancreatitis. However, a combination of mentioned techniques can be implemented in clinical practice for the most reliable and accurate diagnosis. Treatment: Careful monitoring and supportive veterinary care should be given in acute cases to prevent systemic complications. If a dog with chronic pancreatitis has no sign of improvement, additional trial therapy with an immunosuppressive agent such as prednisone, prednisolone, or cyclosporine may be prescribed for the treatment. Treatment for chronic pancreatitis is challenging because of systemic complications such as hypothermia, acidosis, hypocalcemia, and single- or multiple-organ failure. Reference: Watson, P. (2015), Pancreatitis in dogs and cats: definitions and pathophysiology. J Small Anim Pract, 56: 3-12. Whitley EM. Comparative Pancreatic Pathology. Pathobiology of Human Disease. 2014:1101–23. doi: 10.1016/B978-0-12-386456-7.03415-8. Epub 2014 Aug 21. PMCID: PMC7149520. Xenoulis, P.G. (2015), diagnosis of pancreatitis in dogs and cats. J Small Anim Pract, 56: 13-26.
Kidney Diseases in Cats
Lloyd Alexandria Chavez, R.M.T Cats possess a pair of kidneys located on either side of their abdomen, playing a crucial role in eliminating waste from their system. These organs are also key in regulating the balance of fluids, minerals, and electrolytes in the body, conserving water and protein, and supporting blood pressure and the production of red blood cells through the production of the hormone erythropoietin. Kidney disease in cats can manifest in several forms and can stem from various causes, typically classified into either acute or chronic categories. Acute kidney injury occurs when the kidneys are suddenly damaged, potentially impairing their function. This condition can affect both pets and humans and may result in diminished kidney performance. Fortunately, acute kidney injury can often be reversible, with approximately half of those affected—be they pets or humans—able to recover. The kidneys have a remarkable capacity for self-repair, provided the initial cause of injury is addressed and any exacerbating factors are eliminated. Recovery prospects depend on several factors, including the cause of the injury, its severity, whether other bodily systems are involved, the availability of treatments such as hemodialysis, and adherence to medical guidance.Chronic kidney disease (CKD), on the other hand, is frequently diagnosed in older cats and is characterized by a progressive decline in kidney function. Symptoms of CKD in cats include increased thirst and urination, reduced appetite, weight loss, vomiting, and a dull coat. CKD is an incurable condition that worsens over time, resulting from gradual kidney damage over months or years. Its progression and symptom onset are more gradual compared to acute kidney disease, which can emerge rapidly following significant kidney damage from causes such as infections or toxic substances like antifreeze or lilies. Cats with acute kidney disease typically exhibit severe symptoms swiftly. SYMPTOMS In the initial stages of chronic kidney disease (CKD), there may be no noticeable symptoms as the kidneys are still able to function adequately. However, as the disease progresses and the kidneys become increasingly impaired, symptoms will begin to manifest. These symptoms can develop gradually and may be subtle, making them difficult to detect. They include: DIAGNOSIS Chronic kidney disease is diagnosed through a series of blood and urine tests that measure levels of specific substances indicative of kidney function. These tests not only confirm the presence of kidney issues but also aid veterinarians in staging the disease, which helps in understanding its severity. The key laboratory tests include: Together, these tests provide a comprehensive assessment of kidney health, allowing for accurate diagnosis and staging of chronic kidney disease in cats. TREATMENT While it’s not possible to cure chronic kidney disease (CKD) or undo the damage that has occurred, steps can be taken to slow its progression and alleviate the symptoms. In cases where a cat is diagnosed with CKD and is showing signs of illness, the initial course of treatment may include: This treatment regimen aims to manage the symptoms and complications associated with CKD, improving the quality of life for cats living with this condition. Sources: https://www.pdsa.org.uk/pet-help-and-advice/pet-health-hub/conditions/chronic-kidney-disease-in-cats#:~:text=FAQs-,Overview,vomiting%2C%20and%20poor%20coat%20condition. https://www.petmd.com/cat/conditions/urinary/kidney-disease-cats https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7379052/
C-Reactive Protein
Sushant Sadotra The acute phase response (APR) is the early typical systemic response prompted by homeostasis disturbances such as injuries, infection, neoplasia, and other pathologies. Acute phase proteins get released from the liver into the blood after such stimulations. Therefore, elevated levels of such proteins can be used to indicate systemic inflammation. C-reactive protein, also called CRP, is an acute-phase protein synthesized in the liver and acts as a marker of the innate immune system response during inflammatory reactions. It is a 120 kDa composed of five identical subunits to form a pentamer structure. In Dogs, proinflammatory cytokines cause a rapid rise in the blood CRP concentration that also returns to normal without the provocative cause. Therefore it serves as an indicator and a crucial biomarker of inflammation. Besides projecting the degree of inflammation, CRP is helpful as a marker to examine the severity of a specific disease, such as gastrointestinal issues or diseases of other organs. Some of the biological functions of CRP are mentioned below: Factors inducing acute phase response, including CRP: CRP has been widely used in Europe and Japan to examine dogs with gastrointestinal and nongastrointestinal disorders. Some of the pathophysiologic conditions where CRP is frequently used as a biomarker are: CRP is a marker for chronic gastrointestinal signs, mucosal inflammation, systemic or gastrointestinal diseases, etc. Measurement of CRP and pancreatic lipase provide more sensitive and specific results. CRP can provide predictive information in dogs with CPV-2 infection. Dogs with hepatic disease have shown evaluated serum CRP levels. CRP is also the indicator of an acute abdomen in dogs with symptoms of abdominal pain, gastric dilatation or volvulus, small bowel obstruction, and peritonitis. CRP concentrations are higher in dogs with PLE, a disorder where excessive protein loss occurs through gastrointestinal mucosa. Dogs with Immune-mediated hemolytic anemia have high CRP levels. Tumor-associated inflammation or cytokine production leads to higher CRP concentrations in dogs with cancer of hematopoietic origins, such as lymphoma and leukemia. Measurement of canine CRP: POCTs track the inflammatory response in dogs as a rapid ancillary test or emergency. Evaluating CRP levels can be tested using available POCTs like the Point Strip canine CRP assay, LifeAssays canine CRP test, EURO-Lyser solo CRP test, and TECOdogCRP-quant. This commercially available test can estimate the scattering of light from a laser interacting with the CRP and anti-canine CRP antibody complex. This test is developed as Laser CRP-2 by Arrows Co., Ltd., Osaka, Japan. Many laboratories can estimate CRP at a large scale using commercially available multiple canine-specific CRP ELISA Tests such as Phase Range canine CRP ELISA37 (developed by Tridelta Development Ltd, Kildare, UK) and test invented by Waritani et al. Measurement of CRP in dogs can also be done through many automated immunoturbidimetric assays like the Turbovet canine CRP assay by Acuvet Biotech, Zaragoza, Spain; the Gentian canine CRP assay by Gentian AS, Moss, Norway; and TR-IMFA developed by Parra et al. Reference:
Respiratory Tract Disease Complex in Cats
Sushant Sadotra, PhD/Diagnostic specialist Feline respiratory disease (FRD) syndrome or feline upper respiratory tract disease complex is a common infection in cats caused mainly by Feline Herpesvirus (FHV-1), Feline Calicivirus (FCV), Chlamydophila felis, Mycoplasma spp., and Bordetella bronchiseptica. About 90% of all upper respiratory infections are caused by FHV-1 and FCV. Common Symptoms: · Sneezing · Nasal congestion · Conjunctivitis (inflammation of the membranes lining the eyelids) · Discharge from the nose or eyes (clear, purulent, or cloudy containing pus). · Difficulty breathing · Ulcers in the mouth Less specific symptom · Less appetite · Lethargy · Fever · Enlarged lymph nodes · Blepharospasm (squinting) Sources of infection: · Susceptible cats can get an infection by contagious particles in saliva or secretions from the nose or eyes shredded by an infected cat. · Most cases are associated with direct contact · Natural transmissions can also occur via aerosol droplets. Stress may also cause a secondary course of illness. Real-Time PCR for Diagnosis: A definitive diagnosis is based on clinical signs and laboratory testing for the isolation and identification of the infection. The Polymerase chain reaction (PCR) test is one of the sensitive tests and most reliable for detecting the presence of infectious agents. PCR detects the genomic material of the pathogen and determines its presence in the host. It is often more sensitive and specific than other available tests. However, false negative results are still expected. In the case of patients with latent herpes infections where the FHV-1 is found in the trigeminal ganglion can give negative PCR results. In the case of Chlamydophila, 2-3 days of antibiotic treatment for patients can also have negative PCR results. Samples of ocular, nasal, or caudal pharyngeal secretions for PCR assay are best for the diagnosis and identification of causative agents. Sample collection tips: · Ocular: Moisten with tears/exudate well or firmly swab both of the conjunctival sacs with a sterile swab. · Clinical lesions: Prefer to swab from the nasal and pharyngeal areas. After sample collection, place the swab into the preservation buffer and mix thoroughly. If not for immediately use, please keep the mixture at 4°C (no more than 3 days) until nucleic acid extraction.
Feline Herpesvirus Infection- Diagnosis
Trinh Mai Nguyen Tang Feline herpesvirus-1 (FHV-1) is a feline respiratory infection virus also known as feline viral rhinotracheitis (FVR) [1]. The Herpes virus was first isolated by scientists Crandell and Maurer in 1958 in cats with respiratory infections [2]. This virus has a prominent genome with large double stranded DNA, belonging to the family Herpesviridae [3]. This virus is characterized by cat-to-cat transmission with an exposure rate of up to 97% [4]. Herpes virus can be inactivated at 37oC around 3 hours or at 56oC in 5 mins. Meanwhile, the virus can remains infective in the enviroment approximately 5 months and a month at 25oC [5]. Once a cat is infected with the herpes virus, it is incredibly difficult to completely treat it since the virus can enter a dormant state and continue to survive in the cat for the remainder of its life [6]. Cats are not infectious during this latent period, but if they are sick or going through a stressful period, the virus may be reactivate. If this occurs, the cat will once more get the infection and may represent symptoms [7]. Herpes viruses can be latent in the ganglion, attach to sensory nerves and reach nerve cells, persist in the nucleus of infected nerve cells and do not replicate, leading to the process of detecting this virus becomes difficult [7-8]. As reported by Ngoc.N.T and her colleagues, herpes virus can infect cats of any age, however, kittens are more susceptible [9]. Specifically, the prevalence of virus infection in cats younger than 6 months old, 6-12 months old and over 12 months old were 52.17%, 33.33% and 19.05%, respectively [9]. Although previous reports have demonstrate that gender has no effect on the incidence of herpes virus infection [7-8], but Henzel et al. (2002) found that isolates from female cats are substantially taller than isolates from male cats [10]. Clinical Symptoms Herpes virus enters the cat’s body by contact with infected tears, nose, saliva, or items, and then multiplies rapidly in the epithelium of the nose, nasopharynx, and conjunctival mucosa leading to primary infection [11]. In cats infected with FHV-1, signs of sadness, moodiness, lethargy, sneezing, fever, and discharge from the eyes and nose have been noted (figure 1-A), a process that is frequently extended 2-4 days or longer, depending on the immunological system of the cat [11]. Secondary infection occurred after the fourth day of incubation, with symptoms of infection in the throat, bronchi, and bronchioles, and the nasal and conjunctival epithelium necrosing [12]. Conjunctivitis is a common herpes virus symptom, indicated by congestive and exudative symptoms that develop over many days to purulent discharge (figure 1-B) [13]. Gaskell and Dawson (1988) found lung infection or bronchitis in cats, with kittens dying from pneumonia at a greater incidence than adult cats [11,14]. Some other atypical symptoms such as mouth and skin ulcers, dermatitis or neurological signs are rarely seen [7]. Furthermore, the mean white blood cell (WBC) count of cats infected with FHV-1 (17.77 ± 0.70 x103/μl) was slightly increased compared with that of normal cats (4.6-12.8 x 103/μl) [9], in which neutrophils, eosinophils and monocytes all showed signs of slight increase compared. Secondary infections of the eyes, upper respiratory tract, and necrotic ulcers of the mouth can all cause high white blood cell counts [11]. Table 1 displays the white blood cell count. Table 1. Hematological results of cats was infected with FHV-1 [9]. Targets Unit Reference ± SE Red blood cells ´ 106/μl 7-10,7 10,20 ± 0,64 Hemoglobin content g/dl 11,3-15,5 13,47 ± 0,54 RBC mass % 33-45 38,78 ± 1,41 Average volume of red blood cells fl 41-49 45,16 ± 0,75 Average amount of hemoglobin in red blood cells pg 14-17 15,57 ± 0,24 Platelet count ´ 103/μl 180-680 362,50 ± 30,82 WBC count ´ 103/μl 4,6-12,8 17,77 ± 0,70 Lymphocytes ´ 103/μl 1,05-6,00 4,50 ± 0,36 Mono leukocytes ´ 103/μl 0,05-0,68 0,96 ± 0,13 Neutrophils polymorphonuclear leukocytes ´ 103/μl 2,32-10,01 11,47 ± 0,45 Eosinophils ´ 103/μl 0,1-0,6 0,78 ± 0,08 Basophils ´ 103/μl 0-0,14 0,07 ± 0,01 Laboratory Diagnosis In the laboratory, there are many different methods used to determine FHV. Common approaches include PCR, virus isolation in cell culture, and indirect fluorescent antibody staining of tissue samples for viral antibody detection [8,16]. PCR FHV is one of the most common causes of upper respiratory tract illness in cats. Infected cats would show upper respiratory signs. Co-infection of FHV with other pathogens makes the clinical signs more severe, particularly feline calicivirus, Chlamydophila felis, Bordetella pneumoniaseptica, Mycoplasma species, Staphylococcus spp., or Escherichia coli [6]. When a cat is suspected of having a viral infection, a swab can be used to collect nasal, ocular, oropharyngeal secretions, corneal debris, aqueous humor, corneal samples, blood, or biopsies. By amplifying viral DNA, tPCR can detect genetic material of FHV in specimen. However, if the cat is not in the infectious phase, no virus particles will be shed, rendering the PCR test ineffective [19-20]. ELISA method – detecting IgG antibodies The enzyme-linked immunosorbent test (ELISA) is used to determine IgG antibodies against FHV or FHV-1 utilizing serum, aqueous humor, and cerebrospinal fluid samples [15]. This approach, however, cannot discriminate between diseased and vaccinated cats. Due to the extended latent period of FHV, the cat’s body will generate antibodies to combat it [8]. These neutralizing antibodies manifest 20-30 days after the first infection. As a result, the presence of antibodies in the serum signals a prior infection but does not always correspond with clinical signs [8]. Immunofluorescent antibody assay Another approach for detecting FHV is immunofluorescence antibody (IFA) testing on corneal or conjunctival smears or biopsiengs. Through an antigen-antibody response, this assay may identify viral proteins produced in cells. However, this approach is thought to be less sensitive than viral isolation or PCR [16]. Virus isolation This is a traditional method that can detect viruses through isolation of conjunctival debris, nose, oropharynx, or postmortem lung samples from infected cats [8]. This traditional method can detect
Canine Lyme Disease
Oliver Organista, LA Lyme disease is a disease caused by the bacterium Borellia burdorgferi; a worm like, spiral-shape bacterium of spirochete class in the genus Borellia. The bacterium B. burgdorferi is transmitted through a bite of infected blacklegged tick or deer tick (Ixodes scapularis) to dogs and humans[1]. Different life-stage of I. scapularis ticks emerge at different times of the year (varies according to geographic location), giving a seasonality to Lyme disease transmission dynamics. It appears primarily in specific areas including the southern New England states; eastern Mid-Atlantic states; the upper Midwest, particularly Wisconsin and Minnesota; and on the West Coast, particularly northern California in the United States. It is also present in Europe and Asia[7]. Most of the areas where to find them are in forest or grassy, wooded, marshy areas near rivers, lakes or ocean, and are common in homes and buildings in secluded or rural areas. In Canada, there 2 types of blacklegged or deer tick that can spread Lyme disease. The blacklegged tick (Ixodes scapularis) and the blacklegged (Ixodes pacificus) [3] . Dogs tend to be bitten by infected I. scapularis adults, which are most active in the cooler early spring and late fall months [2]. An adult female tick is rarely (if ever) transmitted the B. burgdorferi to her offspring. Ticks most commonly become infected as juveniles after a bloodmeal on an infected wildlife host (most commonly rodents). Because ticks typically feed only one time per life stage, the next opportunity for B. burgdorferi transmission is during the next bloodmeal in the tick’s next life stage[2]. Typically, Lyme disease symptoms will take a couple of months or more to appear (2-5 months) after getting infected [8]. Symptomatically, Lyme disease can be difficult to distinguish from anaplasmosis because the signs of the diseases are very similar, and they occur in essentially the same areas of the country. Lyme disease is diagnosed through a blood test that shows whether an animal has been exposed to the bacterium[11]. Common symptoms that will appear are: Lameness: An inability to use one or more limbs is one of the most common symptoms of Lyme disease in dogs. Swollen lymph nodes: found in the neck, chest, armpits, groin, and behind the knees, are typically the first to show swelling. Lymph node swelling indicates an immune response triggered to fight the disease. Joint swelling: Swollen joints, stiff walking, or avoidance to touch may be other signs of the disease. Fatigue: Dogs with Lyme disease may also exhibit flu-like symptoms of low energy and lethargy. Loss of appetite: Losing interest in eating, especially if it leads to weight loss, is another sign that a dog may have Lyme. Fever: In addition to the above symptoms, a dog may have a fever caused by the Lyme disease infection. In rare cases, if Lyme disease is left untreated it can lead to damage in the kidneys, nervous system, and heart. Lyme disease affecting the kidneys is the second most common syndrome in dogs and is generally fatal. Facial paralysis and seizure disorders have been reported in the disease form affecting the nervous system. The form of the disease that affects the heart is rare. [10]. The most commonly used to diagnose Lyme disease in dogs are the serologic assays. Although some laboratories still use traditional serologic methods (e.g., whole-cell enzyme-linked immunosorbent assay and immunofluorescence assay), these assays have largely been replaced by serologic assays that detect host antibodies to specific B. burgdorferi proteins. These assays are qualitative, providing a yes/no answer regarding B. burgdorferi serostatus[3]. Treatment is generally recommended for seropositive dogs that display clinical signs of Lyme disease or are asymptomatic but have evidence of protein-losing nephropathy[4]. Most frequently antibiotics used to treat Lyme disease in dogs are doxyclycline and monicycline, at a dosage of 10mg/kg PO q12h to q24h for 30 days [2][5]. Amoxicillin and erythromycin are other antibiotics that can be used for treating the disease. A non-steroidal anti-inflammatory (carprofen or deracoxib) may also be given to the patient [6]. A possible complications may occur when treating Lyme disease. Some dogs who take antibiotics can develop loss of appetite, vomiting and diarrhea. Once infected, a dog will always have the bacteria that cause Lyme disease in his or her body. Therefore, relapses are possible; lookout for unexplained fever, swollen lymph nodes, and/or lameness. A small percentage of dogs develop kidney failure as a result of Lyme disease. Clinical signs include vomiting, weight loss, poor appetite, lethargy, increased thirst and urination, and abnormal accumulations of fluid within the body. [6] The best way to protect from Lyme disease is to use tick-preventive products year-round. Several safe and effective commercial parasiticides are available for tick control on dogs and cats, including systemics (isoxazolines), topicals (permethrin, fipronil), and collars. Another effective strategy is vaccination. Other prevention strategies include reducing exposure to ticks and avoiding areas with ticks [2]. References [1] Lyme Disease Diagnostic Market – Growth, Trends, COVID-19 Impact, and Forecasts (2022 – 2027), MOdor Intelligence, January 202 [2] Lyme Disease in Dogs: Signs and Prevention, Kathryn E. Reif, MSPH, PhD.,April 2020, https://todaysveterinarypractice.com/parasitology/lyme-disease/ [3] Lyme Disease, IPAC (https://ipac-canada.org/lyme-disease.php) [4] / Littman MP, Gerber B, Goldstein RE, et al. ACVIM consensus update on Lyme borreliosis in dogs and cats. J Vet Intern Med 2018;32(3):887-903. [5] Mullegger RR. Dermatological manifestations of Lyme borreliosis. Eur J Dermatol. 2004 Sep-Oct;14(5):296-309. PMID: 15358567 [6] How to Treat Lyme Disease in Dogs, Jennifer Coates, DVM, December 2014, PETMD (https://www.petmd.com) [7] Lebech AM. Polymerase chain reaction in diagnosis of Borrelia burgdorferi infections and studies on taxonomic classification. APMIS Suppl. 2002;(105):1-40. PMID: 11985118 [8] Could Your Dog Have Lyme Disease? How to Recognize the Symptoms and Get Treatment, Lavanya Sunkara , July 2022, GoodRx Health [9] Everything You Need To Know About Lyme Disease In Dogs, Kimberly Alt, July 2022, Canine Journal [10] Lyme Disease (Lyme Borreliosis) in Dogs, Reinhard K. Straubinger, DrMedVetHabil, PhD, Institute for Infectious Diseases and Zoonoses, Department of Veterinary Sciences, Faculty of Veterinary Medicine, LMU, October 2022 [11] Lyme disease: A pet owner’s guide, American Veterinary Medical Association
Psittacine Beak and Feather Disease
Long Pham Introduction Psittacine beak and feather disease (PBFD) is an infectious viral disease that infects psittacine birds. This disease affects Old World (Australian and African) psittacine birds and New World (Americas) psittacine birds (Greenacre, 2005). The peracute and acute form of this disease can cause sudden death, while the chronic form of this disease damages the feather, deforms the beak, and will eventually lead to death. (KATOH et al., 2010) The disease is caused by a small circovirus, which is a single-stranded DNA virus belonging to the Circoviridae family (Hakimuddin et al., 2016). The virus can spreads through direct contact with contaminated surfaces, feces, feather dander, and other bodily excretions (Greenacre, 2005). It can be transmitted horizontally to other birds in the same generation and vertically to eggs and young chicks in the next generation (Hakimuddin et al., 2016). Since the virus has a non-envelope structure, it is able to resist many control measures and is able to persist in the environment and infected substances for a long time. The origin of PBFD was thought of to be from Australia (PASS & PERRY, 1984), where it then spread to the rest of the world. Possibly through pet trades and import of these birds, this disease was able to spread globally. Report of this disease has occurred in other countries located in North America, Europe, Africa, Asia, and even on islands in the Indian and Pacific Oceans (Harkins et al., 2014). Psittacine beak and feather disease prevalence around the world varies and has been reported to be around 41.2% in Taiwan (Hsu et al., 2006), 3.5–4% in USA (de Kloet & de Kloet, 2004) and 23% in Australia (Khalesi et al., 2005). With an increasing trend of live birds being traded globally, the spread of PBFD and other diseases will surely grow. Diagnosis Typical clinical signs of PBFD include lethargy, weight loss, shedding and abnormal development of feathers, beak elongation and deformation, and eventually death (PASS & PERRY, 1984). This disease can occur in three different forms: peracute, acute, and chronic. Progression of the disease depends on the age, with younger birds having a higher progression rate (Greenacre, 2005). Some symptoms of peracute PBFD are weight loss, pneumonia, sepsis, enteritis, liver necrosis, and leukopenia (Schoemaker et al., 2000). Sudden death is likely to occur in peracute PBFD. In acute PBFD, majority of those affected by this phase are between the ages of 0-3 years old and it is thought that their susceptibility is based on their condition instead of the virus’ antigenic or genotypic characteristics (Ritchie et al., 1990). Some clinical signs includes depression and rapidly developing feather dystrophy can occur, affecting 80-100% of the feathers in as little as one week (Ritchie, 1995). Sudden death can also occur in this form. Those that survive this phase will have an incubation period, which may be years, before going to the chronic PBFD phase (Greenacre, 2005). For chronic PBFD, it is typically characterized by symmetrical feather dystrophy that progresses slowly and gets worse over time (Greenacre, 2005). Birds can become completely bald and can have beak deformities (Figure 1), where the beak becomes elongated. Death usually occurs from secondary infections, fungal or bacterial, because lymphoid tissues are usually damaged by the virus and causes the immune system to be suppressed (Ritchie et al., 2003). Figure 1: Cockatoo with advanced PBFD (Harcourt-Brown, 2009) PBFD can be diagnosed successfully from just careful examination. The disease can first be suspected if the bird is progressively losing feathers or has a symmetrical feather dysplasia. However, a loss of feathers does not always mean it is PBFD as the cause can be from other reasons, such as being self-inflicted or from excessive allopreening, which causes injuries that look similar to those caused by the disease (Wellehan et al., 2016). PBFD can be diagnosed though antigen and antibody detection from hemagglutination assay and hemagglutination inhibition. In addition, polymerase chain reaction (PCR) is also used for detecting PBFD, being a standard method of detection in most countries (Wellehan et al., 2016). False positives can occur with this method due to the nature of the virus to easily contaminate and persist in the environment, which will contaminate the samples, such as feathers, that are exposed to this environment (Wellehan et al., 2016). Therefore, the choice of sample collection method can have a major impact to the results. In one study, it was found that the use of blood samples for a PCR test resulted in 47 out 56 birds being positive for PBFD, while only 10 birds had a positive result when feather samples were used (Khalesi et al., 2005). Treatment and Disease Control Current treatment for PBFD is for supportive care to prevent secondary infections as there is no cure for this disease. The disease is fatal when clinical signs appear, while other birds that has an immune response and don’t show any clinical signs, making this naturally vaccinated (Greenacre, 2005). Effective methods of controlling this disease involves isolating suspected carriers, testing, and if necessary, culling to prevent a possible outbreak from occurring. The resilience of the virus to many chemical disinfectants and even extreme temperatures can be based on the physicochemical properties of the virus (Raidal & M.Cross, 1994). However, Virkson S or other peroxide disinfectants have been suggested for use to disinfect contaminated areas (Wellehan et al., 2016). Strict hygiene practices with the right disinfectants is the key to prevent further spread of PBFD. While there are no vaccine for PBFD available commercially, research into developing one is ongoing and currently made vaccines appears to be effective. Future control of the disease will still depend on implementing strict hygiene practices and testing methods since vaccinated birds may still spread the disease. References Greenacre, C.B. (2005) Viral diseases of companion birds. Veterinary Clinics of North America: Exotic Animal Practice, 8, 85–105. KATOH, H., OGAWA, H., OHYA, K. & FUKUSHI, H. (2010) A review of DNA viral infections in Psittacine birds. Journal of
Introduction to Feline Hypertrophic Cardiomyopathy
Maigan Espinili Maruquin It is important to be aware that some of the diseases your pets may have are actually inherited. In cats, there are myocardial diseases that can be breed- related. The most common myocardial disease in cats is Hypertrophic cardiomyopathy (HCM), wherein abnormal thickening of the walls of the left ventricle (LV) is observed [1]. First time described in cats in 1977 [2], it has been reported to have a prevalence of around 14.7% in apparently healthy cats [3-5]. In humans, the HCM is considered a genetic disease [6-8], whereas occurrences of the disease were observed in mix- breeds [9], Persian [10], and American shorthair cats [11], while an HCM caused by mutation was identified in Maine coon [12] and ragdoll [13]. The HCM are diagnosed at mean of 5-7 years, although all ages can get the disease [6]. On the other hand, some cat breeds including Maine Coons [14]; Sphynx [15], and Ragdoll [16] were reported on earlier onset of under 2 years old [3]. Cats that are diagnosed with HCM are also recorded to develop congestive heart failure (CHF), arterial thromboembolism (ATE), or sudden cardiac death (SCD) [1, 17, 18]. Clinical Presentation When cats visit the clinics, routine veterinary examinations are conducted, and during auscultation, signs like arrhythmias, gallop sounds, or murmurs can be detected [6, 19, 20]. Respiratory distress is a manifestation of heart failure in diseased cats, whereas, some cats display hypothermia and pre-renal azotemia. On the other hand, the murmurs in cats may vary in intensity form moment to moment, and are commonly associated with dynamic and labile phenomena [6]. Diagnosis Fig. 1. Approach to the asymptomatic cat with suspected heart disease. BP, blood pressure; PCV, packed cell volume; T4, thyroxine [1] The feline HCM are primarily diagnosed on echocardiographic examination, which recognizes basic patterns that are intuitive [21], with ventricular wall thickness that is equal to or exceed 6 mm [6, 22]. Respiratory distress is reported to display left atrial enlargement. However, echocardiographic examination has limitations [1] and there is no definitive, gold-standard to diagnose HCM, unless there is a hypothetical and flawless molecular or genetic testing [6]. The LV wall thickness has no exact value allowable, and body weight can affect its thickness [1]. An increase of cTn-I in plasma concentration indicates its sensitivity and specificity as a biomarker to provide myocardial damage severity and prognosis information. On the other hand, the N-terminal pro B-type natriuretic peptide (NT-proBNP) assay may provide ongoing myocardial stress, however, full cardiac evaluation shall be performed to detect its cause of elevation [1]. Myocyte enlargement and interstitial fibrosis were observed, along with disorganized spatial arrangement of myocytes in histopathological examination [3, 23] Genetic testing for single point mutation that affects MYBPC3 in Maine coon cats (A31P) [12] and ragdolls (R820W) [13] are commercially available. Autosomal dominant inheritance were reported in both breeds [1]. Therapy and Management For asymptomatic cats with HCM, diltiazem or beta-blockers were reported to improve physical condition. Meanwhile, Diltiazem is administered at three times a day as a licensed formulation in UK to manage cases of HCM [21]. In a study conducted by Rishniw, M. and P.D. Pion in 2011, participatiing clinicians used furosemide for evident CHF, and most of them also used and ACEIs, while for cases with substantial dynamic LVOT obstruction, β-blockers were used by most [24]. Altering the progression of HCM in the pre- or subclinical stage is an approach that is ideal in the absence of safe and efficient therapy [1]. References Luis Fuentes, V. and L.J. Wilkie, Asymptomatic Hypertrophic Cardiomyopathy: Diagnosis and Therapy. Veterinary Clinics: Small Animal Practice, 2017. 47(5): p. 1041-1054. Tilley, L.P., et al., Primary myocardial disease in the cat. A model for human cardiomyopathy. Am J Pathol, 1977. 86(3): p. 493-522. Gil-Ortuño, C., et al., Genetics of feline hypertrophic cardiomyopathy. 2020. 98(3): p. 203-214. Paige, C.F., et al., Prevalence of cardiomyopathy in apparently healthy cats. J Am Vet Med Assoc, 2009. 234(11): p. 1398-403. Payne, J.R., D.C. Brodbelt, and V. Luis Fuentes, Cardiomyopathy prevalence in 780 apparently healthy cats in rehoming centres (the CatScan study). J Vet Cardiol, 2015. 17 Suppl 1: p. S244-57. Abbott, J.A., Feline Hypertrophic Cardiomyopathy: An Update. Veterinary Clinics: Small Animal Practice, 2010. 40(4): p. 685-700. Maron, B.J., et al., American College of Cardiology/European Society of Cardiology clinical expert consensus document on hypertrophic cardiomyopathy. A report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines. J Am Coll Cardiol, 2003. 42(9): p. 1687-713. Maron, B.J., Hypertrophic cardiomyopathy: a systematic review. Jama, 2002. 287(10): p. 1308-20. Kraus, M.S., C.A. Calvert, and G.J. Jacobs, Hypertrophic cardiomyopathy in a litter of five mixed-breed cats. J Am Anim Hosp Assoc, 1999. 35(4): p. 293-6. Marin L, V.S., Boon J, et al., Left ventricular hypertrophy in a closed colony of Persian cats [abstract]. J Vet Intern Med 1994. 8:143. Meurs KM, K.M., Towbin J, et al., Familial systolic anterior motion of the mitral valve and/or hypertrophic cardiomyopathy is apparently inherited as an autosomal dominant trait in a family of American shorthair cats. J Vet Intern Med, 1997. 11:138. Meurs, K.M., et al., A cardiac myosin binding protein C mutation in the Maine Coon cat with familial hypertrophic cardiomyopathy. Hum Mol Genet, 2005. 14(23): p. 3587-93. Meurs, K.M., et al., A substitution mutation in the myosin binding protein C gene in ragdoll hypertrophic cardiomyopathy. Genomics, 2007. 90(2): p. 261-4. Kittleson, M.D., et al., Familial hypertrophic cardiomyopathy in maine coon cats: an animal model of human disease. Circulation, 1999. 99(24): p. 3172-80. Chetboul, V., et al., Prospective echocardiographic and tissue Doppler screening of a large Sphynx cat population: Reference ranges, heart disease prevalence and genetic aspects. Journal of veterinary cardiology : the official journal of the European Society of Veterinary Cardiology, 2012. 14. Borgeat, K., et al., The influence of clinical and genetic factors on left ventricular wall thickness in Ragdoll cats. J
