Feline Leukemia Virus (FeLV): A Constant Threat to Our Cat Companion
[vc_row][vc_column][vc_column_text] Feline Leukemia Virus (FeLV): A Constant Threat to Our Cat Companion Maigan Espinili Maruquin It was believed that the Feline Leukemia Virus (FeLV) is the one responsible in most disease- related deaths in cats. It was Jarrett, et al., 1964 who first identified FeLV as a causative agent of the viral infection of cats more than 40 years ago by electron microscopy (EM). However, the prevalence of FeLV as the disease- causing agent in cats has declined, and so is the death rate caused by the infection. Despite FeLV being a threat in the life expectancy of the cats, owners still choose to provide the proper treatment for their cats and proper care, leaving FeLV-infected cats live for many years with good quality of life (Hartmann 2012). Structure and Replication (https://veteriankey.com/feline-leukemia-virus-infection/) Fig. 01. The structure of FeLV containing two identical strands of RNA, reverse transcriptase, integrase, and protease inside the capsid protein (p27), surrounded by a matrix and all enclosed by the envelope containing gp70 glycoprotein and the transmembrane protein p15E (https://veteriankey.com/feline-leukemia-virus-infection/). FeLV is approximately 8.4kb in length. It belongs to the genus Gammaretrovirus. Retroviruses have three- layered structure and RNA (two copies of single-stranded RNA), which makes the genetic material, is in the innermost- layer; together with the essential enzymes for its viral activities (including integrase, reverse transcriptase and protease) and nucleocapsid protein. The capsid protein in the middle layer surrounds the genome. And, the outer layer is the envelope from which glycoprotein ‘spikes’ project (Westman, Malik et al. 2019). The envelope spikes are responsible for the attachment of the virus to the target cell surface receptors which also represents an essential target for the host immune response. During replication, RNA is being reverse transcribed into DNA through the enzyme reverse transcriptase. This interrupts the normal cellular flow of genetic information, the Central Dogma, making this enzyme the target of many anti- viral drugs. The synthesized DNA from the RNA integrates into the genome of the target cell as a provirus, which is a required component for the viral replication, assisted by a second viral enzyme, the ‘integrase’. This provirus remains in the genome of the cell and upon cellular division, the provirus is expressed, leading to the production of progeny virions and virus shedding (Lavialle, Cornelis et al. 2013, Willett and Hosie 2013, Chiu, Hoover et al. 2018, Westman, Malik et al. 2019). FeLV Infection On a previous research, there were three important observations following FeLV Infection: (a) some cats can eliminate the virus before it progresses local replication after enough time and appropriate immune response; (b) some cats become persistently viraemic; (c) some cats are viraemic before immunity responds to eliminate the transient viraemia after 2–16 weeks, but not before a latent infection is established as DNA provirus (Westman, Malik et al. 2019). Antigen-negative, provirus positive cats are considered FeLV carriers. This was after cats infected with FeLV were found to remain provirus-positive. Following reactivation, they can act as a source of infection. As FeLV provirus is integrated into the cat’s genome, it is unlikely to be fully cleared over time and possibly in a transcriptionally silent (latent) state. Antigen-negative, provirus-positive cats do not shed the virus, but reactivation is possible (Torres, O’Halloran et al. 2008, Hartmann 2012). FeLV undergoes different stages of infection. On abortive infection, virus starts initial replication but an effective immune response may terminate the viral replication and avoid becoming viraemic by eliminating the FeLV-infected cells (Hofmann-Lehmann, Cattori et al. 2008, Torres, O’Halloran et al. 2008, Hartmann 2012)(Torres, Mathiason et al. 2005). In regressive infection, effective immune response contains the replication of the virus prior to or shortly after bone marrow infection (Hartmann 2012) despite retaining a low level of FeLV-infected cells in circulation and tissues. In some cases, infected cells are also eliminated and undergo abortive infection (Torres, Mathiason et al. 2005). Mainly, virus shed in saliva however, in this infection, viremia is terminated within weeks or months. However, virus undergoes latency since it is not completely eliminated, harboring viral DNA in circulation, and integrating the proviral DNA in the bone marrow stem cells and lymphoid tissues. The proviral DNA is not translated into proteins making it non- infectious. The cats are considered ‘protected’ from the development of viraemia and thus disease, but they remain infected. Under latent infection, viral replication is delayed. Therefore, these regressively infected cats are not infectious to others but the infection could be reactivated when antibody production decreases (Torres, Mathiason et al. 2005, Hofmann-Lehmann, Cattori et al. 2008, Torres, O’Halloran et al. 2008, Hartmann 2012). For the progressive infection, the infection is not contained early, resulting to extensive viral replication. They remain positive after 16 weeks of infection. This makes the cats persistently viraemic and infectious to other cats. They develop FeLV- related diseases, and most of them die within a few years. On the other hand, it is focal or atypical infection if there’s a persistent atypical local viral replication (e.g., in mammary glands, bladder, eyes). This leads to an irregular production of antigen causing alternate results of positive and negative (Hartmann 2012). Clinical Signs/ Pathogenesis There are two possible results following the first 4 weeks FeLV exposure of the host: (a) failure to contain the viral replication; and (b) successful immune response of the host against the virus (Rojko, Hoover et al. 1982, Hoover and Mullins 1991, Torres, Mathiason et al. 2005). After a long asymptomatic phase, cats can develop clinical signs including tumors, hematopoietic disorders, neurologic disorders, immunodeficiency, immune-mediated diseases, stomatitis, immunosuppression, hematologic disorders, immune-mediated diseases, and other syndromes (including neuropathy, reproductive disorders, fading kitten syndrome). This is determined by a combination of viral and host factors (Hartmann 2012). Mostly, tumors in cats are associated with FeLV, commonly lymphoma and leukemia, less often other hematopoietic tumors and rarely other malignancies (including neuroblastoma, osteochondroma, and others). FeLV vaccination resulted to a major decrease of FeLV infection in the overall
Rapid Antimicrobial Susceptibility Testing to Combat Resistance
Introduction Antimicrobial Susceptibility Testing (AST) plays a crucial role in combating bacterial infections and addressing the growing global challenge of antibiotic resistance. Antibiotics, ranging from β-lactams to macrolides, have saved millions of lives since the accidental discovery of penicillin by Alexander Fleming in 1928. Despite their effectiveness, widespread misuse in healthcare and agriculture has accelerated the emergence of resistant pathogens, causing an estimated 700,000 deaths annually, a figure projected to rise to 10 million by 2050 (Brogan & Mossialos, 2016). (https://share.google/images/TSneDwQ3EQjAbSPAX) Importance of AST in Clinical Practice AST allows clinicians to determine which antibiotics are effective against specific bacterial isolates, enabling targeted therapy and reducing reliance on broad-spectrum antibiotics. Timely and accurate AST is critical, as delayed treatment can increase patient mortality and worsen clinical outcomes. Traditional AST Methods Disk Diffusion (Kirby–Bauer Test): Convenient and cost-effective, providing qualitative results based on the zone of inhibition around antibiotic discs. Broth Microdilution: Offers precise Minimum Inhibitory Concentration (MIC) values, essential for correct dosage selection. Miniaturized 96-well plates allow testing of multiple antibiotics simultaneously. Etest: Gradient diffusion method that combines ease of use with quantitative MIC determination, correlating well with broth microdilution results. Automated AST Systems Modern laboratories increasingly rely on automated systems like VITEK®, BD Phoenix™, Sensititre™, and MicroScan WalkAway®. These platforms streamline bacterial identification and susceptibility testing, reduce manual workload, and provide faster results for effective patient care. Emerging Technologies Rapid AST innovations using optical imaging, micro-channel resonators, and biosensors are being developed. Some technologies can deliver results within hours and may allow direct testing on patient samples without pre-culturing, which is essential for timely therapy, especially in critical care. Conclusion AST remains an essential practice of modern clinical microbiology. By providing rapid and accurate results, AST enables targeted antibiotic therapy, reduces the use of broad-spectrum drugs, and improves patient outcomes. Continued innovation and integration of rapid AST technologies into routine practice are vital to combating antibiotic-resistant infections worldwide. The miniAST Veterinary Antibiotic Susceptibility Test Analyzer, a tool designed to help combat antimicrobial resistance with game-changing features: Feature Benefit Fast Results Get results in just 6 hours, enabling swift and confident treatment. Automated Interpretations Instantly deliver precise susceptibility profiles, supporting faster, more informed clinical decisions and optimizing patient care. Dual-Sample Testing Double the efficiency with simultaneous analysis of two samples at once. High Accuracy Achieve an impressive 92% accuracy rate compared to traditional disc diffusion tests. 📌 Note for Veterinarians: The miniAST Veterinary Antibiotic Susceptibility Test Analyzer is available exclusively to licensed veterinarians and veterinary hospitals. 📩 How to Order miniAST To purchase miniAST or request a quotation, please contact our sales team or email our customer service: 📧 service@bioguardlabs.com ☎️ Please include your hospital name and contact number so our sales representative can follow up with you directly. Source: World Health Organization (WHO) – Antimicrobial Resistance 🔗 https://www.who.int/news-room/fact-sheets/detail/antimicrobial-resistance Clinical and Laboratory Standards Institute (CLSI) 🔗 https://clsi.org/standards/products/microbiology/ European Committee on Antimicrobial Susceptibility Testing (EUCAST) MIC cut-offs and AST interpretation standards. 🔗 https://www.eucast.org/clinical_breakpoints/ Bauer AW, Kirby WMM, Sherris JC, Turk M. (1966) Antibiotic susceptibility testing by a standardized single disk method. Jorgensen JH, Ferraro MJ. (2009) Antimicrobial susceptibility testing: a review of general principles and contemporary practices. Clin Infect Dis. 49:1749–1755. Puskarich MA et al. (2011) Association between timing of antibiotic administration and mortality from septic shock.
Canine Parvovirus
Canine Parvovirus CHINESE EDITION IS WRITTEN BY DR. WANG, SHIH-HAO / ENGLISH EDITION IS TRANSLATED AND EDITED BY DR. LIN, WEN-YANG (WESLEY) Abstract The canine parvovirus (CPV) is a common, acute, high morbidity and high morality virus that mainly infect canine population. This virus possess highly survival rate for 5 weeks in the natural environment. It is highly contagious and easily transmitting among canine population by the fecal-oral route through contacting contaminated feces. CPV usually attack digestive system. Sometimes it may induce myocarditis among canine and cause sudden death. All ages, sexes and breeds of dogs could be susceptible to CPV, especially puppies. Clinical sighs of infected dogs may include fever, lethargy, continuous vomiting, continuous diarrhea, stinky viscous diarrhea with blood, dehydration and abdominal pain etc. Canine show signs of the disease would usually die within 3 to 5 days. There are no specific drugs for curing CPV until now. Supportive care such as consuming water-electrolyte fluid is the only present solution to maintain physiological function and relieve symptoms. The infected canine should have medical care as soon as possible; otherwise, more severe conditions like acute dehydration, hypovolemic shock, bacterial infections and death will occur. Infection prevention measures include environmental disinfection and routine vaccines. Pathogens The canine parvovirus (CPV) is an ssDNA virus, which belongs to the species carnivore protoparvovirus 1 within the genus protoparvovirus in the family parvovirus (parvoviridae). CPV is 98% identical to feline panleukopenia virus (FPLV) with variant in six coding nucleotide of structural proteins VP2: 3025, 3065, 3094, 3753, 4477, 4498 that makes CPV-2 infect canine host instead of replicating in cats. Two types of canine parvovirus were discovered – canine minute virus (CPV1) and CPV2, both can attack canine population and canidae family such as raccoons, wolves and foxes. Canine parvovirus may be susceptible to cats without pathogenic, and it is an inapparent infection. CPV2 could stably survive in feces for 5 months with ideal condition. Furthermore, CPV-2a, CPV-2b and CPV-2c type viruses have been isolated and sequenced from animals. Other than targeting on canine, large cats are susceptible to CPV-2a, CPV-2b. CPV-2c type viruses have high prevalence on infecting leopard cats. Figure 1. Model of CPV evolution showing VP2 amino acid differences between each virus and indicating the virus host ranges. (Karla M. Stucker, Virus Evolution In A Novel Host: Studies Of Host Adaptation By Canine Parvovirus, Published in 2010) Epidemiology In 1978, a novel infectious canine disease was firstly occurring in the east coast of America. Within 12 months, scientists identified CPV-2 as the aetiological key of severe symptoms among canine. Due to characters of highly contagious and potential environmental resistance, CPV-2 spread swiftly over entire USA, European countries, Australia and Asia. In 1978, canine parvovirus also invade among canine in Taiwan. Therefore, CPV caused large scale of canine death at the early stage of pandemic. By the establishment and development of CPV vaccine, global wide spreading of CPV has been rarely happen today. However, canine parvovirus still widely exists in domestic dogs and wild canidae. It became one of the canine endemic disease. Pathogenesis Incubation period of CPV-2 lasts 4 to 5 days. The virus mostly attacks rapidly dividing cells especially lymphopoietic tissues, the bone marrow, crypt epithelia of the jejunum, ileum and (in young dogs under 4 weeks old) myocardial cells. Rottweilers, black Labrador Retrievers, Doberman Pinschers, and American Pit Bull Terriers are more susceptible than other species; once they are infected, would suffer severer conditions. Besides, CPV-2 take the major place to affect canine and wild canids. After entering into hosts’ body, CPV-2 firstly replicates in oropharynx lymphoid tissues, mesenteric lymph nodes and thymus gland, then spreading to other lymph nodes, lung, liver, kidney and rapidly dividing tissues (e.g. bone marrow, intestinal epithelial cell and myocardial cell) by the blood stream. 4 to 5 days after, clinical sighs like diarrhea, vomiting, lymphopenia, anorexia, depression, dehydration, hypothermia, thrombocytopenia and neutropenia would appear. Severe dehydration and hypovolemic shock may happen due to lose large amount of fluid and protein by vomiting and diarrhea. Transmission Fecal-oral route is the main transmission pathway of CPV-2. Large amount of virus would be detected in feces of infected canine within 1 to 2 weeks of acute phase. An infected pregnant canine could transmit virus to fetus through placenta. Fomites include contaminated shoes, cages, food bowls and other utensils could serve as CPV transmitting objects also. Clinical forms There are four clinical forms according to distinct signs and lesions: enteric, myocardial, systemic infection and inapparent Infection. A. Enteric form : It is known that CPV-2 caused enteritis symptoms. This form infect host with low virus titers (around 100 TCID50). Symptoms in initial stage are sopor, loss of appetite, acute diarrhea, vomiting, dehydration, slight elevated body temperature, frailty and acting like in extreme pain. Severity of illness vary according to the age of canine, healthy condition, infectious dose of the virus, and other pathogens in intestine and so on. Typical signs of CPV induced enteritis and its course include loss of appetite, sopor, fever (39.5℃-41.5℃) within 48 hours follow vomiting. 6 to 24 hour after vomiting follow watery stool in yellow or white color, mucus stool or bloody stool with stench in severe cases. Due to consistent diarrhea and vomiting, dogs suffer worsen dehydrated condition. Common clinical pathologic examination consist assessing dehydrated condition and significant decreasing of white blood cell of dogs (400 to 3000 /μL). B. Myocardial form: This form only appear in puppies around 3 to 12 weeks of age. Major cases show pups’ age under 8 weeks. Mortality rate is extremely high with myocardial form (almost up to 100%). Clinical signs include irregular breathing, cardiac arrhythmia. Collapse, hard breathing may happen to acute cases follow death within 30 minutes. Most cases would die within 2 days. The subacute form would also die from hypoplastic heart syndrome within 60 days. Nevertheless female adult canine acquire antibodies against myocardial form by vaccination or infection, puppies may
Peritonitis in Canine
[vc_row][vc_column][vc_column_text] Peritonitis in Canine Andy Pachikerl, Ph.D Introduction: Peritonitis is the inflammation of the peritoneum, which is a silk-like membrane that lines the inner abdominal wall of mammalian bodies and covers the organs within the abdomen, and it is usually due to a bacterial or fungal infection. Peritonitis typically results in rupture (perforation) in the abdomen or causes other medical conditions. In canine or dogs this condition is not that different compared to other mammals, which is the peritoneum of the abdominal cavity, becomes inflamed. In canines, this normally occurs because of an injury by physical trauma, disease, a stomach ulcer, or other problems (Latimer, et al., 2019). The most common cause of peritonitis in canine is actually bacterial infection that moves to the abdomen from an external wound or from perforation of an internal organ. An affected dog may seem to be well, then suddenly become ill. The condition is usually painful, and most dogs will show signs of discomfort when they are been touched on the abdomen (Kine, et al., 2019). Classification and Etiology Peritonitis in dogs are classified in various ways, but there are two main methods of identification are (1) localized or diffuse and (2) primary, secondary, or tertiary. Localized septic peritonitis occurs when a small amount of contamination, whether bacterial or fungal is confined. The contamination usually originates from an intraabdominal organ due to secondary surgery or an underlying disease process, such as gastrointestinal (GI) perforation due to a foreign body. Diffuse peritonitis arises from either a larger amount of contamination or a failure to control localized septic peritonitis. Primary septic peritonitis is spontaneous, and it is the infection of the peritoneal cavity with no specific intraperitoneal source of infection detected during surgery or necropsy. This type of peritonitis is more common in cats rather than dogs, with 14% of cats with septic peritonitis having primary septic peritonitis in one study (Costello, et al., 2004; Odonez & Puyana, 2006; Culp, et al., 2009). Primary septic peritonitis is usually monomicrobial, whereas secondary septic peritonitis is often polymicrobial (Mueller, et al., 2001). In one study (Mueller, et al., 2001), bacteria cultured from patients with primary peritonitis were gram positive in 80% of dogs and in 60% of cats. It is postulated that primary septic peritonitis may result from hematogenous or lymphogenous bacterial spread, transmural bacterial migration from the GI tract, or bacterial spread from the oviducts (Culp, et al., 2009; Enberg, et al., 2006). Secondary septic peritonitis is a consequence of an underlying primary disease process and is the most common cause of septic peritonitis in dogs and cats (Mueller, et al., 2001). There are many possible causes of secondary septic peritonitis in animals; the most common are loss of integrity of the GI tract (53% to 75% of cases), foreign-body penetration, perforating ulcers (Figure 1) and surgical wound dehiscence (Mueller, et al., 2001; Costello, et al., 2004). It is the upmost recommendation that canines showing peritonitis signs should seek medical help from a veterinarian for a proper diagnosis and treatment, as it can be a life-threatening condition. Figure 1: Septic peritonitis secondary to jejunal rupture from a perforating ulcer (arrow). Symptoms of Peritonitis in Dogs In most cases, the symptoms of peritonitis in canines are easy to recognize. A dog may seem fine, then suddenly become very ill the following day. They will almost certainly show signs of pain when their abdomen is been touched (DeClue, et al., 2011). Canine that has been injured or wounded seemed fine but suddenly develop the following symptoms the next day then one may consider seeking a veterinarian right away. Fever: – normal body temperature in canine ranges from 99.5 – 102.5 ° F, whereas a body temperature of at least 103.5 ° F (39.7 ° C) can be considered as fever. Vomiting Diarrhoea Black stools Anorexia Lethargy Weakness Abdominal pain Taking unusual positions to relieve pain Low blood pressure Increased heart rate Increased respiration rate Low body temperature Pale gums Jaundice: – Jaundice in canines refers to a build-up of yellow pigment in the blood and tissue, which causes a yellow discoloration in the skin, gums, and eyes. Swelling in the abdomen Ascites: – Ascites in canines is an abnormal build-up of fluid in the abdomen. It is also called abdominal effusion. Arrhythmia: – Arrhythmia in canines is an abnormality in the rhythm of the heart, which can include the speed, strength, or regularity of heart beats. There are cases when peritonitis could become severely complicated by gut microbiota of the dog. These can lead to changes in the dog’s micro flora forever. Such a case is shown as follow. Case Presentation: An 11‐year‐old intact male Poodle was brought to Oklahoma State University, Center for Veterinary Health Sciences (OSU‐CVHS), with a record of vomiting, abdominal distention, increased serum activities of alkaline phosphatase, γ‐glutamyl transferase, and hyperbilirubinemia. The dog had received amoxicillin and clindamycin (dosage and administration route unknown) prescribed by a referred veterinarian. An abdominal ultrasonographic examination revealed a moderate amount of peritoneal fluid, widespread vascular mineralization, and a markedly thickened and irregular gallbladder wall. The abdominal fluid had a total nucleated cell count (TNCC) of 51,000/μL (CELL‐DYN 3500 analyzer; Abbott Diagnostics, Abbott Park, IL, USA), and a total protein of 5.6 g/dL via refractometry. Cytologic examination of direct smears of the abdominal fluid stained with an aqueous Romanowsky stain (Hematek 2000; Siemens Healthcare Diagnostics, Deerfield, IL, USA) demonstrated marked pyogranulomatous inflammation with abundant golden‐to‐dark green pigment, consistent with bile, present extracellularly and within macrophages. Cytologic diagnosis was bile peritonitis. No infectious organisms were identified, and successive aerobic and anaerobic bacterial cultures were negative. The dog was intravenously dosed with ampicillin/sulbactam and enrofloxacin. Exploratory abdominal laparotomy revealed a ruptured gall bladder and a cholecystectomy and duodenotomy were performed. Following surgery, the effusion persisted, despite antimicrobial therapy, and the dog’s condition began to deteriorate. Abdominal fluid collected 6 days postsurgery had a TNCC of 96,600/μL, and a total protein of 5.3 g/dL. Cytologic examination was shown to have pyogranulomatous inflammation with several yeast organisms
Feline Blood-Types
[vc_row][vc_column][vc_column_text] Feline Blood-Types Andy Pachikerl, Ph.D Introduction Like humans, cats have blood grouping. However, cats do not have the blood-type O positive. The blood type classification of cats, however, is currently based on the AB system, but like dogs, there are other antigens besides the AB system , such as the Mik blood type. The blood type of cats is composed of mainly A, B, and AB. Type A is the most common, type B is rarer, and type AB is rarest. About 95% of domestic cats are type A blood, and some varieties such as exotic short-haired cats, British short-haired cats, Persian cats, and Scottish folds have a higher percentage of type B blood. As mentioned, the blood-type of cats is mainly A, B, or AB. Peculiarly for AB type, other blood types have innate antibodies. Unlike dogs, cats have antibodies against “non-self” or foreign erythrocytes that can cause lethal immuno -reaction. Therefore, cats cannot obtain a “wrong” blood of different blood types. Before any blood transfusion clinically, cat blood typing is extremely important. Incompatibility of blood type can lead to fatal acute hemolysis reaction, particularly, the blood of a type A cat was given to a type B cat. The anti-type B antibodies found in type A cats have weaker affinity towards each other, causing a mild immune response. However, type B cats have a strong affiliated anti-type A antibody, which can cause a strong immune response. Once type B cat transfuses A-type blood, the red blood cells are rapidly destroyed,resulting in intravascular hemolysis. As little as 1 ml of type A cat blood, it is enough to cause a serious immune reaction in type B cat and then causes absolute lethality. Keep in mind that blood typing is not only extremely vital prior a blood transfusion, but also for cat breeding! Neonatal isoerythrolysis (NI) occurs when a mommy cat with type B blood gives birth to kittens with type A or AB blood and breast-feed them with a high chance of having antigens of type A blood antibodies in the milk, which can cause a severe hemolysis reaction in the kittens. There are no obvious clinical signs to severe hemolytic anemia, but only subtle symptoms such as hemoglobinuria and jaundice. Therefore, we must pay attention to the blood type of the parent before breeding. Despite the best of efforts to prevent them, transfusion reactions may still happen. Depending on the severity, therapy can include glucocorticoids, epinephrine, IV fluids, and discontinuing the transfusion. Fever is usually mild, requiring no treatment. Furosemide should be administered if volume overload occurs. The blood product can be warmed to no more than 37 ° C if hypothermia occurs. Crossmatching blood is the best means of preventing immune-mediated transfusion reactions even if the blood type is known for both cats. It is also imperative blood be collected and administered as aseptically as possible and cats receiving blood products are monitored carefully. The distribution of feline blood types varies by geographic region and breed (Table 1) 1-2. Type-A is the most common type among most cats. There is, however, geographic variation in the prevalence of type-B domestic shorthaired cats. Over 10% of the domestic shorthair cats in Australia, Italy, France and India are type- B. Breed distribution does not vary as much by location because of the international exchange of breeding cats. Over 30% of British Shorthair cats, Cornish and Devon Rex cats, and Turkish Angora or Vans have type-B blood. In contrast, Siamese and related breeds are almost exclusively type-A. Ragdoll cats appear to be unique regarding blood types. Approximately 3.2% of Ragdoll cats are discordant for blood group when genotyping is compared to serology, necessitating further investigation in this breed. Table 1: Selected Blood Type A and B Frequencies in Cats (ignoring AB blood types) The AB blood type is very rare while the frequency of the MiK blood type is unknown. The presence of red blood cell antigens in addition to the AB group may explain why transfusion compatibility is not guaranteed by blood typing; crossmatching is recommended prior to any transfusion 3. Breeding queens, along with blood donors and, if possible, blood recipients should be blood typed. Feline blood-typing methods There are various methods are that can be used to determine blood type, both in a laboratory and veterinarian clinic. Usually in a diagnostic laboratory, they would use various serological methods by adding reagents to samples of blood and observe for any agglutination reactions marking a positive result. In addition, genetic testing is now available to identify blood types A and B using buccal swabs, although it cannot distinguish between A and AB blood groups. In veterinarian clinics, testing may be performed using a card typing system (BIOGUARD® Feline blood -typing kit, New Taipei City, Taiwan and Rapid Vet-H®, Flemington, NJ). If the card-typing system is used, type-AB and type-B results should be confirmed by a referral laboratory as some cross-reactions have been known to occur. Recently,there was an introduction to an alternative novel method for blood typing ie using the gel column agglutination test (DiaMed-Vet® feline typing gel, DiaMed, Switzerland). This test is easier to interpret than the card method, although it requires a specially designed centrifuge that may be cost-prohibitive in some settings. An evaluation of various blood typing kits and methods revealed that accuracy of blood type must be high and working hand in hand with time efficiency. A complete comparison of kits and methods for blood typing is as follow.An evaluation of various blood typing kits and methods revealed that accuracy of blood type must be high and working hand in hand with time efficiency. A complete comparison of kits and methods for blood typing is as follow.An evaluation of various blood typing kits and methods revealed that accuracy of blood type must be high and working hand in hand with time efficiency. A complete comparison of kits and methods for blood typing is
Antibiotic Resistance and Horizontal Gene Transfer in Bacteria
Introduction to Antibiotic Resistance Antimicrobial compounds, including natural and synthetic antibiotics, have been crucial in combating infections. Antibiotic resistance, however, has risen rapidly, threatening public health. Resistance can develop through mutations or acquisition of resistance genes via horizontal gene transfer, which has become the primary driver of the current antimicrobial resistance pandemic. Origins of Antibiotic Resistance Antibiotic resistance is ancient, arising from interactions between organisms and their environment. Many antibiotic-producing bacteria, such as Streptomyces species, carry self-resistance mechanisms. Environmental non-antibiotic-producing bacteria have also evolved resistance to survive alongside these producers. Even ancient permafrost samples reveal genes resistant to β-lactams, tetracyclines, and glycopeptides, showing the long-standing presence of resistance genes. (https://share.google/images/BHfaQxPqmbpyS3GPC) Mechanisms of Horizontal Gene Transfer Conjugation Conjugation involves direct transfer of DNA from one bacterium to another, often via plasmids. Plasmids carrying mobile genetic elements such as transposons or integrons spread resistance genes across bacterial populations, including clinically important genes like blaCTX-M and quinolone resistance genes. Transformation In transformation, bacteria uptake DNA fragments from their environment. For instance, penicillin and streptomycin resistance genes were transferred between Streptococcus pneumoniae strains in early experiments, demonstrating this mechanism’s role in spreading resistance. Transduction Transduction occurs when bacteriophages transfer DNA between bacteria “by accident.” This process contributes to resistance evolution in species like Staphylococcus aureus and other clinically relevant bacteria. Environmental Factors and Antibiotic Use Widespread antibiotic use in medicine, agriculture, and aquaculture accelerates resistance by increasing selective pressure. Most antibiotics are excreted unchanged into the environment, creating hotspots for resistance gene transfer. Increased selection pressure has also accelerated horizontal gene transfer and the abundance of resistome elements. Conclusion Horizontal gene transfer—including conjugation, transformation, and transduction—is key to spreading antibiotic resistance genes among bacteria. Understanding these mechanisms is critical to combating the rise of resistant pathogens and protecting public health. To support responsible antibiotic use, Bioguard offers the miniAST Veterinary Antibiotic Susceptibility Test Analyzer, a tool designed to help combat antimicrobial resistance with game-changing features: Feature Benefit Fast Results Get results in just 6 hours, enabling swift and confident treatment. Automated Interpretations Instantly deliver precise susceptibility profiles, supporting faster, more informed clinical decisions and optimizing patient care. Dual-Sample Testing Double the efficiency with simultaneous analysis of two samples at once. High Accuracy Achieve an impressive 92% accuracy rate compared to traditional disc diffusion tests. 📌 Note for Veterinarians: The miniAST Veterinary Antibiotic Susceptibility Test Analyzer is available exclusively to licensed veterinary clinics and hospitals. 📩 How to Order miniAST To purchase miniAST or request a quotation, please contact our sales team or email our customer service: 📧 service@bioguardlabs.com ☎️ Please include your hospital name and contact number so our sales representative can follow up with you directly. Source: Akrami F, Rajabnia M, Pournajaf A. Resistance integrons; A Mini review. Caspian J Intern Med. 2019. 10(4):370-376. Babakhani S, Oloomi M. Transposons: the agents of antibiotic resistance in bacteria. 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