Cryptosporidiosis
Bioguard Corporation Cryptosporidiosis is an illness you get from the parasite Cryptosporidium. It causes watery diarrhea and other gastrointestinal (gut) symptoms. In addition to stomach infection, this parasite can infect the respiratory system causing a cough and/or problems breathing. The family Cryptosporididae belongs to the phylum Apicomplexa characterized by an anterior (or apical) polar complex (with apical rings, micronemes, and subpellicular microtubules), which allows penetration into host cells. Cryptosporidium species are able to infect a broad range of hosts including humans, domestic and wild animals (mammals, birds, fish, marsupials, reptiles, and amphibians) worldwide. Transmission and Life Cycle Humans and animals become infected with Cryptosporidium by touching anything that has come in contact with contaminated feces, although the most common mode of transmission is represented by ingestion of oocysts in contaminated food and water or air. Cryptosporidium has three developmental stages: meronts, gamonts, and oocysts. They reproduce within the intestinal epithelial cells. Two types of oocysts, thick-walled and thin-walled, are produced during sexual reproduction. Thick-walled oocysts are excreted from the host into the environment, whereas thin-walled oocysts are involved in the internal autoinfective cycle and are not recovered from stools. Oocysts are infectious upon excretion, thus enabling direct and immediate fecal-oral transmission. Clinical Symptoms The most common symptoms of cryptosporidiosis are watery diarrhea and stomach cramps. Other symptoms may include fever, nausea, vomiting, and loss of appetite. Symptoms and severity of infection vary with the age and immune status of the host. Cryptosporidium infections are uncommonly detected in cats and dogs. Cryptosporidiosis can sometimes make dogs and cats sick, but animals with signs are atypical. In most cases, epithelial damage is minimal, but in severe cases, infection is associated with losing the ability to maintain water balance. Clinical signs are usually restricted to mild diarrhea unless the host is immunosuppressed or has another underlying condition such as viral infection or malignancy. Diagnosis Cryptosporidiosis is a diarrheal disease that is spread through contact with the stool of an infected person or animal. The disease is diagnosed by examining stool samples. Oocyst excretion is intermittent, and multiple stool samples may be needed. Diagnostic methods include: Microscopic examination: Typically, stool samples are analyzed microscopically using various techniques, including acid-fast staining and Ziehl-Nielsen staining. Real-time PCR: The most accurate method for detecting Cryptosporidium spp. is through a fecal PCR assay. Immunologic tests: These include direct fluorescent antibody tests and enzyme immunoassays to detect Cryptosporidium sp. antigens. Treatment and Prevention Most patients with healthy immune systems will recover from cryptosporidiosis without treatment. Supportive measures, oral or parenteral rehydration, and hyperalimentation may be needed for immunocompromised patients with severe disease. The best way to prevent the spread of Cryptosporidium at home is by practicing good hygiene. References Sardinha-Silva A, Alves-Ferreira EVC, Grigg ME. Intestinal immune responses to commensal and pathogenic protozoa. Front Immunol. 2022 Sep 16;13:963723. Sponseller JK, Griffiths JK, Tzipori S. The evolution of respiratory Cryptosporidiosis: evidence for transmission by inhalation. Clin Microbiol Rev. 2014 Jul;27(3):575-86. Watier-Grillot S, Costa D, Petit C, et al. Cryptosporidiosis outbreaks linked to the public water supply in a military camp, France. PLoS Negl Trop Dis. 2022 Sep 12;16(9):e0010776.
Ferret Coronavirus
Bioguard Corporation The coronavirus of ferrets was first described in 1993. This ferret enteric coronavirus (FRECV) caused an enteric disease called epizootic catarrhal enteritis (ECE) or green slime disease. Later, a ferret systemic coronavirus (FRSCV)-associated disease, resembling the dry form of feline infectious peritonitis (FIP), was identified. ECE is characterized by high morbidity (nearly 100%) but low mortality (< 5%). FRSCV is associated with a high mortality rate and short duration of illness. Pathogen Coronaviruses are large, enveloped, positive-stranded RNA viruses classified under the genus Coronavirus within the family Coronaviridae, order Nidovirales. Virions are roughly spherical and are notable for the large spike (S) glycoprotein that extends from the virus envelope, which resembles a crown or solar corona when imaged using an electron microscope. The diameter of ferret coronavirus is about 120 nanometers, and its genome is about 28 kilobases. Transmission Both the enteric (FRECV) and systemic (FRSCV) ferret coronaviruses are classified as group 1 coronaviruses (that is, alphacoronaviruses), related to feline coronavirus and canine enteric coronavirus. The routes for transmission of FRECV and the FRSCV are suggested to be fecal–oral. Many facts of the pathogenesis of the virulent systemic ferret coronavirus remain unknown, but similar to FIPV, macrophages appear to play an important role in the inflammatory response. Clinical signs After infection of FRECV, the virus causes blunting of the intestinal villi and consequent maldigestion and malabsorption. Clinical signs include anorexia, vomiting, diarrhea, melena, dehydration, lethargy, and weight loss. The microscopic lesions include diffuse lymphocytic enteritis, with villus atrophy, fusion, and blunting; vacuolar degeneration and necrosis of the apical epithelium; or a combination of all these lesions. FRSCV-associated disease causing FIP-like lesions has been reported in mostly young (<18 months) ferrets. Clinical signs are nonspecific, including anorexia, weight loss, diarrhea, and enlarged intra-abdominal and, less commonly, peripheral lymph nodes. FRSCV is grossly associated with pale to white nodules (granulomatous inflammation) in multiple organs, including the spleen, kidneys, mesenteric lymph nodes, intestines, liver, lungs, and brains. Granulomas have a heterogenous cellular composition including macrophages, T and B lymphocytes, and plasma cells. Diagnosis Definitive diagnosis requires intestinal biopsy and histopathological examination, with confirmation of viral antigen or nucleic acid by immunohistochemistry or in situ hybridization. RT-PCR and electron microscopy can be used to examine feces from ferrets. Systemic coronavirus disease in ferrets can be confirmed by histological evaluation of biopsies and intralesional coronavirus nucleic acid detection. RT-PCR has been used to identify viruses in tissues and can differentiate ferret enteric coronaviruses from ferret systemic coronaviruses. References 1. Haake C, Cook S, Pusterla N, et al. Coronavirus Infections in Companion Animals: Virology, Epidemiology, Clinical and Pathologic Features. Viruses 2020, 12(9), 1023. 2. Osborne AJ, Hussain SS, Helman EE, et al. Ferret Systemic Coronavirus in Alpha-1 Antitrypsin Knockout Ferrets. Comp Med. 2022 Dec 1;72(6):410-415. 3. Gnirs K, Quinton JF, Dally C, et al. Cerebral pyogranuloma associated with systemic coronavirus infection in a ferret. J Small Anim Pract. 2016 Jan;57(1):36-9.
Infectious Myxomatosis of Rabbits
Bioguard Corporation Myxomatosis is primarily a disease of rabbits caused by infection with the myxoma virus. It mainly occurs in domestic and wild rabbits. The virus is harmless to humans. Myxomatosis can result in lumps developing around the ears and face. These lumps are named myxomas and the disease virus was named after this lesion. It was first discovered in South America, California and Mexico in 1896. Sick animals will die within a few days to two weeks after infection, and the fatality rate is close to 100%. Currently, there is no effective treatment. Pathogen Myxoma virus is the type species of the Leporipoxviruses, a genus of Chordopoxvirinae, double stranded DNA viruses, whose members infect leporids and squirrels, inducing cutaneous fibromas from which virus is mechanically transmitted by biting arthropods. Pathogenesis studies confirm that the virus initially replicates in dermal cells at the inoculation site, likely dendritic cells. From there, the virus spreads to local macrophages and epidermal cells, and to the draining lymph node. Virus replication in the latter results in lymphoid depletion, with extensive loss of cortical and paracortical lymphocytes. From the lymph node the virus spreads via blood leukocytes to distal tissues including the spleen and other lymphoid tissues, testis, lungs, and skin. Transmission and Clinical Signs Currently, myxoma virus is enzootic to the Americas, Europe, Australia and other regions. The principal mode of transmission of the virus is mechanical transport of virus on mouth parts by arthropod vectors such as ticks, mosquitoes, and fleas through bites. It can also transmit the virus to other rabbits via direct contact. The general incubation period is 3-7 days, up to 14 days. The first sign of disease is conjunctivitis that rapidly becomes more severe and is accompanied by a milky discharge from the eye. The rabbit has no energy and no appetite, with a fever that may reach 42°C. In severe outbreaks, some rabbits die within 48 hours after signs appear. Those that survive become progressively weaker and develop a rough coat. The eyelids, nose, lips, and ears become puffy, which gives a swollen appearance to the head. The ears may droop. In females, the vulva becomes inflamed and swollen with fluid; in males, the scrotum swells. Other signs include discharge of pus from the nose, difficulty breathing, and coma. Death usually occurs within 1 to 2 weeks after signs appear, and the fatality rate is close to 100%. Diagnosis Gross lesions: The most prominent gross lesions in in rabbits with myxomatosis are the skin tumors and the pronounced cutaneous and subcutaneous edema, particularly in the area of the face and around body orifices. Hemorrhages of the skin, heart, and subserosa of the gastrointestinal tract may be observed. Microscopic lesions: Lesions in the skin involve epithelial cells, fibroblasts, and endothelial cells and range from proliferative to degenerative, depending on the strain of virus. The skin tumors result from proliferation of undifferentiated mesenchymal cells, which become large stellate (myxoma) cells surrounded by a homogeneous matrix of mucinous material interspersed with capillaries and inflammatory cells Lab tests include serology and molecular diagnosis. Serology: immunofluorescent assay (IFA), ELISA, complement fixation test (CFT) Molecular diagnosis: PCR Treatment and Vaccination Unfortunately, there is no specific treatment for myxomatosis. Vet can only offer supportive care, including fluids, antibiotics to prevent secondary infections, and pain medication. The myxomatosis vaccine is available in some countries. Reference Bertagnoli S, Marchandeau S. Myxomatosis. Rev Sci Tech. 2015 Aug;34(2):549-56. Espinosa J, Ferreras MC, Benavides J, et al. Causes of Mortality and Disease in Rabbits and Hares: A Retrospective Study. Animals (Basel). 2020 Jan 17;10(1):158.
Diagnosis of Feline Respiratory Mycoplasma Infection
Bioguard Corporation In cats, ’mucosal’ mycoplasma infections typically cause ocular and respiratory disease, and less frequently neurological or joint disease. These Mycoplasma species are distinct to the haemotropic mycoplasmas that target red blood cells, causing hemolytic anemia in cats. Mycoplasma felis is typically associated with Upper Respiratory Tract Disease (URTD) in cats. Transmission M. felis is mainly transmitted from an infected cat to an in-contact one by aerosol, but also by grooming. Stresses, including overcrowding environments, concurrent respiratory viral infections, and poor hygienic situations, may promote transmission of the infection between cats. Clinical symptoms Mycoplasma felis is typically associated with URTD but sometimes it may be associated with lower respiratory tract infections. Common clinical signs include clear or colored discharge from the eyes or nose, coughing, sneezing, conjunctivitis, chemosis, lethargy, and anorexia. Lower respiratory tract infections can result in pneumonia with fever, cough, tachypnoea, and lethargy. Diagnosis Culture of mycoplasmas can be used to demonstrate infection, but it takes time for culture and rapid transport of samples to the laboratory is required. Demonstration of organisms via real-time PCR is increasingly being used to circumvent the difficulties with culture, Treatment Antimicrobial therapy is commonly used to treat mycoplasma respiratory infections. Doxycycline is a good first line agent because it is well tolerated by cats and relatively narrow in spectrum. The recommended dose is 5 mg/kg, PO, q12h or 10 mg/kg, PO, q24 (Lappin et al., 2017). Oxytetracycline or chlortetracycline ophthalmic ointment can be used q6h in addition as topical treatment. References: Vekšins A. Feline upper respiratory tract disease – Computed tomography and laboratory diagnostic. Vet World. 2022 Jul;15(7):1880-1886. Framst I, Ramesh P, Cai HY, Maboni G. Complete genome sequences of Mycoplasma cynos and Mycoplasma felis isolated from dogs and cats with infectious respiratory disease. Microbiol Resour Announc. 2024 Apr 11;13(4):e0124323.
Tritrichomonas Infection in Cat
Bioguard Corporation Tritrichomonas foetus is a significant cause of large bowel diarrhea and persistent colitis in cats. These pear-shaped organisms have three anterior flagella and one posterior flagellum. They have a distinctive undulating membrane, which gives them a similar appearance to Giardia. However, they do not form cysts and are transmitted directly from one host to another as trophozoites. The infection is most prevalent among young cats living in close quarters, such as in densely populated catteries and shelters. A notable investigation into purebred show cats discovered a 31% infection rate among 117 cats spanning 89 catteries, as detailed in Gookin’s 2004 study Clinical Signs Some cats infected with T. foetus may not exhibit any symptoms, particularly older cats that are in good health. However, most cats with T. foetus infection suffer from mild to severe lymphoplasmacytic and neutrophilic colitis, which causes recurrent episodes of large bowel diarrhea that may vary in consistency from semiformed to “cow pie” and emit a foul odor. Diarrhea may contain fresh blood or mucus. Insevere cases, kittens may experience painful anal irritation, fecalincontinence, or even rectal prolapse. Affected cats usually maintain a healthy appearance and good body condition overall. The presence of diarrhea can be exacerbated by other intestinal infections or parasites, particularly Giardia and ryptosporidium. Diagnosis To confirm the infection of T. foetus, there are three methods available – direct fecal microscopy, fecal culture, and fecal polymerase chain reaction (PCR) assay. Direct fecal microscopy involves identifying the motile trophozoites T. foetus in fresh wet smears of diarrheic feces taken directly from the rectum. This method identifies the organisms in about 14% of cases and is less effective with formed or dried feces. In cats who have been treated with antibiotics recently, the detection rate decreases. Trichomonads, which resemble Giardia in size and shape, can be distinguished by their unique undulating membrane and rapid, jerky motility, contrasting with Giardia’s “falling leaf” movement. Fecal culture can be done in-house or at a specialized lab. It helps increase the chances of identifying the organisms. In specific cases, a saline flush might be performed by inserting a catheter through the cat’s anus to wash the colon with saline, followed by aspiration of fecal material. Fecal PCR is the most accurate method for identifying T. foetus. To perform this test, the fecal sample should not contain any litter. This technique detects the organism’s DNA traces in the cat’s stool. It’s best to conduct testing on cats that have not received antibiotics for at least two weeks for the most accurate test results. Antibiotics can temporarily reduce the number of T. foetus, leading to false negatives. Treatment Often, many approaches for treating chronic diarrhea have been tried unsuccessfully before a true diagnosis of T. foetus is confirmed. Tritrichomonas foetus is resistant to most antibiotics and is extremely difficult to eradicate (Gookin 2001). Numerous antibiotics have been evaluated. Some antibiotics reduce the number of organisms and improve the diarrhea without eliminating the infection, so diarrhea relapses whenever antibiotics are stopped. Diarrhea is typically refractory to corticosteroids. The most successful treatment for eliminating T. foetus is ronidazole (30 mg/kg PO, once or twice daily for 14 days). The side effects in some cats include lethargy, decreased appetite, and neurotoxicity. Cats with neurotoxic signs usually improve when the drug is stopped, but recovery can take 1 to 4 weeks. Ronidazole should not be used in pregnant and nursing queens or in very young kittens. Ronidazole is not approved for veterinary or human use, but some pharmacies compound chemical grade ronidazole for veterinary use. Because of its bitter taste, ronidazole compounded in gel caps is better tolerated than flavored suspension. When prescribing ronidazole obtain informed consent and instruct owners to wear protective gloves when handling it. Management of Tritrichomonas foetus Infection In cases where cats show mild or sporadic symptoms of diarrhea caused by T. foetus, and treatment is not possible due to potential side effects, costs, or the owner’s preferences, it is important to know that diarrhea may naturally go away with time, which can take up to two years. However, such cats are likely to remain lifelong carriers of the parasite. The outlook for cats receiving treatment is generally positive. A majority of treated cats exhibit better stool consistency in just a few days, though diarrhea might linger briefly as related secondary inflammation subsides. Nonetheless, around 25% of cases might experience a continuous infection despite initial treatment. Fortunately, T. foetus has a short lifespan outside its host and is easily neutralized by common disinfectants. To mitigate infection risks, it’s advised to uphold strict litter box cleanliness through daily cleansing, isolate cats under treatment, minimize stress factors, prevent overcrowding, and implement regular screenings in breeding and shelter settings whenever feasible.
Encephalitozoon cuniculi in Rabbits
Bioguard Corporation Encephalitozoon cuniculi is a microsporidial, unicellular, spore-forming, obligate intracellular parasite. It can invade the host’s central nervous system, kidneys, crystals, etc. E. cuniculi affects rabbits by causing damage to the brain, nervous system, kidneys, and other important organs. E. cuniculi pose a zoonotic risk to immune-compromised humans. In addition, it can infect various mammals, such as rabbits, rats, mice, horses, foxes, cats, dogs, muskrats, leopards, and baboons. Transmission and Life Cycle E. cuniculi has a direct life cycle with both horizontal and vertical (transplacental) transmission. In rabbits, the common routes of natural horizontal infection are via the ingestion of contaminated food or water or, less commonly, via inhalation of spores. After ingestion, the spores invade enterocytes and then spread through bloodstream or the lymphatic system. Then, it is carried into the blood circulation to target organs (kidney, central nervous system, eye, liver, and heart) where it causes inflammation. Antibody can be detected 2-3 weeks after infection, and IgM are usually detectable up to 18 weeks post-exposure. Spores are passed in the urine of rabbits, beginning around 35 days after infection, and continue to be excreted for 2 to 3 months. Serological surveys show high seroprevalence rates (23-75%) of E. cuniculi in rabbits. The seroprevalence rate of E. cuniculi is about 63.2-67.8% in Taiwan. However, most are asymptomatic and few are found to be affected by disease. Clinical signs When E. cuniculi infect the rabbits, the common clinical signs include head tilt (vestibular disease), hind limb paresis (weakness of the hind limbs), urinary incontinence, renal failure, cloudy eyes (anterior uveitis), cloudy lenses of the eyes (cataracts), or even blindness. Diagnosis Clinical diagnosis of encephalitozoonosis can be challenging because of the following reasons. 1. Serologic evidence is strong evidence of infection but not indicative of clinical signs. 2. Seroconversion does not result in a protective response for the patient. 3. Histologic severity and distribution of lesions are not directly correlated with the severity of clinical signs. 4. Most infected rabbits are asymptomatic or carriers. Diagnostic methods of encephalitozoonosis include histopathology, serology, and molecular diagnosis. • Histopathology- histological examination combined with special staining, or concentrated urine for cytological microsporidia detection • Serology- indirect immune fluorescence antibody test, direct agglutination test, ELISA, western blot • Molecular diagnosis- PCR Treatment and Prevention No uniformly effective treatment has been established. Fenbendazole, Albendazole, and Oxibendazole may be effective in vivo. The treatment of choice generally is fenbendazole, because it has been shown to both prevent and treat E cuniculi infections. To reduce the inflammatory reaction, steroids or NSAIDS may be applied. The use of systemic steroid therapy, although controversial, has been advocated to reduce severe CNS inflammation. The risk with this treatment is that corticosteroids might suppress the immune system to the point that E cuniculi or other infectious organisms may create additional problems. Cases involving the ocular form need to be referred to a veterinary ophthalmologist if surgery is recommended. Prevention of the disease from spreading includes thoroughly cleaning the rabbit’s environment, applying a diluted solution of bleach (1:32) for disinfection, and providing clean water and food to rabbits.
Psittacosis in Birds
Bioguard Corporation Psittacosis (parrot fever), also known as ornithosis, is a bacterial zoonotic disease caused by the bacterium Chlamydia psittaci. It is usually spread by exposure to infected birds at home, pet stores, pigeon stalls and other locations where birds are kept or displayed. The disease was first reported in Switzerland in 1879, and then occurred successively in Britain, Europe, USA, Central and South America and other regions. The incubation period varies from 5-28 days. The clinical symptoms are nonspecific and may include fever, chills, headache, muscle aches, and cough. Etiology Chlamydia psittaci includes six avian (A–F) and two mammalians (WC in cattle and M56 in muskrat) serotypes with distinct host specificity, based on serotyping using monoclonal antibodies in the 1990s. Different serotypes have been isolated from different avian species like serotype A in psittacine birds, B and C in both ducks and geese, D in turkeys, E mainly in pigeons (also in other avian species), and F in parakeets and turkeys. Serotype A is often reported in human zoonotic cases. Based on recent genotypic classification, C. psittaci has several classical genotypes with relevant host specificity. The genomic sequence encoding the outer membrane protein (ompA) is used to classify genotypes, which are employed to study isolates from infected birds and isolates in mammals. All identified genotypes are considered capable of transmission to humans. Transmission Infected birds may shed C psittaci in their droppings, saliva, mucus, feather dust and eye/nasal discharge. Healthy birds may then inhale the bacteria in airborne particles, such as dust from dried droppings and feathers. Birds may also ingest C psittaci from contaminated food, water, perches, and toys. Some infected birds don’t show any signof illness. However, they may become ill and shed the bacteria during times of stress (e.g., battling another infection, changing diet, or living in a crowded environment). Humans most commonly catch the disease from infected birds by breathing in the dust from shed feathers, secretions, and droppings. Less commonly, birds infect people through bites and beak-to-mouth contact. Clinical symptoms The incubation time for infected birds is about 3 days to several weeks up to a month. In birds, the symptoms include poor appetite, ruffled appearance, eye or nose discharge, green or yellow-green droppings, and diarrhea (loose droppings). Occasionally, birds may die from the disease. Some birds may shed the bacteria while exhibiting only mild or no symptoms. C. psittaci may affect some or all of a bird’s organ systems, most commonly the liver, spleen, respiratory tract, and digestive tract. Diagnosis Since psittacosis symptoms can look like an array of other diseases in birds, special tests are needed to diagnose the presence of C. psittaci. Methods to diagnose chlamydial infections include: Antigen detection- immunohistochemistry, immunofluorescence test and ELISA Serology- complement fixation, ELISAs, and indirect immunofluorescence test Molecular diagnosis- PCR Treatment Treatment is usually with oral or injectable doxycycline antibiotic. Since doxycycline only kills the Chlamydia organisms when they are active and dividing, and the lifecycle of these organisms is prolonged, with possible periods of dormancy (ceasing to be active for a period of time), drug treatment should go on continuously for the recommended period of 45 days, without interruption.
Pigeon Circovirus
Bioguard Corporation Pigeon circovirus (PiCV) is an infectious disease that mainly affects young pigeons between 1 and 4 months of age. Mortality is variable, but it can approach 100%. Pigeon circovirus infections have led to the loss of lymphoid tissue in immune system organs, and for this reason, PiCV is regarded as an immunosuppressive agent in pigeons. Etiology Pigeon circoviruses, also known as columbid circovirus (CoCV), belong to the genus Circovirus in the family of the Circoviridae. They are small, non-enveloped viruses consisting of single-stranded circular DNA. Pigeon circovirus is antigenically distinct from the psittacine beak and feather disease (PBFD) virus, which also belongs to the genus Circovirus, but does share some homologous. Transmission The pigeon circovirus is transmitted mainly horizontally. Detection of the virus in the intestine, cloaca, and feces support fecal–oral route transmission. Also, inhalation of other fecal-contaminated materials, such as feather dust, has been suggested as a potential respiratory route of infection. Vertical transmission of PiCV is also possible by the detection of the virus in testis and semen samples of breeding cocks, the ovary but not in the oviduct of the hens, in embryonated eggs, and chicks recovered from eggs shortly before hatching. Clinical signs and lesions The clinical signs of PiCV infections in pigeons is highly varied. In pigeons between 1 and 4 months of age, circovirus infections are associated with lethargy, anorexia, ruffled feathers, dyspnea, diarrhea, and fluid-filled crop, also known as ‘young pigeon disease syndrome’ (YPDS). However, this syndrome should be considered a multifactorial disease. In most cases, concurrent infections can be demonstrated with all possible viral, bacterial, and parasitic agents hampering the assessment of the exact role of the circovirus. The most obvious lesion is a swollen, edematous bursa in the acute phase of infection. However, more chronic infections result in atrophy of the bursa. Histological lesions consist of lymphocyte depletion in lymphoid tissue and characteristic intracytoplasmic basophilic inclusion bodies (mainly in macrophages) in the lymphoid tissue. Diagnosis and Prevention Before having the sequence of the pigeon circovirus, diagnosis of PiCV infections mainly depended on histopathological examinations and electron microscopy findings of the intracytoplasmic and/or intranuclear inclusion bodies in lymphoreticular and hepato-intestinal tissues. Since publication of PiCV sequence, the virus now can be detected by polymerase chain reaction (PCR), in situ hybridization, and dot blot analysis. Currently, there is no specific treatment or effective vaccine against PiCV since pigeons infected with PiCV could die from secondary infections caused by the virus. At the moment, protection against potential detrimental effects of PiCV infection relies on good biosecurity measures in the loft. Reference1. Schmidt R.E. Circovirus in Pigeons. J. Assoc. Avian Vet. 1992;6:204.2. Woods L.W., Latimer K.S., Niagro F.D., Riddell C., Crowley A.M., Anderson M.L., Daft B.M., Moore J.D., Campagnoli R.P., Nordhausen R.W. A retrospective study of circovirus infection in pigeons: Nine cases (1986–1993) J. Vet. Diagn. Investig. 1994;6:156–164.3. Tian D. Bibliometric analysis of pathogenic organisms. Biosaf. Health. 2020;2:95–103.
Lyme Disease in Dogs
Oliver Organista, LA Lyme disease is triggered by the bacterium Borrelia burgdorferi, which belongs to the spirochete class, characterized by its worm-like, spiral shape within the genus Borrelia. This bacterium is spread to both dogs and humans through the bite of an infected black legged tick, also known as the deer tick (Ixodes scapularis). The lifecycle of the I. scapularis tick occurs at various times throughout the year, influenced by geographic location, which in turn affects the timing of Lyme disease transmission. This disease is predominantly found in certain regions, including southern New England, the eastern Mid-Atlantic, the upper Midwest (notably Wisconsin and Minnesota), and parts of the West Coast such as northern California in the United States. Lyme disease is also encountered in Europe and Asia. Typical habitats for these ticks include forests, grassy areas, wooded and marshy zones near bodies of water, and secluded or rural parts of homes and buildings. In Canada, Lyme disease can be spread by two types of black legged ticks: Ixodes scapularis and Ixodes pacificus. Dogs are most often bitten by adult I. scapularis ticks, which are particularly active during the cooler months of early spring and late fall. It is rare for a female tick to pass B. burgdorferi directly to her offspring. Ticks generally acquire the infection during their juvenile stages after feeding on an infected wildlife host, typically rodents. Since ticks feed only once at each life stage, the bacterium’s next chance to spread occurs with the tick’s subsequent blood meal in its next developmental stage. Clinical symptoms Symptoms of Lyme disease typically emerge several months after infection, often between two to five months post-exposure. The clinical presentation of Lyme disease can closely resemble that of anaplasmosis, as both diseases share similar symptoms and occur in similar regions of the country. The most common indicators of Lyme disease in dogs include: Lameness: One of the hallmark signs of Lyme disease is the inability to properly use one or more limbs, often due to pain. Swollen lymph nodes: The swelling of lymph nodes, located in areas such as the neck, chest, armpits, groin, and behind the knees, often signals an immune response to the infection. Joint swelling: Dogs may show signs of swollen joints, which can lead to stiff movements or reluctance to be touched, indicative of discomfort. Fatigue: Affected dogs may display flu-like symptoms, including a noticeable decrease in energy and increased lethargy. Loss of appetite: A reduction in eating habits, particularly if it results in weight loss, can be a symptom of Lyme disease. Fever: A fever is another possible symptom that can accompany the other signs mentioned. In some uncommon instances, untreated Lyme disease can lead to serious complications involving the kidneys, nervous system, and heart. Kidney involvement is the second most frequent severe manifestation of Lyme disease in dogs and often proves to be fatal. Cases involving the nervous system may present with facial paralysis and seizures. Heart-related complications, while rarer, have also been documented. Diagnosis To diagnose Lyme disease in dogs, serologic assays are the most widely used methods. While some laboratories continue to utilize traditional approaches like the whole-cell enzyme-linked immunosorbent assay (ELISA) , the immunofluorescence assay (IFA), and rapid tests. These tests identify the presence of antibodies against specific proteins of B. burgdorferi, offering a simple yes/no result regarding the dog’s serology status. Treatment Treatment is advised for dogs that test positive for Lyme disease and show clinical symptoms, as well as for asymptomatic dogs that have signs of protein-losing nephropathy. The antibiotics doxycycline and minocycline are the primary medications used, administered at a dose of 10mg/kg orally every 12 to 24 hours for 30 days. Amoxicillin and erythromycin are alternative antibiotic options. Additionally, a non-steroidal anti-inflammatory drug (NSAID), such as carprofen or deracoxib, may be prescribed to manage symptoms. Prevention To safeguard against Lyme disease, the most effective approach is the consistent use of tick-prevention products throughout the year. There are numerous commercial options available for controlling ticks on both dogs and cats, such as systemic treatments (like isoxazolines), topical applications (such as permethrin and fipronil), and tick-preventive collars. Vaccination also serves as an effective means of protection. Additionally, limiting exposure to tick-infested areas and practicing caution in environments known to harbor ticks are important preventive strategies. References 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
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.
