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
Feline Hyperthyroidism
Sushant Sadotra Introduction: One of the most common diseases in middle-aged and older cats is hyperthyroidism. An increase in the production of thyroid hormones, i.e., T4 and T3, is the primary cause of this disorder. The enlarged thyroid gland in the neck region of the cat is the most common visible sign identifying hyperthyroidism. This enlargement is a non-cancerous tumor known as an adenoma. However, in some rare cases, it can also be caused by malignant tumors known as thyroid adenocarcinomas. Hyperthyroidism, also called thyrotoxicosis, increases the metabolic rate in an animal’s body because of high circulating thyroid hormone and often causes secondary problems by affecting all of the organs in the body. The reason for feline hyperthyroidism is unfamiliar. However, deficiencies or excesses of some elements in the diet and thyroid-disrupting could be responsible for the onset of hyperthyroidism. Hyperthyroidism is rare in dogs. However, if it occurs, it is primarily because of thyroid carcinoma. This contrasts with the case in hyperthyroid cats, where less than 5% of a thyroid tumor is carcinoma. Clinical signs: Cats’ most common clinical signs of hyperthyroidism are weight loss, increased appetite, vomiting, diarrhea, increased fecal volume, hyperexcitability, polydipsia, polyuria, enlargement of the thyroid gland, cardiomegaly, and congestive heart failure. Diagnosis A high thyroid hormone concentration in serum is the primary indication of hyperthyroidism. Therefore measuring serum total T4 concentration is the standard procedure that can confirm the diagnosis of hyperthyroidism in cats. In 5% – 10% of cases, it is also seen that cats so have normal T4 levels. It could be an indication of early or mild hyperthyroidism. Suppression of a high total T4 level to within reference range limits can also be caused by a nonthyroidal illness concurrent with hyperthyroidism. High free T4 concentration, medical history, and physical examination diagnose hyperthyroidism in cats with normal T4 levels. Treatment Radioiodine Therapy The radioiodine can be concentrated within the thyroid gland, where it targets the tumor by selectively irradiating and destroying hyper-functioning tissue. Radioactive iodine therapy is a simple, effective, and safe treatment for cat hyperthyroidism. Thyroidectomy Unilateral thyroid tumors can be easily treatable with surgical thyroidectomy without requiring thyroxine supplementation. Thyroidectomy can also be used for bilateral thyroid tumors. However, to avoid postoperative hypocalcemia, the functioning of the parathyroid gland must be preserved. After complete thyroidectomy, thyroxine should be administered for one to two days. Vitamin D and calcium treatment are also indicated if iatrogenic hypoparathyroidism develops. Chronic administration of an antithyroid drug An antithyroid drug acts by blocking thyroid hormone synthesis. Methimazole, carbimazole, and propylthiouracil are some of the most commonly used antithyroid drugs that are used to control hyperthyroidism. An initial dose of methimazole is 2.5 mg to 5 mg and is divided into two equal amounts to be given daily. Propylthiouracil has shown some adverse effects (hemolytic anemia and thrombocytopenia) and therefore is not recommended in cats. In less than 5% of treated cats, methimazole may have adverse effects such as agranulocytosis and thrombocytopenia. Besides lowering the circulating T4 concentration, cardiovascular signs such as tachycardia, tachypnea, hypertension, and hyperexcitability are often treated using β-adrenoceptor blocking agents such as propranolol and atenolol. Another strategic drug that inhibits the conversion of peripheral T4 to T3 is the oral cholecystographic agents such as ipodate, iopanoic acid, and diatrizoate meglumine. Lifelong nutritional therapy A diet with iodine levels below the minimum daily requirement is mainly prescribed for cats that are not suitable as a candidate for surgery or radioiodine therapy or in cats that develop adverse effects from oral medication. Compared to cats with severe hyperthyroidism, this nutritional therapy is more effective if the cat has a moderate increase in T4 levels. Hill’s® y/d Feline Thyroid HealthTM is one of the prescription diets available in the market with severely restricted iodine levels. The therapy can only control but not wholly treat hyperthyroidism. Also, cats on an iodine-deficient diet must not eat any other diet or food. If the diet is stopped, a setback will occur, and the therapy will be ineffective in regulating hyperthyroidism. References Vaske, Heather H et al. “Diagnosis and management of feline hyperthyroidism: current perspectives.” Veterinary medicine (Auckland, N.Z.) vol. 5 85-96. 20 Aug. 2014, doi:10.2147/VMRR.S39985 Carney, Hazel C et al. “2016 AAFP Guidelines for the Management of Feline Hyperthyroidism.” Journal of feline medicine and surgery vol. 18, 5 (2016): 400-16. doi:10.1177/1098612X16643252 Mark E. Peterson. Hyperthyroidism in Animals. Last full review/revision Jul 2019 | Content last modified Oct 2020. MSD MANUAL Veterinary Manual.
Canine Ehrlichiosis
Oliver Organista, LA Ehrlichiosis (also known as canine rickettsiosis, canine hemorrhagic fever, canine typhus, tracker dog disease, and tropical canine pancytopenia) is a tick-borne disease of dogs usually caused by organism Ehrlichia canis. Ehrlichia canis was first identified in 1935 in Algeria; dogs infested with ticks showed fever and anemia [1]. Later, during the Vietnam War, many military working dogs brought to Vietnam by the US army exhibited a severe disease called Tropical Canine Pancytopenia [3]. Later, it was renamed canine monocytic ehrlichiosis (CME). Canine monocytotropic ehrlichiosis (CME), caused by the rickettsia E. canis, is an important canine disease with a worldwide distribution. Diagnosis of the disease can be challenging because of its different phases and multiple clinical manifestations. CME should be suspected when a compatible history (living in or traveling to an endemic region, previous tick exposure), typical clinical signs and characteristic hematological and biochemical abnormalities are present [4]. German shepherd dogs are thought to be particularly affected by the disease, other breeds generally have milder clinical signs. Cats can also be infected [2] Figure 1a. Peripheral blood smear from a dog. On the feathered edge, monocytes rarely contain cytoplasmic morula (arrow) consistent with Ehrlichia canis. Source: https://tvmdl.tamu.edu/2019/10/01/ehrlichia-canis-discovered-in-dog/. 1b. Photomicrograph of an E. canis strain isolated from the leukocytes of a dog Uberlandia, Brazil. Andia,dia, , Brazil. Note the multiple mourale in the DH82 cell cytopolasm (arrows). Source: DOI:10.4142/jvs.2014.15.2.241 Ehrlichiosis symptoms in dogs can be classified into three stages: early disease (acute phase), sub-clinical (no outward appearance of disease), and clinical or chronic (long-standing infection) [5]. Acute Phase The acute stage of ehrlichiosis can last 2 to 4 weeks, during which the infection is either eliminated or your dog will progress to the sub-clinical phase. Symptoms of the acute stage include: Swollen lymph nodes Weight loss Respiratory distress Bleeding disorders (spontaneous hemorrhage or bleeding) Fever Neurological disturbances (meningitis or unsteady on feet) Sub-Clinical Phase In the sub-clinical phase, the Ehrlichia organism is present but there may not be any outward signs of disease. This is often considered the worst phase of the disease because it is able to progress undetected. In some cases the disease is detected when the vet notices prolonged bleeding from the injection site after taking a blood sample. If the organisms are not eliminated in this stage, your pooch’s infection may move to the next stage – clinical ehrlichiosis. Clinical Phase Clinical ehrlichiosis happens when the organism isn’t eliminated by the immune system in one of the previous stages. This stage can lead to several serious symptoms, including: Lameness Swollen limbs Neurological problems Bleeding episodes Anemia Eye problems (such as blindness or hemorrhage into eyes) This phase becomes extremely serious if the bone marrow (where blood cells are produced) fails, meaning that your pup will be unable to create any blood cells he needs to sustain life (platelets, white blood cells and red blood cells). Diagnosis can be performed using visual, serologic, or molecular methods. Erhlichia spp. replicate inside a membrane-bound vacuole (i.e., morula) that can sometimes be observed by light microscopic examination of stained blood smears inside either monocytes (E. canis and E. chaffeensis) or granulocytes (E. ewingii). A cross-reactivity between antibodies is possible when performing an immunofluorescent assay (IFA) or enzyme linked immunosorbant assays (ELISA) [7]. The most common molecular method used to diagnose an Ehrlichia spp. infection, particularly in dogs with acute illness where the onset of clinical signs may precede a measurable antibody response is by polymerase chain reaction (PCR) [8]. In Canines, blood counts and hematological tests are crucial to the diagnosis of Canine monocytic ehrlichiosis. Low blood counts or thrombocytopenia are often critical signs of ehrlichial infection. In a study conducted by Shipov et. al red blood cell count and hemoglobin were used as the diagnostic indicators for canine ehrlichiosis (2008). Within the study dogs were assigned to two categories: survivors and non- survivors. Within each group the prognostic indicators and treatment protocols were observed and compared. Most commonly the dogs under examination exhibited symptoms such as weakness pale mucous membranes, fever, and bleeding tendencies [9]. Ehrlichiosis is typically treated with a 28- to 30-day course of antibiotics, most often prescribing doxycycline [11,14]. Doxycycline tablets were administered orally once a day for 20 consecutive days, at a target dose level of 10 mg/kg. The actual dose administered was calculated as ranging between 10 mg/kg and 11.7 mg/kg [12] .Most dogs in the acute or subclinical phases will not require hospitalization and can be managed as outpatients at home with minimal supportive care (pain medications and appetite stimulants). Dogs with chronic ehrlichiosis may require hospitalization for aggressive supportive care that includes blood transfusions, steroids, IV fluids, and nutritional support [10]. Minocycline can be an effective alternative to doxycycline for clearing E. canis from the blood in nonacute infections [13]. Fortunately, most tick bites can be prevented through monthly flea and tick preventative care. There are plenty of options available, including topical, tablet, and chewable medications. Your veterinarian will be able to help you find the best option for your pet. If you live near wooded areas where ticks are prone, it is best to keep your dog away from these areas, since there currently is no vaccine for ehrlichiosis. When your dog comes back from any outdoor adventure, it’s important to inspect them for any ticks or fleas and remove them safely. Early removal of ticks is the best defense against the spread of any infection [15]. Reference Donatien, A., and F. Lestoquard. “Existence en Algerie d’une Rickettsia du chien.” Bull. Soc. Pathol. Exot 28 (1935): 418-419. Eddlestone, S.M., et al., Doxycycline clearance of experimentally induced chronic Ehrlichia canis infection in dogs. J Vet Intern Med, 2007. 21(6): p. 1237-42. Huxsoll DL, Hildebrandt PK, Nims RM, Walker JS. Tropical canine pancytopenia. J Am Vet Med Assoc. 1970;157(11):1627–32. Harrus S, Waner T. Diagnosis of canine monocytotropic ehrlichiosis (Ehrlichia canis): an overview. Vet J. 2011 Mar;187(3):292-6. doi: 10.1016/j.tvjl.2010.02.001. Epub 2010 Mar 11. PMID: 20226700. Veterinary Specialty Center Tucson (www.vscot.com), Ehrlichiosis in
An Overview Of Feline Parvovirus
Trinh Mai Nguyen Tang Feline panleukopenia virus (FPV) is a single-stranded DNA virus that causes feline leukopenia disease. It belongs to the family Parvoviridae, and is also known as Parvo in cats [1]. In the early years of the twentieth century, the first cases of FPV were reported in cats [2]. This is a common and dangerous disease in cats worldwide that occurs seasonally, especially from early summer to autumn with the highest peak in July, August, and September [3]. The virus usually resides in the everyday items of cats such as cages, beds, food bowls, etc [4]. Moreover, it has high resistance to physical factors and disinfectants, they can still survive for 30 minutes at temperatures up to 560C, and can even survive in contaminated environments for months or even years, which is why FPV is highly lethal and contagious in cats [4-5]. Transmission and clinical signs FPV is spread by the fecal-oral route when cats come into contact with food, water, objects, or secretions that contain the virus. The virus enters and infects cells through the feline transferrin receptor (fTfR) [6-7]. Previous reports also showed that the two main types of cells that FPV replicate are small intestinal crypt cells and lymphoid cells [8-9]. The replication of virus leads to impaired white blood cell function, and bleeding in the small intestine and stomach is the cause of hemorrhagic diarrhea in cats [10]. According to Yen et al.’s report in 2021, the percentage of small intestine congested is 100% in a total of 8 cats examined (Figure 1A-B), and 75% of intestinal mucosal ulcerations appear. Meanwhile, there are 6 cats with gastric congestion in 75% (Figure 1C) and 2 cats with pneumonia accounting for 25% (Figure 1-D). In addition, other lesions were also detected, such as enlarged lymph nodes in the mesentery, and infarcted spleen [10]. These lesions can cause symptoms such as anorexia, fever, vomiting, and hair loss in the early stages [11], followed by diarrhea, severe dehydration, electrolyte imbalance, hypoglycemia, hemorrhage or sepsis and endotoxins in the blood cause rapid death in cats if not treated promptly [12-15]. Furthermore, in some kittens, there is damage to the central nervous system such as hydrocephalus, and cerebellar hypoplasia [16]. According to Reif (1976), cats infected with FPV have an incubation period of 4 to 6 days [16], during infection can excrete virus-containing feces for up to 43 days, and they even can survive for more than 1 year in the lungs and kidneys [17] Figure 1. Symptoms of cat infection with FPV. A, B: Intestinal congestion, scattered or intermittent bleeding; C: Congested stomach contains a lot of fluid; D: Mild pneumonia [10] FPV can cause infection in cats 3 to 5 months of age when infected with them or in unvaccinated cats, especially kittens, with an almost 90% chance of mortality due to maternally derived antibodies (MDAs) weakened [18]. MDAs may protect kittens against disease during the first weeks of life, and they are mainly transmitted through colostrum [19-20]. However, a kitten’s immunity will depend on factors such as the length of the lactation, the quality of the colostrum, and the amount of milk they are ingested [21]. Figure 2. The immunity gap and maternally derived antibodies (MDAs) [24] Although kittens all have antibodies inherited from the mother, these antibodies can only protect for 6-8 weeks, these antibodies gradually disappear and create an immunity gap that makes it easier for the virus to attack [19]. The immunological gap (Figure 2) is the distance that the maternally derived antibodies from the mother cat to the kittens are reduced. This gap usually occurs when kittens reach the age of 8-12 weeks and interferes with the development of immunization immunity [24]. There is evidence that there is seroconversion with long-term antibody titers after administration of modified live vaccines (MLV) in kittens lacking MDAs compared with kittens receiving MDAs [22–23]. When MDA titres ≥1:10 as measured by inhibition of coagulation (HI), MLV vaccination should not be given because of seroconversion [19, 24]. Diagnosis FPV can be difficult to diagnose accurately because it has similar symptoms to feline immunodeficiency virus (FIV) infection. Symptoms of feline leukemia virus (FeLV) infection and pancreatitis vary depending on the extent of the infection. FPV detection using PCR There are many methods to detect the presence of FPV in the cat. One of the most widely used and informative methods today is PCR testing, which can use whole blood samples or feces [26]. FPV detection using ELISA method or Rapid test kit The ELISA method can detect the presence of FPV-specific antigens in cat feces. When cats show clinical symptoms, they can be tested by ELISA or using the FPV antigen rapid test kit. The FPV Antigen test kit made by Bioguard Corporation is simple, fast, and accurate with a specificity and sensitivity of 92.54%. FPV detection using blood test method One of the methods of FPV diagnosing is to count white blood cells through a blood test. Other reports have also shown that markedly reduced leukocyte counts in hematologic parameters are very common in cats with FPV usually below 3000 and may reach less than 200/mm3 [3]. Prevention and Treatment Because the FPV virus can survive for a long time in the environment and has high resistance to physical factors and disinfectants so it is necessary to clean the barn, shelter, and food bowl after the cat has been infected. In addition, it is necessary to isolate infected cats to avoid infecting other cats and becoming an outbreak FPV in cats is a dangerous disease with no cure. All treatment for leukopenia in cats is for symptomatic treatment. Although there is no cure for feline leukopenia, if detected in time, the symptoms can be treated and the cat can recover. Prevention The way to prevent cats from contracting FPV is vaccination. Atteunuated live virus vaccines can be used, but should not be given to kittens < 4 weeks of
Feline Polycystic Kidney Disease (PKD)
Maigan Espinili Maruquin Introduction Cats, as a fur family, require health attention. However, some felines can get infected with certain types of inherited diseases. One of the most prevalent genetic diseases is the Feline Polycystic Kidney Disease (PKD) [1, 2], which causes the progressive development of multiple fluid-filled cysts in the kidney and in some cases extends to the liver and pancreas [2-5]. Prevalence of the PKD in Persian cats has been studied in different countries including, the United Kingdom (49.2%) [6], Japan (46%) [7], Australia (45%) [8], and France (40.45%) [9]. Reports suggest that the disease is not related to the sex of the feline, after results show no statistical differences between males and females [9, 10]. Different species of felines can get the said disease like Charteux [11], Neva Masquerade cat [12], and Scottish Fold and American Shorthair [7], however, it is most commonly inherited by the Persian and Persian- related breeds [3] with 35 to 57% detection via ultrasonography or genetic testing [13]. It is suspected that all the feline breeds could have inherited the mutation where the disease starts, considering that around 80% of all current feline breeds have had some type of cross with Persian breed [3, 14]. In humans, 1 in 500–1000 of the general population can inherit Autosomal dominant polycystic kidney disease (ADPKD) [15], which is characterized by increase in kidney size caused by the development and progressive enlargement of renal cysts, eventually leading to a steady decline in glomerular filtration rate [16]. The PKD1 and PKD2 genes, which are responsible for coding the polycystin-1 and 2 proteins, where 85 % and 15%, respectively, are responsible for the mutations [17]. Relative to the cases recorded with ADPKD in cats, the feline ortholog of the human PKD1 gene, which is also named PKD1, were recorded to have a single germline mutation. During the mutation, at exon 29 of the feline PKD1 gene, position 3284, a pyrimidine base (cytosine, C) is substituted by a purine base (adenine, A), wherein the premature stop codon produced causes the 25% loss in the C- Terminal formation of polycystin-1 protein [3, 18, 19]. With similar features clinically and morphologically in both human and feline ADPKD [2], feline PKD is a good representation for human ADPKD [7]. Clinical Presentations Fig. 1. Postmortem images, including cross-section of the polycystic kidneys of a seven-year-old, entire male British shorthair cat (cat 4), tested positive for the PKD1 mutation, demonstrating multiple cysts of variable sizes in both kidneys (a, b). [4] The polycystin-1 is suggested to play a role in cell–cell and matrix–cell interactions [20]. The primary cilium, where this protein is expressed, functions in fluid transport and chemo and mechanoreceptors [21, 22]. Cysts of different sizes were presented in renal cortex and medulla, sometimes occurs in the liver and pancreas, as well [8], and increases both in size and quantity as they age [23]. With slow growth and progression, affected cats start to deteriorate renal functions [7]. The cysts develop by different scenarios including the increase of cell proliferation, fluid secretion, and extracellular matrix alterations, cilia with lost polarization would then alter the water reabsorption function [3, 24]. Secondary to renal cysts development, obstruction due to nephrolithiasis, lymphoma and chronic kidney disease with interstitial nephritis are also displayed, especially in old cats [8, 25] In a study conducted among cats in Turkey, some diagnosed cats were reported for fatigue, anorexia, and vomiting. During palpation, an increase in total kidney volume was discovered, and cystic lesions were seen in the cortex of both kidneys when ultrasonography was performed [19]. Generally, apathy, anorexia, weight loss, bad appearance of the coat, polyuria and polydipsia, and gastrointestinal disorders could be observed [26-28], while general dehydration and pale mucous membranes are also noticeable on clinical examinations [3]. Elevated serum Cre concentration has been presented as one of the clinical signs in cats from three years old, while other cats at nine showed normal concentration. This suggests variable clinical courses of the disease [7]. Whereas, few cases showed hepatic cysts an extrarenal manifestation [6]. Diagnosis Imaging Diagnosis Fig. 2. Ultrasound picture of a 2.5 year old Persian cat, positive for PKD. Note the distal enhancement beyond the anechoic cyst structures (arrow). The largest cyst measures 29 mm in diameter [8]. The Ultrasound is known to be with the highest successful diagnosis, allowing quick and reliable diagnosis [23], and is considered due to availability and non-invasive, safe, cheap and effectivity in detecting the presence of kidney cysts [28]. Whereas, radiography and intravenous urography are usually used in more advanced cases, like when there is a presence of multiple, large cysts [3]. Molecular Approach Various PCR methods have been used to identify and amplify the DNA fragment of interest [3]. The RFLP-PCR was developed and used [18], real-time PCR or quantitative PCR is known to be reliable and faster than the earlier technique [29]. Whereas, ARMS-PCR (Amplification-refractory mutation system-Polymerase Chain Reaction) presented its advantages in time, low quantity of samples needed and its low cost, which has resulted in 100% sensitivity and specificity [30]. The synergistic use of genetic testing to confirm the presence of the causal mutation and make an early diagnosis; and the ultrasound to diagnose polycystic kidney disease and to monitor the progression of the disease has been agreed by several authors to plan detection programs for feline PKD [3, 30-32]. For as early as three years old, affected felines can develop signs of impaired renal function, and thus, positive cats are strongly discouraged for breeding [7]. References Young, A.E., et al., Feline polycystic kidney disease is linked to the PKD1 region. Mamm Genome, 2005. 16(1): p. 59-65. Eaton, K.A., et al., Autosomal dominant polycystic kidney disease in Persian and Persian-cross cats. Vet Pathol, 1997. 34(2): p. 117-26. Schirrer, L., P.J. Marín-García, and L. Llobat, Feline Polycystic Kidney Disease: An Update. 2021. 8(11): p. 269. Nivy, R., et al., Polycystic kidney
Canine Hypothyroidism
Sushant Sadotra Introduction: Hypothyroidism is a prevalent thyroid disorder that is caused due to the deficiency of thyroid hormone. In this condition, there is an irregular short production and improper secretion of thyroid hormones into the blood from the thyroid gland. This leads to a slow metabolic rate and loss of proper body functions. Regarding pet animals, hypothyroidism is mostly occurring among dogs and rarely in cats and other pet animals. Hypothyroidism Etiology in canines: Imbalance at any level of the hypothalamic-pituitary-thyroid axis can cause hypothyroidism in animals, especially dogs. In Adult dogs, the onset of primary hypothyroidism can cause either because of lymphocytic thyroiditis or idiopathic atrophy of the thyroid gland. The gradual destruction of follicles and secondary fibrosis on the gland because of diffuse infiltration by lymphocytes, plasma cells, and macrophages into the thyroid gland. This condition is known as lymphocytic thyroiditis. Loss of thyroid parenchyma leads to the idiopathic atrophy of the thyroid gland, in which fatty tissue will replace the lost thyroid parenchyma. The condition can occur due to autoimmune thyroiditis. Secondary hypothyroidism can be caused due to the damage of pituitary thyrotrophs by tumor growth, leading to the deficiency of one or more pituitary hormones. Hypothyroidism in dogs can occur due to other rare causes such as congenital hypothyroidism or neoplastic destruction of thyroid tissue. Congenital hypothyroidism can be primary or secondary. Thyroid dysgenesis and dyshormonogenesis can cause congenital primary hypothyroidism in dogs. Congenital secondary hypothyroidism can show clinical signs caused by the deficiency of growth hormones such as dwarfism, lethargy, gait abnormalities, or pituitary dwarfism. Diagnosis of hypothyroidism in canines: A variety of nonthyroidal factors and other conditions can mimic thyroid disorder and mislead the correct diagnosis of canine hypothyroidism. The severity and chronicity of the clinical findings associated with hypothyroidism and other clinicopathologic abnormalities of the hypothyroid state can be a basis for the choice of a proper diagnostic test. Tests that could confirm the diagnosis of hypothyroidism in canines are mentioned below: Total T4: The initial screening test for hypothyroidism can determine Total T4 concentration. A dog with a T4 concentration lower than the reference range limits may be anticipated to have a hypothyroid issue. However, it can also indicate that the dog can have a nonthyroidal illness such as sick euthyroid syndrome. Therefore, the total T4 test alone cannot be a proper diagnosis. Free T4: In serum, unbound T4 is supposed to be biologically active. Therefore, it is a very used test to differentiate between hypothyroid and euthyroid dogs. Also, a free T4 assay can give a better diagnosis with high sensitivity and specificity. Most commercial Free T4 tests use the method of single-stage solid phase (analogue) assays. However, an equilibrium dialysis step can improve the accuracy. Free T3: Among T4 and T3, T3 is the most potent hormone in animals. Therefore, measuring Free T3 is also a sensitive diagnostic step. However, during the onset of the primary hypothyroidism, serum T3 determination is weak. Also, it is found that in hypothyroidism dogs, serum T3 concentrations could be low, normal, or high. If the serum concentration of T3 is high, it is to be checked whether or not anti-T3 antibodies are producing false results in the T3 radioimmunoassay. Serum TSH concertation: In primary hypothyroidism, high serum TSH concentrations are expected that further may lead to low serum concentrations of T4 and free T4. A species-specific TSH assay can be used to check the high level of serum TSH. However, a false-negative result showing normal TSH concentrations may indicate a condition of primary hypothyroidism; a false-positive result showing high serum TSH concentrations may indicate a nonthyroidal illness in a euthyroid dog. A normal serum TSH concentration can indicate secondary hypothyroidism in a few cases. Therefore, serum TSH concentration results should always be coupled with other tests for definite confirmations. TSH stimulation test: In this particular test, bovine TSH is introduced exogenously into the dog’s body, and the thyroid gland’s response is evaluated. Firstly, a basal T4 is measured. Then bovine TSH is administrated at a dosage of 0.1 U/kg. After 6 hours, T4 levels are calculated for the second time to check the response of the thyroid gland. Result interpretations could be a no response for hypothyroidism, a normal and blunted response for the sick euthyroid syndrome. Although the TSH stimulation test is one of the accurate tests to check thyroid function, it is expensive and less available. Imaging: Thyroid Ultrasonography can detect the decreased echogenicity followed by decreased thyroid volume. The procedure can take the best imaging of the thyroid gland by technetium 99m (99mTc). This diagnostic tool can differentiate between hypothyroidism and euthyroid sickness. Therapeutic trial: In this approach, a thyroxine supplementation is given to a dog at a particular dosage. If the response is positive, the supplementation is stopped to check for the return of clinical signs related to hypothyroidism. This can confirm that the dog has thyroid-responsive diseases rather than other nonthyroidal issues. However, before starting a therapeutic trial, every attempt should eliminate nonthyroidal sickness. Also, therapeutic monitoring should be performed in case the therapy is unsuccessful. Treatment of hypothyroidism in canines: The typical treatment of hypothyroidism in dogs is the oral medication of levothyroxine (L-T4). L-T4 is a synthetic thyroid hormone that can restore blood thyroid hormone concentrations and reverse hypothyroidism’s effects. The replacement of natural with synthetic hormones will be used for the rest of the animal’s life. However, a great precaution is needed with the initial dose and tailoring of the drug. The dosages of L-T4 in d are 0.01–0.02 mg/lb (0.02–0.04 mg/kg). The drug is given every day once or twice without food. Reference: Hypothyroidism is the Most Common Hormone Imbalance of Dogs; Wendy Brooks, DVM, DABVP. Date Published: 02/26/2002, Date Reviewed/Revised: 08/16/2019. Strey S, Mischke R, Rieder J. Hypothyreose beim Hund: eine Übersicht [Hypothyroidism in dogs: an overview]. Tierarztl Prax Ausg K Kleintiere Heimtiere. 2021 Jun; 49(3):195-205. German. doi: 10.1055/a-1367-3387. Epub 2021 Jun 22. PMID: 34157761 Mark E. Peterson. Hypothyroidism in Animals. Last
Canine Distemper Virus
Canine Distemper Virus Tang Nguyen Mai Trinh Infection of canine distemper virus (CDV) is common in most terrestrial carnivores in the wild, especially in the Canidae family (eg, wolves, foxes, domestic dogs, etc.), as well as certain ferrets, otters, raccoons, cats, and even marine animals [1]. CDV is a member of the Paramyxoviridae family which the genus Morbilivirus was first described in the 1970s, however, it was only isolated in 1905 from the nasal secretions of infected dogs by a French veterinarian, [2]. CDV is now known as the most dangerous disease in dogs because of its propensity to infect through respiratory and digestive pathways and cause death in virtually all canines. When infected with it, the unvaccinated host has a 100% mortality rate [3]. Structure of Canine distemper virus CDV is known as a single-stranded RNA virus, like many other viruses CDV has an N nucleocapsid protein that is responsible for genome replication, matrix (M), fusion (F), phosphoprotein (P), and polymerase (L) which are involved in genomic and mRNA transcription. Whereas nonstructural proteins C and V have been identified as virulence factors involved in the modulation of immune responses and innate immunity, proteins like H and F are essential for viral attachment, invasion, and fusion into host cells [4-6]. Transmission Puppies and dogs most often become infected through airborne exposure to the virus from an infected dog or wild animal. CDV enter the dog’s body through respiratory secretions, most notably coughing and sneezing. Virus particles can spread about 25 feet with a single sneeze, then proliferate in immune cells such as macrophages, T and B cells via the SLAM receptor within 24 hours [8] and spreads to tonsils and lymph nodes via the lymphatic vessels, causing long-term immunosuppression [9-11]. The amount of virus in the lymph nodes of the throat, tonsils, and bronchi will go up after 2 to 4 days of infection, and the virus continues to release and replicate in multiple organs. This process takes 4 to 6 days after infection and affects organs such as the thymus, spleen, lymph nodes, stomach cells, lungs, and bone marrow. The increased concentration of virus in the lymph node tissue at this time causes the number of white blood cells to decrease, resulting in the infected dog’s body temperature increasing [12]. The virus begins to migrate to specific epithelium and the central nervous system (CNS) via the blood or CSF after around 8 –10 days [10]. Simultaneously, organs such as the respiratory tract, intestines, and urinary tract begin to experience significant infections as lymphocytes are destroyed, resulting in a massive release of viruses into these organs [13]. Figure 2. The process of entry and replication of CDV in dogs.1, The CDV virus enters the dog’s body through the respiratory tract. 2, the virus begins to multiply in the tonsils, bronchial lymph nodes, oropharyngeal nodes, and gastrointestinal lymphoid tissues. 3, the virus attacks immune cells such as macrophages and is released to other organs such as the heart. 4, The virus enters the central nervous system (CNS) through the circulatory system. 5, Virus enters the cerebrospinal fluid (CFS). 6, Viral migration to the pyramidal lobes of the cerebral cortex through the nasal passages to the central nervous system [14]. Clinical Symptoms of Canine Distemper Virus infection in dogs The CDV virus can cause disease in dogs of any age, although it is more common in pups aged 12 to 16 weeks and in unvaccinated dogs. Because pups’ immune systems are so immature, they are easily infected by the virus if they come into touch with dogs that have already been afflicted with CDV. When the dog get infected with the CDV virus, early symptoms include fever, weariness, lack of appetite, apathy, and a reluctance to be active [9]. However, these symptoms are quite similar to those of the parvovirus, which primarily infects the digestive system, whereas CDV not only assaults the digestive system but also damage to the respiratory system, neurological system, bones, arthritis, eyes, and skin [13]. Prolonged vomiting, diarrhea, severe dehydration, and stool abnormalities in color, consistency, and blood and mucus contribute to gastritis and intestinal inflammation in the early stages. Finally, the dog was unable to defecate, resulting in death (Figure 3A). Pus discharge, ulcers, and progressively becoming clouded eyes can lead to conjunctivitis and even blindness, while the skin appears as spots with pus within, then gradually changes from red to yellow (Figures 3 B and C). Signs such as a runny nose with green mucus in the early stage, shortness of breath in the latter stage, and shortness of breath lead to pneumonia in the respiratory system (Figure 3B). Figure 3. Signs of CDV infection in dogs. A, Dogs have digestive system damage, diarrhea with blood [17]. B, Eyes are damaged causing pus discharge, ulcers, while the nose shows signs of runny nose with green mucus [15]. C, The skin also appears spots that have pus inside. D and E, the dog’s paw and nose epithelium show basal keratinocytes. F, enamel deterioration in adult dogs following neonatal CDV infection [13]. When the disease is severe, evidence of central nervous system damage such as convulsions, hemiplegia, or quadriplegia will occur; at this stage, 99% of infected dogs will die. Furthermore, the CDV virus can attach to lymphocytes and enter the cerebrospinal fluid (CSF), causing harm to the central nervous system. In addition, CDV was discovered in the foot and nasal epithelium, promoting basal keratinocyte growth, which was clearly recognized in the Figures 3D and E. Although CDV infection leads to the above clinical signs, however the appearance of these signs is also dependent on habitat, age, host immunity, and virulence of the virus strain [13]. Studies have also demonstrated that CDV can be passed from mother to puppy through the placenta during pregnancy. When the mother dog is infected with the virus, it can lead to miscarriage, stillbirth, but this depends on the pregnancy stage of the mother dog [16]. For the lucky puppies
Canine Babesiosis
Oliver Organista, LA Canine babesiosis is a tick-borne, protozoal, haemoparasitic disease that can cause varying degrees of haemolytic anaemia, splenomegaly, thrombocytopenia and fever. It is very endemic to different parts of the world, and presents varying clinical, hematological, and pathological manifestation depending on the species and subspecies involved.1,2 There are two hosts for the transmission of Babesia spp., viz. invertebrate (tick) and vertebrate host. Dogs are one among the many targets of Babesia spp., causing canine babesiosis, and now there are clinical evidences of possible vertical transmission too. Dogs of all ages can be affected with Babesia spp., but young puppies are more commonly affected. Two Babesia parasites were thought to occur in dogs; the relatively large intra-erythrocytic piroplasm referred to as Babesia canis and a smaller parasite, known predominantly as the cause of canine babesiosis in Asia, Babesia gibsoni. B. canis has been reclassified into three separate species (B. canis, B. rosi, B. vogeli) on the basis of immunity, serological testing, vector specificity and molecular phylogeny At least 4 genetically and clinically distinct small piroplasms affect dogs which include: Babesia gibsoni–originally described in India nearly a century ago and now occurring sporadically in other parts of the world including the Australia; Babesia conradae, a piroplasm that occasionally infects dogs in California; Theileria annae, a Babesia microti-like parasite that has so far been reported only in northwest Spain, transmitted by Ixodes hexagonus ; and a fourth small piroplasm, B. (=T.) equi has also been reported in dogs in Spain.³ Prevalence of Babesiosis The incidence of canine babesiosis vary considerably from one country to another depending on the distribution of the causative parasite and their specific vectors. Table below shows the data gathered during the Questionnaire-based survey on the distribution and incidence of canine babesiosis in countries of Western Europe.5 DIAGNOSIS, SYMPTOMS, AND TREATMENT Diagnosis. In the past, babesiosis was diagnosed by seeing the parasite on a blood smear. Other diagnostic tests are becoming more readily available, including FA (fluorescent antibody) staining of the organism and ELISA (enzyme-linked immunosorbent assay) tests. A PCR (polymerase chain reaction) test is also available and is commonly used to diagnose babesiosis. The PCR test has the advantage in that it can detect all four species of Babesia. Serologic or antibody titer testing in the diagnosis of babesiosis has limitations. A positive test result is dependent on an antibody response by the infected dog, which may take up to ten days to develop. Once a dog has developed antibodies to babesiosis, they may persist for years and this must be considered when performing follow-up tests.6 Symptoms. Dogs typically present with the acute, severe form of babesiosis, which is characterized by findings such as abnormally dark urine, fever, weakness, pale mucous membranes, depression, swollen lymph nodes, and an enlarged spleen. Potential complications: Bleeding problems, a severe type of anemia that leads to jaundice, organ damage, death.7 Treatment. The FDA approved treatment for babesiosis is imidocarb diproprionate. A combination therapy of quinine, azithromycin, atovaquone, and/or clindamycin is being researched and may become more common to treat dogs within the US or Canada in the future. Clindamycin, the treatment of choice for Babesia microti, the main Babesia species that infects humans, can also be used against Babesia in dogs. Clindamycin is a readily available antibiotic and is an excellent starting point for treatment in many dogs. Your veterinarian will discuss any alternative and adjunctive treatments with you.7 TRANSMISSION AND PREVENTION OF BABESIOSIS How is dog Babesia transmitted? Transmission. In most cases, Babesia organisms are spread to dogs through the bite of an infected tick but is not likely to be transmitted until a tick is attached for 36 hours. However, some studies suggest that infected dogs with open mouth sores can pass on the infection to other dogs through a bite, and infected pregnant females can transmit babesiosis to their unborn puppies. It can also be transmitted by the needle passage of infected blood, inadvertently in the case of blood transfusion or deliberately during experimental studies. Generic Life Cycle of Babesia spp.10 Generic life cycle of Babesia spp. Sporozoites (Sz) are injected into a vertebrate host blood system, during the blood meal of an infected tick. After invasion, Sz differentiate into trophozoites (T). Trophozoites undergo asexual division into two or four merozoites (M) in the infected red blood cells. Merozoites exit the red blood cells and invade new ones. Some groups of merozoites transform into gamonts or pregamotyces (G). The process of gamogony and sporogony takes place in the tick. Gamonts ingested by a tick feeding on an infected host differentiate in the gut into gametes (called ray bodies or Strahlenkorper – (Sk)) that fuse forming a diploid zygote (Z, gamogony). Via meiosis division, zygotes give rise to motile haploid kinetes. After haploid kinetes multiply by sporogony, they penetrate the tick haemolymph and organs. The final stage of the development occurs in the salivary glands (Sg), where differentiation and multiplication occur. Kinetes transform into sporozoites that infect the vertebrate host after vector development into a subsequent life stage – larvae to nymph, nymph to adult (transstadial transmission, Ts). In large Babesia spp. kinetes also invade the tick ovaries and eggs, and infective sporozoites are formed in the salivary glands of the next generation larvae. This process is called transovarial transmission (To). Adopted and reproducted from Schnittger et al. 9 How ticks spread disease11 Ticks transmit pathogens that cause disease through the process of feeding. Depending on the tick species and its stage of life, preparing to feed can take from 10 minutes to 2 hours. When the tick finds a feeding spot, it grasps the skin and cuts into the surface. The tick then inserts its feeding tube. Many species also secrete a cement-like substance that keeps them firmly attached during the meal. The feeding tube can have barbs which help keep the tick in place. Ticks also can secrete small amounts of saliva with anesthetic properties so that the animal or person can’t feel that the tick has attached itself. If the tick is in a sheltered spot, it can go unnoticed. A tick will suck the blood slowly for several days. If the host animal has a bloodborne infection, the tick will ingest the pathogens with the blood. Small amounts of saliva from
Thyroid Function in Animals
Sushant Sadotra Introduction: The thyroid is one of the endocrine glands in vertebrates. The thyroid gland has a bilobed structure located below the larynx and overlays the trachea in animals. In different animals, Anatomical variations of the thyroid are primarily seen in the isthmus connecting the gland’s two lobes. The size of the gland approximates 0.20% of body weight. However, the size may increase due to iodine deficiency, ingestion of goitrogenic toxins, tumors, and hyperactivity of the gland, or maybe reduced to fibrotic due to hyperthyroidism. Thyroid follicles are the thyroid gland’s functional units with a spherical structure composed of an inner core of the thyroglobulin-hormone complex, colloid. The colloid is surrounded by an outer monolayer of follicular cells and acts as the storage tank of thyroid hormone. The overall size of the follicles and the shape of their follicular cells may differ due to the functional activity of the thyroid gland. The dormant follicular cells are squamous-shaped compared to the tall columnar, highly active follicular cells. Other than colloid, the thyroid C-cells are interspersed between the follicles. The thyroid C-cells are the source of the hypocalcemic hormone calcitonin that is associated with calcium metabolism. The third type of tissue embedded in the thyroid gland is the parathyroid. The parathyroid is the source of the hypercalcemic hormone parathormone. Functions of the thyroid gland: The thyroid gland functions the same in all animals. There are four primary functions of the thyroid gland in animals; trapping the iodide, synthesis of thyroid hormones, storage, and release of hormones. All these activities of the thyroid gland are usually regulated by thyroid-stimulating hormone (TSH), a pituitary hormone. Hormonogenesis and release of thyroid hormone mainly have four stages: Trapping of Iodide: The follicular cells trap the circulating I– from the blood against the concentration gradient mediated by a sodium iodide symporter (NIS) protein present on the thyroid follicular cell membrane. A trapping enzyme catalyzes the trapping process via a mode of active transport catalyzed by an ATP-dependent Na+K+-ATPase. This trapping system’s high efficiency can concentrate most blood iodine in the thyroid gland. This process is stimulated by TSH and blocked by large amounts of I– or goitrogenic agents. (Figure 1) Synthesis of Thyroid Hormones: The trapping of I- is followed by its oxidation, catalyzed by peroxidase to form a highly active free radical I*. This reaction is also stimulated by TSH and inhibited by thyrotoxic agents (thiouracils or thioureas). At the follicular cell membrane-colloid interface, highly active I* binds to thyroglobulin, a thyroidal glycoprotein of a high molecular weight of 660 kDa. I* binds to thyroglobulin at its tyrosine moieties to form monoiodotyrosine (MIT) or a diiodotyrosine (DIT). After that, the iodinated phenyl groups of the tyrosine undergo oxidative condensation resulting in the synthesis of thyroid hormones. The thyroid gland produces two active hormones: 3,5,3’-triiodothyronine (T3) and 3,5,3′,5,-tetraiodothyronine (T4). T3 is formed by the oxidative condensation of an iodinated phenyl group of one DIT to an MIT group or of one DIT to another DIT to create T4. The inner deiodination product of the T4 is the inactive hormone is 3,3′,5’-triiodothyronine (rT3). Storage of hormones: Thyroid follicular cells synthesized thyroglobulin and localized it to the cell membrane for the iodination process. Iodinated thyroglobulin, also known as a colloid, is released and stored in the lumen of the follicle. Release of hormone: TSH stimulates the release process of hormones. TSH acts at the follicular cell membrane, the second site of action for TSH. Colloid from the lumen is taken up to the follicular membrane, where they are taken in as vesicles into the follicular cells by the process of endocytosis. Lysosomes merge with these vesicles to release lysosomal proteases that hydrolyze the colloid. Hydrolyses of colloid release their T3, T4, DIT, and MIT. Microsomal tyrosine deiodinases enzymatically degrade the released DIT and MIT, and their iodine is recycled within the follicular cell. A simple diffusion process releases the T4 and T3 into circulation. Out of the total hormone released from the gland, 90% is T4, and only 10% is T3. The phenyl group of T4 may also undergo some deiodination within the gland or in the peripheral tissues to form rT3. rT3 is an inactive form of the T3 hormone. Therefore it undergoes a degradation pathway. (Figure 1) The regulation of T3 and T4 secretion starts in the hypothalamus. The thyrotropin-releasing hormone secreted from the hypothalamus acts on the pituitary gland. This stimulates TSH secretion, which ultimately acts on the thyroid gland, producing and releasing thyroid hormones. The action and disorder of Thyroid Hormones: In humans and animals, thyroid hormones play a vital role in regulating metabolic and cellular mechanisms. The mode of action can be quick in minutes or prolonged to hours or longer. Thyroid hormones in normal levels work together with other hormones like insulin (beta cells of the pancreatic islets) and growth hormone (pituitary gland) to work on protein synthesis in different cellular processes. However, thyroid hormones can be catabolic in excess (hyperthyroidism), with increased protein breakdown and gluconeogenesis. Hyperthyroidism is more common in cats middle-aged to old cats than in dogs. However, thyroid carcinoma could be a cause when it occurs in dogs. Decreased levels of thyroid hormones (hypothyroidism) cause a slower metabolic rate in animals. This disorder is most likely seen in middle-aged (4-10 Years) dogs and mid to large-size dog breeds (Doberman pinscher, Golden retriever, etc.). Also, spayed female dogs have a higher hypothyroidism risk than unspayed ones. On the contrary, naturally occurring hypothyroidism is rare in cats. Reference: Kaneko, J. J. (2008). Clinical biochemistry of domestic animals. San Diego: Academic Press. Thanas C, Ziros PG, Chartoumpekis DV, Renaud CO, Sykiotis GP. The Keap1/Nrf2 Signaling Pathway in the Thyroid—2020 Update. Antioxidants. 2020; 9(11):1082. https://doi.org/10.3390/antiox9111082 Mark E. Peterson. The Thyroid Gland in Animals. Last full review/revision Jul 2019 | Content last modified Oct 2020. MSD MANUAL Veterinary Manual, https://www.msdvetmanual.com/endocrine-system/the-thyroid-gland/the-thyroid-gland-in-animals
