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Canine distemper (CD) is one of the most severe infectious diseases affecting wild and domestic canidae as well as many other species of carnivores.
It is caused by canine distemper virus (CDV) which is an enveloped negative strand RNA virus classified under family Paramyxoviridae and genus Morbillivirus.

The virus mainly affects respiratory system, gastrointestinal tract, lymphoid organs, urinary bladder and the central nervous system.

Generally young, unvaccinated or not fully vaccinated puppies, under 6 months of age, are most susceptible to canine distemper virus. Very young puppies (under 3 months old unable to get their mother’s colostrums (maternal immunity) are also at high risk. Older, unvaccinated dogs can also contract the disease.
Viral shedding occurs by 7 days following experimental inoculation. CDV, most abundant in respiratory exudates, is commonly spread by aerosol or droplet exposure; however, it can be isolated from most other body tissues and secretions, including urine. Transplacental infection can occur from viremic dams. Virus can be excreted up to 60 to 90 days after infection, although shorter periods of shedding are more typical. Contact among recently infected (subclinical or diseased) animals maintains the virus in a population, and a constant supply of puppies helps provide a susceptible population for infection. Although immunity to virulent canine distemper is prolonged or lifelong, it is not as absolute after vaccination. Dogs that do not receive periodic immunizations can lose their protection and become infected after stress, immunosuppression, or contact with diseased individuals. Based on results of serosurveys, the infection rate is considered to be higher than the disease rate, which reflects a certain degree of natural and vaccine-induced immunity in the general dog population. Many susceptible dogs can become subclinically infected but clear the virus from the body without showing signs of illness. Although most recovered dogs clear the virus completely, some may harbor virus in their CNS.
The prevalence rate of spontaneous distemper in cosmopolitan dogs is greatest between 3 and 6 months of age, correlating with the loss of maternal-derived antibodies (MDAs) in puppies after weaning.
In contrast, in susceptible, isolated populations of dogs, the disease is severe and widespread, affecting all ages. Increased susceptibility among breeds has been suspected but not proved. Brachiocephalic dogs have been reported to have a lower prevalence of disease, mortality, and sequelae compared with dolichocephalic breeds.
Concurrent infections, such as with CDV and canine adenovirus (CAV)-2, can cause severe fatal pneumonia in pups.

Clinical signs
Clinical signs of canine distemper vary depending on virulence of the virus strain, levels of environmental stress, and host age and immune status. More than 50% of CDV infections are probably subclinical.
In mild:
• Fever
• Signs of upper respiratory tract infection
• Listless
• Inappetant
• Bilateral serous ocular discharges can become mucopurulent with coughing
• Labored breathing; “kennel cough” (acute respiratory disease of canines)
• Keratoconjunctivitis
In severe:
• Fever after an incubation period of 3–6 days
• Profound leukopenia.
• Anorexia,
• Serous or mucopurulent nasal discharge
• Vomiting
• Conjunctivitis
• Depression
• Diarrhea (May be mucoid or bloody)
• Dehydration and emaciation
• Dry cough
• Productive cough
• Bronchitis
• Interstitial pneumonia follow
• Tenesmus
• Intussusceptions
• Vesicular and pustular dermatitis

• Virus isolation, or antigen detection tests
• ELISA or indirect fluorescent antibody test

Prevention and control-
Virus is very fragile, and susceptible to standard disinfectants.
Successful immunization of pups with attenuated canine distemper virus vaccines depends on the absence of interfering maternal antibody.
Puppy that has not received colostrum is probably protected for at least 1 to 4 weeks. MDA are usually absent by 12 to 14 weeks of age.
Alternatively, pups can be vaccinated with modified live-virus vaccine at 6 weeks of age and then at 2- to 4-week intervals until 16 weeks of age.
Hyperimmune serum or immunoglobulin can be used prophylactically immediately after exposure.

Dogs with upper respiratory infections should be kept in environments that are clean, warm, and free of drafts. Oculonasal discharges should be cleaned from the face. Pneumonia is frequently complicated by secondary bacterial infection, usually with Bordetella bronchiseptica , which requires broad-spectrum antibacterial therapy and expectorants or nebulization and coupage. Good initial antibacterial choices for bronchopneumonia include ampicillin, tetracycline, and chloramphenicol. Parenteral florfenicol might be considered. Parenteral therapy is essential when GI signs are present. Food and water and oral medications or fluids should be discontinued if vomiting and diarrhea are present. Parenteral antiemetics may be required. Supplementation with polyionic isotonic fluids such as lactated Ringer ’ s solution should be given intravenously or subcutaneously, depending on the hydration status of the patient. B vitamins should be administered as nonspecific therapy to replace vitamins lost from anorexia and diuresis and to stimulate the appetite. Two 100,000-IU- 200,000-IU (30-60-mg, intramuscularly [IM]) doses of vitamin A may be administered. Specific antiviral therapy against CDV has not been evaluated in infected dogs; however, ribavirin and a closely related compound were shown to have antiviral efficacy. Therapy for neurologic disturbances in canine distemper is less rewarding. Variable or temporary success in halting neurologic signs in some dogs can result from a single anti-CNS edema dose (2.2 m g/kg, given intravenously [IV]) of dexamethasone. Subsequent maintenance therapy with anti-inflammatory doses may be needed, and this treatment can be tapered with time. Seizures, myoclonus, or optic neuritis are three neurologic manifestations in dogs that can be tolerated by many owners. Myoclonus is usually untreatable and irreversible. Drugs such as benzodiazepines or levetiracetam have been used with variable efficacy. For seizure control, recommendations have been made to administer anticonvulsants after the onset of systemic disease but before the development of seizures. Seizures are best treated with parenteral diazepam (0.5- to 2-mg/kg rectally or slow IV). Glucocorticoid therapy in anti-inflammatory to anti-CNS edema dosages may have variable success.

Fowl Cholera

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Newcastle Disease

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