* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download VIRAL DISEASES
Meningococcal disease wikipedia , lookup
Sexually transmitted infection wikipedia , lookup
Human cytomegalovirus wikipedia , lookup
Orthohantavirus wikipedia , lookup
Sarcocystis wikipedia , lookup
Chagas disease wikipedia , lookup
Onchocerciasis wikipedia , lookup
Gastroenteritis wikipedia , lookup
Ebola virus disease wikipedia , lookup
Herpes simplex virus wikipedia , lookup
Oesophagostomum wikipedia , lookup
Visceral leishmaniasis wikipedia , lookup
Coccidioidomycosis wikipedia , lookup
Leishmaniasis wikipedia , lookup
Eradication of infectious diseases wikipedia , lookup
West Nile fever wikipedia , lookup
Schistosomiasis wikipedia , lookup
African trypanosomiasis wikipedia , lookup
Henipavirus wikipedia , lookup
Leptospirosis wikipedia , lookup
Hepatitis C wikipedia , lookup
Middle East respiratory syndrome wikipedia , lookup
Marburg virus disease wikipedia , lookup
Dirofilaria immitis wikipedia , lookup
FELINE INFECTIOUS PERITONITIS INTRODUCTION Affects both domestic and wild cats. Highly fatal and characterized by prolonged progressively debilitating course, anorexia, depression, weight loss and anemia. Usually refractory to treatment. It is an immulogical reaction to some viral diseases manifesting as either effusive (wet or serositis) or non-effusive granulomatous form. Etiology – RNA virus 70-94nm Cats usually have both leukemia virus and FIP virus. Transmission:Oral, nasal and ectoparasites Transplacental transmission • All age groups and sex can be infected but young animals are more susceptible. Clinical Signs: There are two forms: Effusive (wet) Noneffusive form (Parenchymal or dry and granulomatus form) Clinical Signs: There are two forms: Effusive (wet) form characterized Ascites Hydrothorax Pleuritis Dyspnoea. Affected cat dies within 1-8 weeks Clinical Signs: Noneffusive form (Parenchymal or dry form and granulomatus) characterized by the involvement of specific organs e.g. The brain (causing pyogranulomatous meningoencephalitis) The eye causing pyogranlomatous uveitis, bilateral iritis, ocular discharges, keratic precipitates in the anterior chamber of the eye. Kidney Spleen, Liver Pancreas. Several clinical forms may coexist in young adults, 6 months – 3 years are mostly affected. There is Fluctuating fever, progressive anorexia, depression, weight loss and dehydration. Non regenerative anaemia. A few patients may vomit or have diarrhea. Diagnosis: Hemogram – moderate to marked leukocytosis increase in icterus index 10-50 units (normal 2.5 – 7.5 units), non regenerateive anaemia Hyperproteinaemia due to hypoglobulinaemia peritoneal fluid can clot because it contains high concentration of protein and flecked fibrin. Radiography. Treatment: Temporary remission may occur, seemingly recovered cats relapse and ultimately die. 1. Peritoneal lavage with balanced electrolyte solution. 2. Administration of chloramphenicol or tylosin and flumethasone. 3. Oral antibiotic and steroid combined with lavage. 4. Most effective is a combination of oral tylosin and prednisolone. Prevention:Difficult. Vaccine not presently available. Prevent contact between susceptible and ill cats. FELINE LEUKEMIA INTRODUCTION Malignant proliferative or degenerative disease of the hematopoietic tissue of the domestic cat Etiology: caused by feline leukemia virus (RNA) an RNA retrovirus Transmission:- The virus is present in the saliva, urine, feces, milk and nasal discharges of the affected cat. Transmission is both horizontal (cat to cat) and vertical (mother to foetus) Clinical signs: Variable because of the various body systems that might have been affected. The proliferative forms (Myelo-proliferative) always affect the bone marrow resulting in pallor of mucous membranes, enlargement of liver and spleen and fluctuating fever, anorexia, malaise. In non-regenerative anaemia panluekopenia like syndrome, thymic atrophy. Diagnosis 1. Clinical signs 2. Cytologiy of the body fluid and histological examination at post mortem. Treatment Not advisable because they constitute a distinct hazard to cats, other species and man. CANINE ADENOVIRUS INFECTIONS (Double straded DNA cubic sysmetry) (Infectious canine hepatitis) Synonyms: Contagious canine Hepatitis or Rubarth’s Disease. INTRODUCTION It is a multisystemic acute viral disease which primarily affects the liver of dogs and other canids. Characterized by very rapid course, tonsillitis, oedema of the subcutaneous tissues (especially of the neck regions). Aetiology There are two serologically distinct adenoviruses responsible for disease of dogs. CAV-1 CAV-2 Aetiology Epizootiology and Dermology Adenoviruses are more stable than canine distemper virus under moist condition and out of direct sunlight. One strain of CAV-ICH in urine can survive up to 5-6 days on soil or concrete floor. The disease is widely spread but only a small proportion of dogs come down with the disease. Clinical signs may be so slight that they pass unnoticed, while definite clinical signs may be diagnosed in some dogs. A small minority come down with severe clinical signs in that case there is high mortality. In endemic areas sporadic epidemics may occur. Young puppies 3-6 months are most susceptible. About 20% occur in 18 months and above old dogs. Transmission:Ingestion of food or water contaminated with infected urine but the respiratory form can be transmitted through aerosol during coughing. Clinical Signs 1. 2. 3. 4. Liver GIT Cardiovascular Eye Clinical signs Acute fulminating, high temperature, (1060F). Death may occur within a few hours. This condition may be severe and acute that it can be confused with poisoning. The mucus membrane of the tonsil is inflamed. High temperature becomes subnormal just before death. Clinical signs Extreme apathy depression, sudden onset of anorexia, vomiting, which may be severe and contains blood terminally, as a result of liver damage in about 35% of the cases. Bilirubinuria, increase in liver enzymes (ALP, ALT) Damage to the vascular endothelium manifest as perivascular haemorrhage cardiovascular system, thymus, brain, lungs, epi and endocardium, lymph nodes, spleen and subsutaneous tissues. Vomiting and diarrheoa may become haemorragic. Clinical signs Presence of blood in faeces signifies grave prognosis. There is an intense thirst The mucous membranes may be extremely pale. Jaundice may occur in 25-34% cases. In some cases there may be petichial haemorrhage on the mucous membrane of the mouth. Tenderness and pain in the abdominal region which can be induced by palpation especially toward the xiphisternum. There is hepatomegaly. The abdomen contains some fluid. There may be tachypnoea in some cases. Clinical signs There is cornea opacity which may be unilateral or bilateral referred to as “hepatitis blue eye”. When this occurs it is diagnostic and prognosis is good. Subcutaneous oedema of the head region i.e. head, neck and sternum. CNS involvement is low (5%) showing signs such as restlessness (moving, pacing around the room) and posterior incoordination. Excitability and hyper asthesia may be evident. Sometimes epileptiform convulsions progressing to coma. The pulse is usually fast and weak. High temperature (105-1060F) and remains so until the animal collapses when it becomes subnormal. There is high protein in the urine. Superficial lymph nodes are enlarged, tonsil is swollen and inflamed. The course is usually rapid therefore no room for weight loss. Diagnosis:Clinical signs Sudden onset, pallor of mucous membrane, palpable enlarged liver, corneal opacity, leucopenia, increase coagulation due prothrombinemia thromibocytopenia, increased liver enzymes. Virus isolation from tonsil, swab or clotted blood samples. Serum assay – paired sera. Serum neutralization test CFT. Immunofluorescence and histopathology, intranuclear inclusion bodies in liver and spleen. Material becomes useless 48 hours after death. Treatment:Antibiotic to control 20 bacterial infection. Supportive treatment: Blood transfusion, vitamins, Vit K. i/v glucose saline, specific antiserum. If nervous signs appear, administer primidone. Prognosis:In clinically diagnosed cases the prognosis is poor but good when corneal opacity occurs. Prophylaxis:Vaccination, hygiene. FELINE RESPIRATORY DISEASE INTRODUCTION • Respiratory disease is common among cats. The term “cat flu” is widely used to describe the clinical signs associated with infection. • Feline respiratory disease is a syndrome that may be cause by one or a number of infectious agents. It is thus similar to Kennel cough of dogs. • Morbidity of viral respiratory disease in cats is high but the mortality is low. • Severity of the disease varies, with subclinical or mild infections being more common, though more serious cases may occur. AETIOLOGY are The two major causes of upper respiratory disease (URD) in cats 1.) Feline viral rhinotracheitis (FVR), virus, also known as feline herpersvirus 1 (FHV 1) 2.) Feline calicivirus (FCV). Together, these two viruses are responsible for majority of cases of URD. Others are Feline reovirus, Feline poxvirus Bacteria such as Clamydia psitacci, staphylococci, haemolytic stereptococci, pasteurella spp, coliforms and mycoplasmas have been isolated from causes of URD. Their main importance may be as secondary invaders following primary viral damage. Bordetella bronchiseptica has been isolated in some cases of feline URD but its significance has not been determined. EPIZOOTIOLOGY Feline viral respiratory disease is more common in colony cats than individual house pets. The disease appears commonly in situations where cats have been brought together e.g. catteries, breeding colonies, stray-cat homes etc. Feline upper respiratory disease (URD) is widespread worldwide. Most cases are due to infection by FHV and FCV. In endemic situations, URD is generally acute in young kittens especially after weaning. Older cats usually suffer a milder disease which is characterized by persistent, or recurrent rhinitis, sinusitis. TRANSMISSION Occurs from sick or carrier cats to susceptible ones through transfer of virus-containing oral or nasal secretions. Close contact, rather than aerosol, is responsible for virus spread. The viruses persist in cat populations in 3 ways: 1. Direct transmission from acutely infected to susceptible cats. 2. In the environment for short periods of time. 3. Persistence through a carrier state in recovered cats. PATHOGENESIS FVR Following infection, upper respiratory tract secretions carry the virus into the nasal passages, oropharynx, and trachea. FCV Infection leads to growth of the virus in the epithelia of the tongue, palate, external nares and lungs. CLINICAL SIGNS FVR The incubation period is usually 2-4 days but may be up to 10 days depending on the virus dose. PHV infection generally produces a severe disease. The initial stages are characterized by depression, anorexia, pyrexia (400C) and sneezing. Conjuctival oedema occurs commonly. In the later stages, ocular and nasal discharge become more copious and are often purulent. Drooling of saliva due to hypersalivation is common. Mouth breathing occurs as a result of obstruction of the nasal passages. Recovery begins 7 to 10 days after the initial clinical signs but complete recover may take several weeks. In a few cases chronic rhinitis and sinusitis may persists. Recovered cats are resistant to re-infection and do not develop clinical signs. FCV The incubation period is short, 1-3 days. FCV usually produces a milder disease than FHV though severe cases may be similar to FVR. General malaise, coughing and oculo-nasal discharges are less copious. Nasal discharges usually occur with sneezing. Initially there is usually depression and anorexia associated with pyrexia. The characteristic sign is ulceration of the anterior border and dorsum of the tongue, hard palate and external nares. Since there is a large number of strains of feline calicivirus, the pathogencity and clinical signs may vary slightly. Some strains produce primary interstitial pneumonia, others pyrexia, myalgia and limping, while infection with some strains may be subclinical.