Canine Viral Diseases PDF

 Rabies Hydrophobia Lyssa Rage ‫السعار‬ ‫الكلب‬  Definition ❖ Acute fatal encephalitis of all warm-blooded mammals but most common in carnivores. ❖ Transmitted by saliva of rabid animals. ❖ Characterized by encephalomyelitis manifested by:...

 Rabies Hydrophobia Lyssa Rage ‫السعار‬ ‫الكلب‬  Definition ❖ Acute fatal encephalitis of all warm-blooded mammals but most common in carnivores. ❖ Transmitted by saliva of rabid animals. ❖ Characterized by encephalomyelitis manifested by: Altered behavior. Motor irritation with signs of mania. Inability to swallow. Progressive ascending paralysis beginning in hind limbs & forward to trunk & the fore limbs followed by death.  Etiology ❖ Neurotropic lyssa virus, family Rhabdoviridae (large RNA). ❖ Street viruses: Strains isolated from naturally infected cases. ❖ Fixed viruses: Strains adapted to secondary hosts for experimental use. ❖ Flury strain: Isolated from brain of human patient & passed in several host systems. Standard strain for vaccine preparation. ❖ Sensitive to standard disinfectants as 1% formalin & 3% cresol. ❖ Inactivated in dry saliva within few hours, sunlight & boiling.  Etiology Types of rabies virus Street virus Fixed virus Recovered from natural cases Prepared in the laboratory In saliva of infected animals Repeated culture in brain of rabbit Produces Negri bodies Does not form Negri bodies Incubation period long (20-60 days) Incubation period constant 4-6 days Pathogenic for humans under certain Pathogenic for all mammals conditions Not used for preparation of vaccines Used for preparation of vaccines  Epidemiology ❖ Distribution: Worldwide & endemic in Africa including Egypt. Only few countries free as Australia & New Zealand. ❖ Animal susceptibility: All mammals. High susceptible: Wolves, coyotes & jackals. Moderate susceptible: Dogs, cats, humans, racoons & skunks. Bats are important vectors: Asymptomatic infection because the virus multiplies in fatty tissue without nervous system invasion. Highest incidence during summer & autumn because of large scale movements of wild animals for mating or pursuit of food.  Epidemiology ❖ Transmission: Source of infection: ✓ Virus intermittently excreted in saliva of infected animals 2-5 days before signs & throughout course of the disease. ✓ Virus may exist in saliva of about 5% of normal dogs. ✓ Vampire bats are important source of virus in USA where virus is excreted for several months. Mode of infection: ✓ Biting by infected vectors. ✓ Contamination of wound by saliva may cause infection. ✓ Not all bites cause infection because virus exists in saliva intermittently or if saliva wiped from teeth by closing.  Pathogenesis CNS Afferent fibers Efferent fibers Muscles Nerve endings Salivary gland Organs & tissues Virus Pathogenesis  Clinical signs in dog & cat ❖ Incubation period: 3-8 weeks but may be longer up to few months. ❖ Length of incubation depends on distance between inoculation site & CNS, severity of bite & virulence of virus & quantity of virus in saliva. ❖ Sporadic. ❖ Mortality: 100%. ❖ Course: 7-10 days. ❖ Three clinical phases: Prodromal phase. Excitative (furious) phase. Paralytic (dumb) phase.  Clinical signs in dog & cat ❖ Prodromal phase: Change in normal behavior. Fever. Salivation. Stop eating & drinking. Ataxia. Slow eye reflexes. Friendly dogs become irritable. Chewing at the bite site. Persists: 2-3 days in dogs & 1 day in cats.  Clinical signs in dog & cat ❖ Excitative phase (furious form): Hypersensitive. Irritability. Aggressive attack. Bite without warning. Facial expressions show alertness, anxiety, dilated pupils, erected ears & reddening of eyes. Fear of natural enemies is lost. Unequal dilatation of pupils with increased corneal reflex. Sexual stimulation & bitches come in estrus in unusual time.  Clinical signs in dog & cat ❖ Excitative phase (furious form): Wander aimless & run for long distances. Attack other animals & any moving objects. Saliva dribbles from lips. Depraved appetite: Swallowing soil, stones & grass. Hydrophobia. Voice changes: Low-pitched hoarse howling. Cats mew continuously. This phase persists for 2-4 days (dogs rarely live beyond 10 days after onset of signs).  Clinical signs in dog & cat ❖ Paralytic phase: Start by paralysis of throat & masseter muscles accompanied with: ✓ Profuse salivation. ✓ Inability to swallow. ✓ Dropping of lower jaw. Paralysis progresses rapidly to cover entire body muscles. Seeking for calm sheltered place. Depression & coma. Death. This phase persists: 2-4 days.  Clinical signs in cattle & buffaloes ❖ Paralytic form: Stray from herd. Sudden drop in milk yield. Loss of appetite, depression, weakness. Drooling of saliva, inability to swallow & esophageal choke. Deprived appetite: Chewing wood, stones, non-digestible objects. Deviation of tail to one side. Hind limb lameness or hind fetlock knuckling & swaying of hind quarters on walking. Yawing movement or voiceless attempts to bellow. Diarrhea or tenesmus with paralysis of anus & bladder & bloat. Ataxia, reduced sensation, paresis & paralysis. Death after 6-7 days of onset of signs.  Clinical signs in cattle and buffaloes ❖ Furious form: Alert apprehensive appearance. Hypersensitivity to sound & touch. Violent attack other animals or inanimate objects. Incoordination of gait. Muscular tremors. Head pressing against fixed objects. Bellow constantly in low-pitched voice. Sexual excitement. Aimless movement.  Clinical signs in cattle and buffaloes ❖ Furious form: Blindness. Dysphagia. Salivation. Grind of teeth. Inability to eat or drink. Local or generalized pruritus. Convulsion. Recumbency & paralysis. Death.  Clinical signs in sheep & goats ❖ Signs present in number of animals at one time. ❖ Majority of sheep show: Sexual excitement. Attacking human or other animals. Vigorous wool pulling. Violent exertion. Muscular tremors & Salivation. Sudden falling & death. ❖ In goats: Signs are similar in addition to: Aggressive behavior. Continuous bleating.  Clinical signs in camels ❖ Incubation period is 15-60 days. ❖ Excitative stage: Restlessness, aggression, biting. Itching & scratching. Hypersalivation & muscle tremors. Lasts for 1-3 days & followed by paralytic stage. ❖ Paralytic stage: Camel lies on side. Wave with its limbs. Yawns continuously. Lasts for 1-2 days before death.  Diagnosis ❖ Field diagnosis: History of being bitten by rabid animal, clinical signs & death of affected animal within 5 days from onset of clinical attack. ❖ Laboratory diagnosis: Detection of Negri bodies in impression smear and tissue section. Detection of virus antigens by FAT. Isolation of virus. Experimental transmission. ❖ Differential diagnosis: Encephalomyelitis as canine distemper, canine hepatitis. In endemic area, any case of encephalomyelitis considered rabies until proven negative.  Treatment ❖ Treatment: After appearance of signs, no treatment is attempted. Immediately after biting: Wound is irrigated with 20% soaps & water, cresol or 2% quaternary ammonium compounds to prevent virus attachment. Post exposure vaccination not useful in animals as death occurs before immunity developed, but anti-rabies immune sera may be used. Post biting vaccination can be used in human.  Control ❖ Prevention of exposure: Bite wounds & scratches immediately washed with soap & antiseptics as 70% alcohol. Rabid animal destroyed with elimination of stray dogs. Other dogs: Muzzled, restraint, licensed & vaccinated. When rabies suspected: Handlers should wear gloves. If bovine bitten by rabid animal: Destroyed immediately. If animal slaughtered within 7 days after exposure: Portions that exposed to bite discarded & other part can be eaten.  Control ❖ Prevention of exposure: Meat & milk from rabid animal: Not used for human. Control of vampire bats in America depends on vaccination of bovine hosts & injection of anticoagulants that are harmless for cattle & kill bats within 4 days. Dogs or other suspected animals isolated for 10-15 days ✓ If still alive: They considered rabies-free. ✓ If they die: They considered rabies-infected.  Control ❖ Vaccination: Dogs and cats: ✓ Inactivated tissue culture vaccine, vials 2 ml one dose, I/M. ✓ At any age but preferably at 3 months then annually. Calves from vaccinated dams: ✓ Vaccinated at 4 & 10 months of age, IM. Humans: ✓ Single dose inactivated concentrated vaccine. ✓ At high-risk people: Pre-exposure vaccination.  Canine distemper Hard pad disease ‫طاعون الكالب‬  Definition ❖ Acute & subacute contagious, incurable, often fatal, multisystemic viral disease of carnivora mainly dogs & foxes. ❖ Characterized by: Diphasic fever. Conjunctivitis. Bronchitis. Gastroenteritis. Nervous signs. Hardening of pads of nose. ❖ Infection rates are higher than disease rates. ❖ About 25-75% of dogs become subclinically infected.  Etiology ❖ The canine distemper virus (CDV) is Morbillivirus belongs to family Paramyxoviridae. ❖ Closely related to the human measles virus (MV), rinderpest virus (RPV), and peste de petits ruminants virus (PPRV). ❖ Epitheliotropic RNA virus. ❖ Virus strains differ in virulence. ❖ Not very resistant, readily destroyed by most disinfectants. ❖ It does not persist in kennels after removal of infected dogs.  Epidemiology ❖ Distribution: Worldwide. Endemic in Egypt. ❖ Animal susceptibility: Domestic dogs & many other carnivores. Young puppies of 3-6 months old are most susceptible especially those did not receive maternal antibodies. Nonimmunized older dogs are also highly susceptible. Stress factors: Immunosuppression, poor feeding, debility, Vit A deficiency & parasitism.  Epidemiology ❖ Transmission: Source of infection: ✓ Infected dogs shed the virus through bodily secretions & excretions, especially respiratory secretions for 60-90 days after infection. Mode of infection: ✓ Aerosol inhalation is main route of infection. ✓ Contact with contaminated objects. ✓ Flies & insects may transmit virus mechanically. ✓ Transplacental or in-utero infection is reported. Pathogenesis  Clinical signs ❖ Incubation: 2-9 days but usually varies. ❖ Morbidity & mortality: Variable. ❖ Course: 10 days but may extend for weeks or months.  Clinical signs ❖ Systemic manifestations: Diphasic fever for 1-3 days then temperature subsides for several days then second elevation for week or more. Loss of appetite, depression & lethargy. Cough, sneezing, dyspnea. Purulent oculo-nasal discharges. Vomiting, diarrhea, feces contain blood & mucous, tenesmus, dehydration & emaciation followed by death. Affected bitches abort. Hyperkeratosis of foot pads & nose with pustular dermatitis of abdomen & scruff & dandruff throughout the coat.  Clinical signs ❖ Neurological form: May occur at the time of systemic disease then after 3-6 weeks & after few months even years without history of disease (old dog encephalitis). May occur without visceral distemper. Hyperesthesia & cervical rigidity. Circling or running in place. Disturbance of balance, straddling gait, tremor, ataxia & paralysis. Chewing gum seizures: Chewing of jaw with salivation.  Clinical signs ❖ Transplacental transmission form: Mild or unapparent infection, abortion, stillbirth or birth of weak puppies. Young puppies infected transplacentally develop nervous signs in first 4-6 weeks of life. Permanent immunodeficiency. ❖ Neonatal infection form: Infection of puppies before eruption of permanent dentition causes severe damage of their enamel. Teeth become irregular or there is enamel hypoplasia.  Clinical signs ❖ Ocular form: Serous to mucopurulent conjunctivitis. Optic neuritis (blindness with dilated pupil) after systemic or subclinical infections. Degeneration & necrosis of retina causing gray to pink irregular densities on funds resulting in atrophy & complete retinal detachment. Circumscribed hyper-reflective areas termed as “gold medallion” lesions (characteristic of previous infection). Normal paws Affected paws Hyperkeratosis of the digital pads  Postmortem lesions ❖ Thymic atrophy in prenatally infected puppies. ❖ Catarrhal enteritis, conjunctivitis, rhinitis, pneumonia & inflammation of tracheobronchial tree. ❖ Hyperkeratosis: Nose, foot pads & pustular dermatitis of lower abdomen are found in dogs suffered from neurological disease. ❖ Meningeal congestion, ventricular dilatation & brain edema. ❖ On histopathology: Lymphoid depletion, neuronal & myelin degenerations (demyelination) & inclusion bodies (intracytoplasmic).  Laboratory diagnosis ❖ Isolation & identification: Cell culture, identified by FAT. ❖ Detection of virus antigens: FAT & PCR. ❖ Serological examinations: NT, FAT & ELISA. ❖ Experimental transmission: Mice, ferrets & hamsters. Rabbits & rats are resistant. ❖ Histopathological examinations: Intracytoplasmic & intranuclear in epithelial cells, neurons & leukocytes. ❖ Cell-mediated immune response (lymphocyte transformation test): Depression of lymphocyte because of immunosuppression. ❖ Hematological & serum analysis: Thrombocytopenia, lymphopenia, reduction in albumin & increase of globulins.  Differential diagnosis ❖ Infectious hepatitis: Prolonged bleeding time, liver enlarged & friable. ❖ Leptospirosis: Ulcers & bleeding of gums, bloody urine & Leptospira in urine. ❖ Tonsillitis: Due to Strep. or Staph. ❖ Toxoplasmosis. ❖ Bacterial gastroenteritis. ❖ Lead poisoning.  Treatment ❖ No specific treatment. ❖ Dogs suffering from respiratory signs kept in clean warm place away from drafts. ❖ Oculonasal discharges removed frequently. ❖ Food & water is withheld if there is vomiting & diarrhea. ❖ General tonics, multivitamins, antiemetic, antidiarrheal & minerals. ❖ Electrolytes (ringer’s solution & glucose). ❖ Neurological signs: Anticonvulsants, analgesics or sedatives. ❖ Broad-spectrum antibiotic to avoid bacterial infection: Ampicillin, chloramphenicol & amoxicillin 20-40 mg/kg daily in two or three divided doses or trimethoprim sulfonamide 30 mg/kg daily.  Control ❖ Proper management & hygiene: Infected dogs isolated & symptomatically treated. Kennels & living places cleaned & disinfected. All sources of infection are destroyed. ❖ Vaccination: Modified live attenuated vaccine: Ferret, egg & tissue culture. Inactivated vaccines: In exotic area & neonates. Combined vaccine: Canine distemper, hepatitis & leptospirosis. Puppies from non-vaccinated bitches: 1-4 weeks. Puppies from vaccinated bitches: 6-16 weeks. Program: 2 doses, 2-4 weeks intervals, booster dose annually. Post-vaccinal encephalitis may develop.  Control ❖ Vaccination in Egypt: Live attenuated tissue culture vaccine. Vial contains one dose dissolved in 1 ml saline, S/C in inner aspect of thigh, 3 months of age. Revaccinated annually. Give protection for one year. Infectious canine hepatitis Adenovirus infection Contagious hepatitis ‫التهاب الكبد المعدي فى الكالب‬  Definition ❖ Highly contagious disease affecting liver & other organs. ❖ Caused by Canine Adenovirus type 1 (CAV-1). ❖ Characterized by: ❖ Fever, depression, vomiting & diarrhea. ❖ Loss of appetite & abdominal pain. ❖ Jaundice & hepatitis. ❖ Conjunctivitis & blue eye. ❖ Prolonged bleeding time. ❖ Subclinical infection in adults.  Etiology ❖ Canine adenovirus 1 (CAV-1). ❖ Nonenveloped double-stranded DNA virus. ❖ Antigenically related only to CAV-2 (one of the causes of infectious canine tracheobronchitis). ❖ Resistant to lipid solvents, acids, formalin. ❖ 1-3% solution of sodium hypochlorite (household bleach) is an effective disinfectant.  Epidemiology ❖ Distribution: Worldwide. Not reported Egypt. ❖ Animal susceptibility: Dogs: Highly susceptible. Foxes & canines: Susceptible. Dogs less than 1 year highly susceptible.  Epidemiology ❖ Transmission: Source of infection: ✓ The infected animals shed the virus in secretion & excretion (urine, saliva, feces) during acute stage. ✓ Remain in renal tubules & shed in urine for 1 year after recovery. Mode of infection: ✓ Ingestion. ✓ Contact with fomites. ✓ Inhalation. ✓ Vectors: Fleas, ticks & mosquitoes.  Virus enters through the oral route Pathogenesis Multiplication in tonsils & spread to local lymph nodes Viremia (4-8 days) Dissemination to other tissues Bone marrow & Hepatic- Renal- Endothelial cells lymphoid tissues ocular parenchyma of many tissues Hepatitis, Uveitis Leukopenia & anaemia Glomerulonephritis Serosal haemorrhages  Clinical signs ❖ Incubation: 4-10 days. ❖ Morbidity & mortality: Variable (around 5%). ❖ Course: 5-7 days in uncomplicated cases. ❖ Clinical signs: Vary from mild to severe. ❖ Peracute form: Sudden death.  Clinical signs ❖ Acute form: Diphasic fever for 1-6 days: Anorexia, thirst, depression, Increased pulse & respiration rates. Tonsillar enlargement & cervical lymphadenopathy. Edema of head, neck & trunk. Abdominal distension due to ascites & hepatomegaly. Epistaxis & bleeding time is increased. Respiratory signs: Serous discharges from nose, cough & harsh respiratory sounds. GIT signs: Vomiting, abdominal pain, diarrhea with or without hemorrhage. Nervous signs: Disorientation, seizures & coma.  Clinical signs Ocular signs: Conjunctivitis, corneal edema, ulceration & uveitis results in blepharospasm, photophobia & ocular discharges. Unilateral or bilateral corneal opacity (blue eye). About 30% of dogs develop blue eye in 1-3 weeks after remission of signs (temporary or permanent). Petechial hemorrhage around teeth (paint brush hemorrhage), mucous membrane of mouth, abdominal skin & aqueous chamber of eyes with hematoma. Death due to hepatic insufficiency & hepatoencephalopathy.  Postmortem lesions ❖ Dogs die in acute phase: Edema & hemorrhage of cervical LN. ❖ Serous surfaces: Petechial & ecchymotic hemorrhages. ❖ Abdominal cavity: Clear to bright red fluid. ❖ Lungs: Multiple areas of consolidation. ❖ Liver: Enlarged, dark & mottled with fibrinous exudates. Dogs survive acute phase show small, firm & nodular liver (hepatic fibrosis). ❖ Gall bladder: Thickened. ❖ Eyes: Corneal opacity & clouding of aqueous humor. ❖ CNS: Hemorrhages in midbrain & brain stem. ❖ Spleen: Enlarged. ❖ Kidneys: White foci & focal hemorrhages in cortex.  Diagnosis ❖ Field diagnosis: History, signs (prolonged bleeding), & PM. ❖ Laboratory diagnosis: Isolation: CPE & intranuclear inclusions, identified by FAT. Detection of virus antigens: FAT & PCR. Serological examinations: HI, NT & CFT. Histopathological examinations: Intranuclear inclusions in hepatic & endothelial cells (pathognomic for ICH). Hematological & serum analysis: In early stage, leukopenia & neutropenia later lymphocytosis & neutrophilia. Increase in bleeding time, increase in ALT, AST, ALP, bilirubinuria, proteinuria & thrombocytopenia. ❖ Differential diagnosis: CD, Herpesvirus, Strep., E. coli, Brucellosis & Toxoplasmosis.  Treatment ❖ Prognosis: Unfavorable. The recovered animals develop lifelong immunity. ❖ Treatment: Protein intake is reduced. Non-absorbable oral antibiotic as neomycin. Broad-spectrum antibiotics: Ampicillin or gentamicin. Fluid therapy as ringer’s solution: 45 ml/kg I/V & glucose 5%, 5 ml/kg. Clotting factors & platelets or whole blood: 80-100 ml. Antiserum in early stages: 2.2 ml/kg & after 48 hours in bad cases. Potassium & ascorbic acid is indicated. Atropine ophthalmic ointment to reduce ciliary spasm.  Control ❖ Proper management & hygiene: Detection of subclinical cases. Infected dogs isolated, treated & good nursed. Kennels cleaned & disinfected & source of infection destroyed. ❖ Vaccination: Live attenuated vaccine (CAV-1 & CAV-2). Single or combined vaccine: Distemper, hepatitis, & leptospirosis. At 12-14 weeks, 2 doses 3-4 weeks intervals. Immunity for 1-3 years. Inactivated vaccines do not produce any lesions. Live vaccines produce respiratory signs or subclinical interstitial nephritis & shedding of vaccinal virus in urine. Canine parvovirus enteritis Hemorrhagic enteritis Panleukopenia of dogs ‫مرض بارفو الفيروسي‬  Definition ❖ Highly contagious disease of dogs that causes acute gastrointestinal illness in puppies. ❖ Enteric disease attacking pups between weaning age & six months of age. ❖ Characterized by: Pyrexia & anorexia. Vomiting. Depression & dehydration. Hemorrhagic enteritis & dysentery. Sudden death in young puppies due to myocarditis.  Etiology ❖ Canine parvovirus 2 (CPV-2), genus parvovirus, family Parvoviridae. ❖ Small single stranded DNA. ❖ Related to feline parvovirus (Feline panleukopenia virus). ❖ Three antigenic types CPV-2 (a, b & c). ❖ Require actively dividing cells for growth. ❖ Very stable and resistant.  Epidemiology ❖ Distribution: Worldwide. Reported in Egypt. ❖ Animal susceptibility: Domestic & wild canines as dogs, foxes, & wolves. Any age but severe in puppies of 6-16 weeks of age. Antibodies (HI) found in serum of 85% of dogs without symptoms.  Epidemiology ❖ Transmission: Source of infection: ✓ Feces of diseased animals (small amount of feces contain billions of viral particles). Mode of infection: ✓ Spread by direct & indirect (contamination with dog feces). ✓ Ingestion of food or water contaminated with feces (fecal- oral infection). ✓ Oro-nasal. ✓ In-utero infection. Pathogenesis Cardiac Intestinal form form Clinical signs  Clinical signs ❖ Myocardial form: Less common. Attack heart muscle of young puppies (puppies infected in uterus or shortly after birth until 8 weeks of age). Sudden death after a brief illness with or without bloody diarrhea. They suffer from myocarditis with signs of: ✓ Cardiac arrhythmia. ✓ Dyspnea & Coughing. ✓ Pulmonary edema. ✓ Death (20-100%) due to progressive myocardial necrosis.  Clinical signs ❖ Intestinal form: Common in age of 6 weeks-9 months. May express unapparent, subclincal, acute or subacute disease. Fever & anorexia. Depression & lethargy. Weight loss & dehydration. Abdominal discomfort. Repeated episodes of vomiting. Severe enteritis with bloody diarrhea. Diarrhea is foul smelling & sometimes yellow in color. Hemorrhagic enteritis Hemorrhagic enteritis  Postmortem lesions ❖ Subserosal congestions & hemorrhages in intestinal lumen. ❖ Necrosis of intestinal crypts. ❖ Intestine contain yellow or blood-tinged fluid. ❖ Lymph nodes are enlarged & edematous with hemorrhages. ❖ Thymic edema & atrophy in young dogs. ❖ Myocarditis in puppies died with cardiac form. ❖ Pulmonary edema. ❖ Hydropericardium.  Hemorrhagic enteritis Affected cardiac muscle  Diagnosis ❖ Field diagnosis: Sudden bloody diarrhea, anorexia & repeated vomiting. In breeding kennels: Several littermate puppies may become ill simultaneously or within short period. ❖ Differential diagnosis: Canine coronavirus. Salmonellosis. Colibacillosis. Enteric bacterial infection. Gastrointestinal parasitism as giardiasis. Toxin enteritis.  Diagnosis ❖ Laboratory diagnosis: Detection of the virus: In feces or intestinal contents by ELISA, latex agglutination, electron-microscope & in tissue sections by immunofluorescence. Isolation & identification: In canine fetal lung cells. Serological examinations: HI & NT. Histopathological examinations: Interstitial fibrosis of myocardium with intranuclear inclusions & destruction of intestinal epithelium resulting in shortening of villi. Detection of cardiac abnormalities: Radiography & ECG. Hematological examinations: Lymphopenia is characteristic. In severely affected dogs, neutropenia & intestinal damage.  Treatment ❖ No specific treatment. ❖ Symptomatic & supportive. ❖ Food & water withheld for 12-24 hours. ❖ Electrolytes: I/V or S/C fluid therapy as ringer’s solution with potassium chloride & sodium bicarbonate in acidosis. ❖ Glucose 5% and amino acids if blood glucose decreased. ❖ Broad spectrum antibiotics as ampicillin or gentamicin. ❖ Intestinal coating. ❖ Antiemetics & corticosteroids. ❖ Multivitamins as Vit B.  Control ❖ Proper management & hygiene: Difficult to exclude from breeding centers because infected dogs shed virus in feces. Infected dogs isolated, treated & good nursed. Young puppies isolated in separate place. Kennels & living places cleaned & disinfected. ❖ Vaccination: Inactivated & live attenuated vaccines. Bitches vaccinated prior breeding. Puppies from immunized bitches have immunity for 8-16 weeks. They vaccinated for three times at 8, 12 & 16 weeks of age & booster dose annually in case of inactivated vaccine.  Control ❖ Vaccination in Egypt: Monovalent living attenuated tissue culture vaccine in lyophilized form in vials of one dose. ✓ Vial dissolved in 1 ml saline, S/C in inner aspect of thigh. ✓ Puppies vaccinated at 3 months & revaccinated annually. Bivalent parvovirus & distemper living attenuated tissue culture vaccine is produced. ✓ Vaccination program similar to monovalent vaccine. Canine coronavirus and rotavirus enteritis  Definition & etiology ❖ Viral disease caused either by coronavirus or rotavirus. ❖ Characterized by: Enteritis & diarrhea. ❖ Canine coronavirus (CCV) is small RNA virus. Inactivated by detergents & lipid solvents. ❖ Canine rotavirus (CRV) belongs to family Reoviridae. Resist acids & lipid solvents.  Epidemiology ❖ Worldwide distributed. ❖ Not reported in Egypt. ❖ Dogs are susceptible. ❖ High prevalence rates are in housed dogs. ❖ Puppies of 2-12 weeks of age are more susceptible. ❖ Infected dogs shed virus in feces intermittently for several months after recovery. ❖ Transmitted by fecal-oral route, therefore infection spreads rapidly.  Pathogenesis Virus invades mature epithelial cells of small intestinal villi Multiplies causing degeneration intestinal epithelium Villous atrophy with diarrhea.  Clinical signs ❖ In coronavirus: Signs are mild. Pyrexia & anorexia & Vomiting. Enteritis & diarrhea. Depression & dehydration. Watery feces may be tinged with blood. Mortality rate is very low. ❖ In rotavirus: Most of infections result in subclinical infection or mild. Anorexia & Diarrhea. Lethargy.  Diagnosis ❖ Field diagnosis: Clinical signs, PM & History disease. ❖ Laboratory diagnosis: Detection of the virus: In feces or intestinal contents: by FAT, PCR & electron-microscope. Isolation and identification: In tissue culture & identified by FAT. Serological examinations: ELISA & latex agglutination. Histopathological examinations: Destruction & desquamation of intestinal epithelium & shortening of intestinal villi. ❖ Differential diagnosis: Parvovirus, Salmonellosis, Colibacillosis, Giardiasis, Toxin enteritis.  Treatment ❖ Symptomatic & supportive. ❖ Food & water withheld for 12-24 hours. ❖ Fluid therapy as ringer’s solution & glucose 5% supplemented with potassium chloride & sodium bicarbonate in acidosis. ❖ Broad-spectrum antibiotics as: ampicillin or gentamicin. ❖ Intestinal coating. ❖ Multivitamins as Vit B.  Control ❖ Isolation & symptomatic treatment of infected dogs. ❖ Young puppies are isolated in separate place away from general population. ❖ Kennels and living places are cleaned & disinfected. ❖ Inactivated vaccine can be used for CCV. ❖ No available vaccine for CRV.  Infectious canine tracheobronchitis Canine infectious tracheobronchitis (CITB) Kennel cough complex ‫إلتهاب القصبة الهوائية والشعبتين المعدي في الكالب‬  Definition ❖ A collection of highly contagious infectious diseases of the canine respiratory tract. ❖ Characterized by: Acute tracheobronchitis. Sudden onset of paroxysmal cough lasting several days. ❖ Most of infections are self-limiting. ❖ It is one of most prevalent diseases of dogs.  Etiology ❖ Several pathogens. ❖ Two most important causes of canine ITB: Canine parainfluenza virus (CPIV). Bordetella bronchiseptica. ❖ Other infectious agents occasionally isolated from coughing dogs: Canine adenoviruses (especially CAV-2). Canine herpesvirus. Reoviruses (types 1, 2 & 3). Mycoplasmas.  Epidemiology ❖ Distribution: One of most common canine infections worldwide. ❖ Animal susceptibility: All ages susceptible. Immunosuppressed & young dogs more susceptible. Predisposing factors: Weaning, bad weather, overcrowding, immunosuppression.  Epidemiology ❖ Transmission: Source of infection: ✓ Dogs infected with CPIV or CAV-2 shed the virus only 1 week after recovery. ✓ Dogs infected with B. bronchiseptica, or Mycoplasma become chronic carriers with persistent shedding. Mode of infection: ✓ Direct by inhalation. ✓ Indirect contact with infected fomites.  Pathogenesis ❖ Virus multiplies in epithelium of nasal mucosa, trachea, bronchi, bronchioles & peri- bronchial lymph nodes. ❖ Infection causes initial damage of tracheobronchial mucosa which facilitates colonization of bacterial invasion (viral-bacterial synergism).  Clinical signs ❖ Incubation: 10 days. ❖ Morbidity: High. ❖ Mortality: Low. ❖ Course: Several days to weeks.  Clinical signs ❖ Uncomplicated form: Common. Dry hacking cough followed by vomiting. Cough is sudden & paroxysmal or high pitched due to laryngitis & vocal cord swelling. Rhinitis with serous to mucopurulent nasal discharges. Conjunctivitis. Dogs are alert, active & remain eating. Arched back, open mouth & foamy mucoid discharges. Spontaneous recovery in 1-2 weeks or less may occur.  Clinical signs ❖ Complicated form: In puppies or immunosuppressed dogs. Bacterial bronchopneumonia: ✓ Fever. ✓ Purulent nasal & ocular discharges. ✓ Dyspnea. ✓ Weight loss. ✓ Loss of appetite.  Laboratory diagnosis ❖ Isolation of causative agents: Viral & bacterial cultures. ❖ Serological examinations: Antibodies for PI, B. bronchiseptica by ELSA, NT & HI. ❖ Hematological examinations: Neutrophilia, lymphopenia & drop in eosinophils. Examination of tracheal washes reveals high neutrophils. ❖ Radiograph examination: Pulmonary hyperinflation & consolidation. ❖ Histopathological examinations: Inflammation in trachea, bronchi & lungs.  Treatment ❖ Antimicrobial therapy: Antibiotic is chosen on basis of sensitivity test: Tetracycline: 20 mg/kg, PO, every 8 hours for 7 days. Trimethoprim-sulfonamide: 15 mg/kg S/C every 12 h for 7 days. Cephalexin: 30 mg/kg, PO, every 12 hours for 7 days. Doxycycline: 5–10 mg/kg, PO, 12h for 2 to 4 weeks. Amoxicillin/clavulanate: 12.5–25 mg/kg, PO, 12h for 2 to 4 weeks. Azithromycin: 5 mg/kg, PO, once daily for 5 to 7 days. ❖ Expectorants: Patent expectorants or guaifenesin & volatile oil inhalation.  Treatment ❖ Antitussive drugs: Hydrocodone bitartrate: 0.22 mg/kg, PO, every 6-12 hours. Butorphanol tartrate: 0.5-1 mg/kg, S/C, every 6-24 hours. ❖ Bronchodilators: Aminophylline: 11 mg/kg, PO, every 6-12 hours for 5-10 days. Theophylline: 5-10 mg/kg, PO, every 6-12 hours for 5-10 days. ❖ Anti-inflammatory: Glucocorticoids & prednisolone: 0.25-0.5 mg/kg every 12 hours for 5-7 days to reduce cough & respiratory secretions. ❖ Supportive care: Maintenance of adequate caloric & fluid intake.  Control ❖ Proper management and hygiene: Infected dogs isolated, treated & good nursed in hygienic environment. Kennels cleaned & disinfected by sodium hypochlorite or quaternary ammonium compounds. Density of the population minimized with proper ventilation. ❖ Vaccination: Bivalent (PI & B. bronchiseptica) or polyvalent vaccines. Intranasal. Annually.  Canine herpesvirus infection Viral puppy mortality Fading puppy complex Neonatal virus deaths ‫نفوق الجراء‬ ‫عدوي فيروس الهربس في الكالب حديثة الوالدة‬  Definition & etiology ❖ Acute fatal viral disease of young puppies. ❖ Characterized by: Sudden death. Rhinitis. Dyspnea. Serous to mucopurulent nasal discharges. Meningoencephalitis. Conjunctivitis. ❖ Canine herpesvirus. ❖ Only one serotype is described.  Epidemiology ❖ Distribution: Worldwide. Reported in Egypt. ❖ Animal susceptibility: Several canine species as dogs & wolves. Clinical disease is rare in dogs older than 3-4 weeks of age. Puppies die at 9-14 days after birth. This range may extend form 1 day after birth (prenatal infection) to 1 month (neonatal infection).  Epidemiology ❖ Transmission: Source of infection: ✓ Feces & urine of diseased animals. ✓ Virus exists in oral, nasal & vaginal secretions 2 weeks after infection. Mode of infection: ✓ Direct contact. ✓ Puppies may be infected in-utero, during passage through birth canal ✓ Inhalation.  Pathogenesis ❖ Virus multiplies in nasal epithelial cells & tonsils causing necrotizing rhinitis. ❖ Viremia ❖ Dissemination via macrophages throughout body. ❖ Localize in various organs causing hemorrhages & focal necrosis. ❖ Transplacental infection during last 3 weeks of gestation may result in fetal deaths with mummification, abortion, or birth of dead or dying puppies. ❖ Remain latent in trigeminal nerve ganglia & excreted in nasal secretions.  Clinical signs ❖ Incubation: 4-6 days. The course is rapid with high mortality rate. ❖ Sudden death of puppies after 12-36 hours of illness. ❖ Some puppies may be found died without signs. ❖ Anorexia, dyspnea & serous to mucopurulent nasal discharges. ❖ Grayish yellow or green soft odorless stool. ❖ Nervous signs & severe gasping before death. ❖ Recovered puppies suffer from deafness, blindness, or renal damage. ❖ Old dogs express rhinitis & conjunctivitis ❖ Urogenital infection: Vesicular vaginitis & reproductive failure as infertility, abortion & stillbirth.  Postmortem lesions ❖ Focal necrosis & hemorrhages: In several organs as kidneys, lungs, liver, adrenal glands & small intestine. ❖ Lymph nodes & spleen are enlarged.  Diagnosis ❖ Field diagnosis: Deaths of young puppies. Respiratory manifestations. Abortion & stillbirth. PM. ❖ Laboratory diagnosis: Detection of virus: NT, FAT, immunofluorescent assay & PCR. Isolation & identification of virus: Identified by FAT & NT. Serological examinations: NT & ELISA. Histopathological examinations: Perivascular necrosis & cellular infiltration in kidneys, lungs, liver, spleen, brain & small intestine. ❖ Differential diagnosis: Parvovirus, distemper, hepatitis, E. coli, Salmonella & Toxoplasmosis  Treatment & control ❖ Prognosis: Bad because of the high mortalities. ❖ Treatment: Not recommended. Antiviral drugs unsuccessful. Immune serum from recovered bitches is beneficial in reducing deaths. among puppies if given before onset of illness. ❖ Control: Infected pregnant bitches are isolated 3 weeks prior to parturition. Puppies upto 3 weeks are reared in incubators at 35°C and 50% humidity. Kennels and living places are cleaned & disinfected. Examination of animals before breeding for vesicular vaginitis. The virus is poorly immunogenic & there is no available vaccine.  Canine infectious diarrhea ‫اإلسهال المعدي في الكالب‬  Definition & etiology ❖ Acute disease of dogs. ❖ Signs of enteritis or gastroenteritis as: Diarrhea, vomiting, dehydration & occasionally death. ❖ Multi factorial causes: Coronavirus, Rotavirus, adenovirus, canine distemper, parvovirus type 2, parvovirus 1 & calcivirus. Campylobacter jejuni, pathogenic serotypes of E. coli, salmonella spp. & Clostridia. Protozoa as Coccidia & Giardia. Helminth infestations.  Clinical signs ❖ Many cases: Apparently self-limiting. The animal does not appear ill & diarrhea resolves spontaneously. ❖ In severe cases: Profuse diarrhea, dullness, inappetance, vomiting, dehydration, electrolyte imbalance. ❖ In some cases: Dysentery & rapid collapse. ❖ Temperature: Raised, especially with acute bacterial infections, but often within the normal range or subnormal in profusely diarrheic & collapsed animals. ❖ On abdominal palpation: Fluid and or gas filled intestinal loops.  Diagnosis ❖ Field diagnosis: History & clinical signs. ❖ Laboratory diagnosis: Isolation & identification of causative agents. ❖ Differential diagnosis: Infectious enteritis should be differentiated from dietary upset, which is the commonest cause of transient diarrhea in the dog.  Treatment & control ❖ Treatment: Reduction in food intake for 24-48 hours. Absorbents as kaolin or bismuth or drugs inhibiting bowel mobility (atropine sulfate & codeine phosphate). Antibiotics as neomycin acts mainly within the gut lumen. Fluid therapy: Lactate Ringer solution by I/V. ❖ Control: Proper management & hygiene. Vaccination. Composed by El-Sayed M. Galila Infectious Diseases Menoufia University Thank you