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VIRAL DISEASESPresented by
EMAD M. A. SAMARA, BVM&S
I- Foot and Mouth Disease
• AKA (FMD, Aftosa)• Causative agent (Virus; Picornaviridae)• History (1921-29,1953,1967-68, 1981, 1993-97,and 2001)• Public Health Significance (not a public health concern; 40
cases since 1921)
• Species Affected (Domestic Cloven-Footed animals)• Animal Transmission (Direct and indirect contact)• Morbidity/ Mortality (100% / 1%; Higher in young animals)
• Economic Impact (Direct and indirect costs, Economically Devastating)
I- Foot and Mouth Disease• Diagnosis (Clinical Signs, Laboratory Tests)• Clinical Signs
– In Cattle (Fever, Vesicles and Erosions on “feet, mouth, nares, muzzle, teats, hoof”, Excess salivation, Serous nasal discharge, Abortion, Death in young animals)
– In sheep and goat (Mild, Fever, Oral lesions, Lameness)• Post Mortem Lesions (indistinguishable from other vesicular diseases,
Single or multiple vesicles, Dry Erosions, Tiger heart)
• Treatment (No treatment available, Supportive and symptomatic, Vaccine available)
• Prevention and Control (Import restrictions, Confirmatory diagnosis, Authorities Notification, Quarantine, Disinfection, Vaccination)
II- Rinderpest
• AKA (RPV, Cattle Plague)• Causative agent (Virus; Paramyxoviridae)• History (1184 BC, 1762, 1885, 1960’s,and 1992)• Public Health Significance (not a public health
concern)
• Species Affected (Domestic Cloven-Footed Animals)• Animal Transmission (Direct and indirect contact) • Mortality (100%; Susceptible stock are immature or
young adults)
• Economic Impact (Direct and indirect costs, Destroys entire populations of cattle)
II- Rinderpest• Clinical Signs (Four forms)
– Classic form (Fever, depression, anorexia, Constipation followed by hemorrhagic diarrhea, Serous to mucopurulent nasal/ocular discharge, Necrosis and erosion of the oral mucosa, Enlarged lymph nodes, Death in 6-12 days)
– Peracute form (Young animals, high fever with congested mucous membranes, death in 2-3 days)
– Subacute form (Mild clinical signs with low mortality)– Atypical form (Irregular fever, mild or no diarrhea, Immunosuppression
leading to secondary infections)
• Post Mortem Lesions – Esophagus (Brown and necrotic foci)– Omasum, Abomasum, Small intestine and cecum ( Tiger striping;
Necrosis, edema and congestion )– Lymph nodes (Swollen and edematous)– Gall Bladder ( Hemorrhagic mucosa)– Lungs (Emphysema, congestion, and areas of pneumonia)
II- Rinderpest
• Treatment (No treatment available, Diagnosis usually means slaughter of effected animals, Supportive care with antibiotics in rare cases of valuable animals, Preventative measures are the keys)
• Prevention and Control (Confirmatory diagnosis, Authorities Notification, Quarantine, Disinfection, Vaccination)
III- Peste des Petits Ruminants
• AKA (Pest of Small Ruminants, Stomatitis-Pneumoenteritis Syndrome, Pseudorinderpest, Contagious Pustular Stomatitis, Kata)
• Causative agent (Virus; Paramyxoviridae)• History (1942, 1972, and 1990’s)• Public Health Significance (not a public health concern)
• Species Affected (Principally goats and sheep, reported in captive wild ungulates, Cattle and pigs seroconvert but do not transmit disease)
• Animal Transmission (Direct and indirect contact)• Morbidity/ Mortality (80-90% / 50-80%, can be up to 100%; More
severe in young animals, poor nutrition, concurrent parasitic infections; Goats more susceptible than sheep)
• Economic Impact (Direct and indirect costs)
III- Peste des Petits Ruminants
• Diagnosis (Clinical Signs, Laboratory Tests)• Clinical Signs (Acute fever, Anorexia, Upper respiratory
discharge progressing to catarrhal exudate, Dyspnea Profuse diarrhea, Dehydration, Emaciation, Abortion and Death in 5-10 days)
• Post Mortem Lesions (Similar to Rinderpest; Carcass emaciation, Bronchopneumonia, “Zebra stripe” lesions of congestion in large intestine, Enlarged lymph nodes)
• Treatment (No specific treatment, Drugs to control bacterial and parasitic complications may decrease mortality, Supportive care)
• Prevention and Control (Import restrictions, Confirmatory diagnosis, Authorities Notification, Quarantine, Disinfection, Vaccination)
IV- Malignant Catarrhal Fever• AKA (Malignant Head Catarrh, Gangrenous Coryza,
Snotsiekte)• Causative agent (Virus; Gamma-herpesviridae)• History (1920’s, 1973, and 2002)• Public Health Significance (not a public health concern)
• Species Affected (Domestic and wild Cloven-Footed Animals)
• Animal Transmission (Direct and indirect contact; Some species ”Dead end hosts” )
• Morbidity/ Mortality (30-40% / 1-100 %; depend on the host; Survival is rare; carrier species asymptomatic)
• Economic Impact (Direct and indirect costs; Variable)
IV- Malignant Catarrhal Fever• Clinical Signs (Five forms)
– Acute form (High fever, Dyspnea, D.I.C., and Sudden death)
– Head and eye form (Bilateral corneal opacity, Crusty muzzle and nares, Nasal discharge, Salivation, Erosions on the tongue and buccal mucosa)
– Intestinal form (Inappetence, Dysphagia, Severe diarrhea)– Nervous form (Depression, Incoordination, head pressing,
nystagmus, hyperesthesia)– Mild form (Inoculated animals recover)
• Post Mortem Lesions (Erosions on the tongue and soft and hard palate, Multiple erosions of intestinal epithelium, Enlarged lymph node, Diptheritic areas in the larynx, Edematous urinary bladder mucosa )
IV- Malignant Catarrhal Fever
• Treatment (Supportive therapy, antibiotics for secondary bacterial infection, Recovered animals will remain virus carriers)
• Prevention and Control (Confirmatory diagnosis, Authorities Notification, Quarantine, Disinfection, No vaccine available)
V- Rift Valley Fever• Causative agent (Virus; Bunyaviridae)• History (1900’s, 1930, 1950-51, 1977-78, 1987, 1997-98, 2000-
01, and 2003)• Public Health Significance (a public health concern; cause
Flu-like illness, Retinopathy, Hemorrhagic fever, and Encephalitis; mortality ~1%, Treatment is supportive care)
• Species Affected (Domestic and wild Cloven-Footed Animals, pet animals)
• Animal Transmission (Direct and indirect contact; ”Dead end hosts” in human)
• Morbidity/ Mortality (100% / 10 -100%, More severe in young animals “week vs. over week” )
• Economic Impact (Direct and indirect costs)
V- Rift Valley Fever• Clinical Signs (High fever, Listless, Anorexia, ptyalism, High
rate of abortion, Fetid diarrhea, Icterus, Mucopurulent nasal discharge, Acute death )
• Post Mortem Lesions (Necrosis and Petechial hemorrhages in Hepatic, abomasum and peritoneal cavity; yellow, enlarged, friable Liver; aborted fetuses)
• Treatment (No specific treatment, Drugs to control bacterial and parasitic complications, Supportive care Preventative measures are keys)
• Prevention and Control (Immunization of ruminants, Avoid and control vectors, Personal protective equipment, Avoid contact with infected tissues and blood, Restrict movement of animals, Precautions when traveling)
VI- Bluetongue Virus• AKA (Sore Muzzle, Pseudo Foot-and-Mouth Disease, Muzzle
Disease)• Causative agent (Virus; Reoviridae)• History (1997-2002)• Public Health Significance (Not a significant threat to
humans; One human infection documented, Reasonable precautions should be taken, Treatment is supportive care)
• Species Affected (Domestic and wild Cloven-Footed Animals)• Animal Transmission (Direct and indirect contact )• Morbidity/ Mortality (100% / 0-50% in Domestic Animals, and
80-90% in wild Animals)
• Economic Impact (Direct and indirect costs; Variable)
VI- Bluetongue Virus• Diagnosis (Clinical Signs, Laboratory Tests)• Clinical Signs (Fever, depression, salivation, Facial swelling,
Oral erosions and ulcerations, Swollen, protuding, and Cyanotic Tongue “Blue-tongue”, Dyspnea, Panting, Nasal discharge, Hyperemia of muzzle, lips, ears, lameness “Coronitis”, abortion, “dummy” lambs)
• Post Mortem Lesions (Edematous face and ears, Dry, crusty exudate on nostrils, Vesicles, ulcers, necrosis in Mouth, Hyperemic coronary bands, Internal hemorrhaging, Hydranencephaly, cerebellar dysplasia)
• Treatment (No specific treatment, Supportive care)• Prevention and Control (Control of vectors, Confirmatory
diagnosis, Authorities Notification, Quarantine, Disinfection, )
VII- Viral Encephalitis• Types (Western equine encephalitis (WEE), Eastern equine
encephalitis (EEE), St. Louis encephalitis (SLE), La Crosse encephalitis (LAC), Venezuelan equine encephalitis (VEE), West Nile virus (WNV)
• Causative agent (Virus; Flaviviridae)• History (1925 -2000, and 2003-04)• Public Health Significance (a public health concern; 1964-
2002, 182 cases; cause Flu-like illness, Sudden fever, headache, myalgia, malaise, encephalitis, Death, mortality ~ 0.1%)
• Species Affected (Equine species; and other animals)• Animal Transmission (indirect contact; Dead end hosts; equine
and human )• Case-fatality rates (Equine: 90%, Human: 30-70%, other
Variable)
VII- Viral Encephalitis
• Diagnosis (Clinical Signs, Laboratory Tests)• Clinical Signs
– Neurological (Paralysis of lips, facial muscles, tongue; Dysphagia; Hyperesthesia; Sound sensitive; torticollis; nystagmus; Seizures; Blindness; Ataxia)
– Other (Flu-like signs, Fever, Depression, Anorexia, Muscle spasm, Skin twitching, Weakness, and recumbency)
• Post Mortem Lesions (Mild to moderate, diffuse, and non-suppurative meningoencephalitis; myocarditis)
VII- Viral Encephalitis
• Treatment (No specific treatment, Supportive care, Fully licensed vaccine)
• Prevention and Control (Vector Management “Surveillance, Source reduction, Personal protection, Biological control, Larvicide, and Adulticide”; Confirmatory diagnosis, Authorities Notification, Quarantine, Disinfection, Vaccination)
VIII- Other Important Dz
• Bovine Viral Diarrhea
• Maedi-Visna
• African Horse Sickness
• Vesicular Stomatitis
• Lumpy Skin Disease
• Sheep and Goat Pox
• Haemorrhagic Fever Disease
The End