RINDERPEST
Cattle Plague
• Rinderpest, also known as cattle plague, is a contagious viral disease affecting clovenhoofed animals (mainly cattle and buffalo).
• In 2011, rinderpest became the second disease to be declared officially eradicated.
• Notifiable disease.
• This virus is separate from but related to CDV, measles
Morbidity % 90 Mortality % 100
Rinderpest, which once devestated cattle herds around the world, has become the second deadly virus to be eliminated
Etiology
• Paramyxoviridae --- Morbillivirus
• RNA
• Enveloped
• Sensitive to Ether and Chloroform
• There is just one serotype of this virus, but three genetically distinct lineages
• – lineage 1, lineage 2, and lineage 3 – have been identified.
• Kabete-O
• Rinderpest historically occurred in Europe, Africa and Asia. The Americas and Oceania never faced rinderpest epizootics.
• Virus forms I.N. and I.S. inclusion bodies.
• Virus was first isolated by French Nicholl and Turkish Adil Bey.
• CPE
• İnterference feature
Transmission
• Transmission of rinderpest virus usually occurs through direct or close indirect contact with infected animals.
• The virus is found in nasal secretions a few days before any clinical signs appear.
• As the disease progresses the virus is found in most body fluids and
• either death ensues,
• or the animal recovers, develops immunity and clears the virus from the body.
• Other than cattle and buffalo, rinderpest can infect zebus, water buffaloes, African buffaloes, eland, kudu, wildebeest, various antelopes, bushpigs, warthogs, giraffes, sheep, and goats.
• Some wild animals can carry the virus without showing signs of disease and in a few cases have made contact with domestic animal populations, leading to
(re)introduction of the disease.
Rinderpest transmission and spread are enhanced by congregation of different herds of animals, as occurs at common watering-points
Clinical Signs
• The incubation period for rinderpest ranges from 3 to 15 days; 4 to 5 days is typical.
• The virulence and dose of virus and the route of exposure affect the incubation period.
• Mild forms of the disease can have an incubation period between one and two weeks.
• The World Organization for Animal Health
(OIE) has established a maximum incubation
period of 21 days for zoosanitary measures.
• In cattle, the most susceptible species, classical signs of the disease include
• fever,
• erosive lesions in the mouth, (foamy saliva)
• discharge from the nose and eyes,
• profuse diarrhea and dehydration,
• often leading to death within 10 to 15 days.
• In other species rinderpest may show milder clinical signs.
• A peracute form, characterized primarily by high fever and sudden death, is mainly seen in young and newborn animals.
Oral legions from Rinderpest, Source:
www.vet.uga.edu
• In the acute (classical) form in cattle,
• a prodromal period of fever,
• depression,
• decreased appetite,
• decreased milk yield,
• congestion of mucous membranes,
• and serous ocular and nasal discharges is followed in approximately 2-5 days by the development of necrotic oral lesions.
• Necrotic epithelium can be found on the lips, tongue, gums, buccal mucosa, soft and hard palates.
• The muzzle eventually dries and develops cracks, and the animal becomes anorexic and develops mucopurulent ocular and nasal discharges.
• Diarrhea is typically profuse and watery at the onset, but may contain mucus, blood and shreds of epithelium in the later stages.
• Enlarged lymph nodes
• Death in 6-12 days
• In endemic areas, cattle may also develop mild subacute disease or atypical forms of rinderpest.
• Rinderpest is usually milder in sheep and goats than cattle, and some infections are subclinical.
• The clinical signs may include fever and anorexia, with diarrhea in some animals.
• Severe cases with necrotic stomatitis, oculonasal discharge, conjunctivitis, pneumonia and diarrhea
(similar to classical disease in cattle) may also be seen.
Pathogenesis, immunity and pathology
• Highly infectious virus is excreted in nasal and ocular exudates and in saliva and faeces. Aerosol virus travels over distances of less than 3 metres.
• Marked necrosis of gut (zebra bands) and resp tract, lymphadenitis, death after haemorrhagic diarrhoea. Cattle will only recover from less virulent infections. Animals that recover are immune for life.
• In endemic areas, newborn animals are protected from 6-11 months
of age by maternal antibodies, so the most susceptible are immature
or young adult animals.
• Esophagus
• Brown and necrotic foci
• Omasum
• Rare erosions and hemorrhage
• Small intestine, abomasum, cecum and colon
• Necrosis, edema and congestion
• Colonic ridges may be congested, this is referred to as
“Tiger striping” or “zebra striping’.
The ileocecal valve, cecal tonsil and crests of the longitudinal folds of the cecal, colonic and rectal mucosae can be greatly congested in animals that die acutely, and may be darkened in more chronic cases, a lesion known as ‘tiger striping’ or ‘zebra striping’.
http://www.vetmed.ucdavis.edu/vetext/INF-DA/INF-DA_Rinderpest.html lower photo: USDA)
Post Mortem Lesions
• Lymph nodes
• Swollen and edematous
• Gall Bladder
• Hemorrhagic mucosa
• Lungs
• Emphysema, congestion and areas of pneumonia
Histologically, evidence of lymphoid and epithelial necrosis accompanied by viral associated syncytia and
intracytoplasmic inclusions
Bovine, oral mucosa. There are numerous small gingival erosions.
Bovine, oral mucosa. There are numerous coalescing erosions on the ventrolateral lingual mucosa.
Bovine, oral mucosa. There is severe diffuse necrosis/coalescing ulceration of the dental pad;
mandibular mucosa contains smaller erosions.
Bovine, colon. There are many petechiae on the crests of the mucosal folds, and there are several small blood clots on the mucosal surface
Bovine, trachea. The mucosa is hyperemic and covered by abundant mucopurulent exudate.
Bovine, ileum. Peyer's patches are depressed and covered by fibrinonecrotic exudate
Diagnosis
• Rinderpest antigens can be detected with various assays including agar gel immunodiffusion (AGID) tests, counterimmunoelectrophoresis or ELISA.
• Virus isolation can be made on calf kidney monolayers. (CPE with inclusion bodies)
• Antigens can be identified in tissues by immuno-peroxidase or immunofluorescence staining.
• neutralization
• PCR
Differential Diagnosis
• Cattle
• Bovine viral diarrhoea/mucosal disease
• Malignant catarrhal fever
• Infectious bovine rhinotracheitis
• Foot and mouth disease
• Papular stomatitis
• Jembrana disease
• Vesicular stomatitis
• Contagious bovine pleuropneumonia
• Theileriosis (East Coast fever)
• Salmonellosis
• Necrobacillosis
• Paratuberculosis
• Arsenic poisoning
• Small ruminants
• Peste des petits ruminants
• Nairobi sheep disease
• Contagious caprine pleuropneumonia
• Pasteurellosis
Vaccines
• 1-Inactive Tissue Culture Vaccine: 75% Chloroform or 1% Formol is added to the infected tissue culture and inactivated. Immunization time is 8-10 months.
• 2-Kaprinize Live Vaccines: Vaccine strains are weakened by making about 600 passages in goats. The vaccine strain is lyophilized goat milk. Provides immunity for 6 months. Not used in calves. Used in other animals over 2 years old.
• 3-Lapinize Live Vaccines: Virus is passaged and weakened in rabbits.
Blood of the rabbit, mesenterial lymph glands and spleen are used as
vaccine material. Immune for 1 year.
• 4-Avianize Live Vaccines; the virus is inoculated in the egg yolk of the embryonic egg and all of the eggs are used as the vaccine material. It is not an effective vaccine.
• 5- Tissue Culture Vaccine; Live vaccine. calf In the Kidney Cell, 100
times passaged Kabete-O is used. Immune for 2 years.
• The most commonly used vaccine is the cell-culture-adapted
vaccines. This is a safe vaccine for many species and produces life- long immunity in cattle (animals challenge-inoculated 7 years after vaccination were protected).
• Colostral immunity interferes with vaccination
• Vaccinate calves annually for 3 years
• Heat stability of vaccine an issue
Kaynaklar
• http://www.oie.int/fileadmin/Home/eng/Media_Center/docs/pdf/Di sease_cards/RINDERPEST-EN.pdf
• http://www.oie.int/fileadmin/Home/eng/Animal_Health_in_the_Worl d/docs/pdf/Disease_cards/RINDERPEST.pdf
• http://www.fao.org/docrep/004/X2720E/X2720E02.htm
• http://www.cfsph.iastate.edu/Factsheets/pdfs/rinderpest.pdf
PESTE DES PETİT RUMİNANT (PPR)
Ovine Rinderpest, Pseudorinderpest
• Peste des petits ruminants (PPR) is a highly contagious viral disease that mainly affects sheep and goats.
• Major losses can be seen, especially in goats, with morbidity and mortality rates sometimes approaching 80-100%.
NOTIFABLE DISEASE
Etiology
• Paramyxoviridae --- Morbillivirus
• It is the same as the etiology of the Rinderpest
• Among domesticated animals, peste des petits ruminants is primarily a disease of goats and sheep. PPRV has also been implicated, either alone or with other pathogens, in a few outbreaks in camels and
water buffalo.
Transmission
• Transmission of PPRV mainly occurs during close contact.
• Inhalation is thought to be an important route.
• This virus can be shed during the incubation period, and has been found in nasal and ocular secretions, saliva, urine and feces. It probably occurs in milk.
• PPRV is relatively fragile in the environment, and
long distance aerosol transmission is unlikely; in cool temperatures and in the dark, this virus has been
shown to spread for approximately 10 meters.
Clinical Signs
• The incubation period can range from 2 to 10 days; in most cases, clinical signs appear in 3-6 days.
• The severity of the clinical signs can vary with the animal’s species, breed and immunity to PPRV. Immunosuppression caused by this
virus can exacerbate concurrent infections, contributing to the clinical
signs.
Acute form
• Sudden rise in body temperature (40–41°C) with effects on the general conditon: animals become depressed or restless, anorexic and a dry muzzle develops and pyrexia may last for 3–5 days
• Serous nasal discharge becoming mucopurulent and resulting in a
profuse catarrhal exudate which crusts over and occludes the nostrils;
signs of respiratory distress in surviving animals, mucopurulent discharge may persist for up to 14 days
• Within 4 days of onset of fever, gums become hyperaemic, and erosive lesions develop in the oral cavity with excessive salivation, necrotic
stomatitis with halitosis is common, erosions may resolve or coalesce
• Small areas of necrosis on the visible mucous membranes
Typical mucopurulent nasal discharge in peste des petits
ruminants in a goat. Vaccines against peste des petits ruminants virus July 2010 DOI: 10.1586/erv.10.74
• Congestion of conjunctiva, crusting on the medial canthus and sometimes profuse catarrhal conjunctivitis
• Severe, watery, blood-stained diarrhoea is common in later stages
• Bronchopneumonia evidenced by coughing is a common feature;
abdominal breathing
• Abortions may occur
• Dehydration, emaciation, dyspnoea, hypothermia and death may occur within 5–10 days
• Survivors undergo long convalescence
Peracute form
• Frequent in goats; especially situations of inmuno-naïve introductions into instances of circulating PPRV
• High fever, depression and death
• Higher mortality Subacute form
• Frequent in some areas because of local breed susceptibility; form commonly seen in experimentally infected animals
• Usually 10–15 days development with inconsistent signs; on or about 6th day post-infection, fever and serous nasal discharge is observed
• Fever falls with onset of diarhea and, if this is severe, may result in
dehydration and prostration
Pathology
• The postmortem lesions are characterized by inflammatory and necrotic lesions in the oral cavity and throughout the gastrointestinal tract.
• The respiratory tract is also affected in many cases.
• The carcass is often emaciated and/or dehydrated, and there may be
evidence of diarrhea, serous or mucopurulent oculonasal discharges, crusted scabs on the lips, and necrotic stomatitis.
• Erosions in the mouth, and sometimes in the pharynx and upper esophagus.
• Similar lesions may be detected on the vulva and vaginal mucous membranes of some animals.
• Erosions are common in the abomasum, but the rumen, reticulum and
omasum are not significantly involved
• The most severe lesions are seen in the large intestine, particularly around the ileocecal valve, at the cecocolic junction and in the
rectum. “Zebra stripes” or “tiger stripes” of congestion, hemorrhage
or darkened tissue are sometimes found in the posterior part of the
colon on the mucosal folds
Diagnosis
• The disease may be suspected when there is sudden onset of fever, nasal discharges, diarrhea in sheep and goats, while cattle are
uninvolved.
• PPRV, its nucleic acids or antigens can be detected in
• whole blood,
• swabs of ocular and nasal discharges and/or
• swabs of buccal and rectal mucosa.
• At present, PPRV is usually isolated in African green monkey kidney
(Vero) cells, although other cell lines have also been employed.
• ELISA (ICE),
• counter immunoelectrophoresis (CIEP)
• agar gel immunodiffusion (AGID).
• RT-PCR
• virus neutralization
• ELISA assays.
Antigenic
Serologic
Differential Diagnosis
• Bluetongue
• Contagious ecthyma
• Foot and mouth disease
• Heartwater
• Coccidiosis
• Mineral poisoning
• Contagious caprine pleuropneumonia
• Pasteurellosis
• Rinderpest
Prevention and Control
• In regions where peste des petits ruminants is not endemic, it can be eradicated with a
combination of quarantines, movement controls, euthanasia of infected and exposed animals, and cleaning and disinfection of infected premises.
• Vaccination of high-risk populations may also be
helpful.
Vaccination
• In an outbreak, ring vaccination and/or vaccination of high-risk populations can be helpful
• Endemic areas
• Used to control disease
• Vaccine types
• Attenuated rinderpest vaccine, previously
• Homologous, attenuated PPR vaccine
• Recombinant vaccine (recombinant capripox-based PPR vaccine)
• http://www.cfsph.iastate.edu/Factsheets/pdfs/peste_des_petits_rumi nants.pdf
• http://www.oie.int/doc/ged/D13983.PDF
• http://www.oie.int/fileadmin/Home/eng/Animal_Health_in_the_Wor
ld/docs/pdf/Disease_cards/PESTE_DES_PETITS_RUMINANTS.pdf
DISTEMPER VIRUS (CDV)
• Canine distemper is a highly contagious, systemic, viral disease of dogs seen worldwide.
• Prior to vaccination this was the major pathogen of dogs and puppies.
• Clinically, it is characterized by a diphasic fever, leukopenia, GI and respiratory catarrh, and frequently pneumonic and neurologic
complications. Its epidemiology is complicated by the large number of species susceptible to infection.
• Dogs, ferrets, seals, lions and mink are susceptible to the virus.
Etiology
• Paramyxoviridae - Morbillivirus
• RNA
• enveloped
• Sensitive to Ether and Chloroform
• HA
• It is in close antigenic relationship with all other morbilliviruses.
(rinderpest and measles)
• It is serologically uniform.
• As a experimental animal Dog puppies and minks are used.
• Virus could be inoculated CAM of ECE.
• As a tissue culture, Vero, MDCK and Dog Kidney Cell cultures are used and virus forms CPE and a Giant Cell.
• For disinfection, 2% NaOH, 0.01% Formol and 1% Lysol are used
Transmission
• the disease is seen in
• Canidae (dog, fox, wolf, raccoon dog), Mustelidae (ferret, mink, skunk, wolverine, marten,
badger, otter), most Procyonidae (raccoon, coatimundi), some Viveridae (binturong, palm civet), Ailuridae (red panda), Ursidae (bear), Elephantidae (Asian elephant), primates (Japanese
monkey), and large Felidae. Domestic dogs (including feral populations) are considered to be the reservoir species in most, if not all, locations.
• The main route of infection is via aerosol droplet secretions from
infected animals. Some infected dogs may shed virus for several months.
• Directly,
• nasal discharge, tear flow, saliva, contact with urine and stool and spread through the droplet.
• Indirectly,
• it is transmitted through infected feed and infected material.
Which animals are at risk?
• 3-6 month olds.
• Mixed races,
• It has been determined that the Greyhounds are the most sensitive race (race predisposition).
• Unvaccinated or improperly vaccinated animals,
• Immunosupressed animals (individuals with T-cell deficiency),
• Animals that contact the infected dog.
Pathogenesis
• Virus initially replicates in the lymphatic tissue of the respiratory tract.
• A cell-associated viremia results in
infection of all lymphatic tissues, which is followed by infection of respiratory, GI, and urogenital epithelium, as well as the CNS and optic nerves.
• Disease follows virus replication in these
tissues.
1, CDV enters the respiratory tract via aerosols and
colonizes the local lymphoid tissues such as the tonsils.
2, Primary viral replication occurs in the tonsils,
retropharyngeal nodes, bronchial lymph nodes, and GI lymphoid tissue.
3, From these sites of primary replication, macrophages containing CDV enter lymphatics traveling back to the heart, where they enter the blood as a mononuclear cell- associated viremia.
4, Virus enters the CNS via the cerebral circulation. There it is deposited in the perivascular spaces of fine blood
vessels.
5, Alternatively, virus enters the vessels of the choroid plexus and eventually the cerebrospinal fluid and
ventricular system.
6, As an uncommon phenomenon in dogs, CDV can travel from the nasal passage, through the cribiform plate and anterograde via the olfactory nerve to the olfactory bulb and CNS. There it localizes, predominantly in the pyriform lobes of the cerebral cortex
.(A, B, and D Art by Kip Carter © 2010 University of Georgia Research Foundation Inc.)
The degree of viremia and extent of viral spread to various tissues is
moderated by the level of specific humoral immunity in the host during the viremic period.
Mortality is variable (average 20%) according to the virulence of the strain; some cases may be subclinical.
However CNS involvement often causes >90% mortality.
The inclusion body in the epithelial cells is pathognomic!
Pathogenesis
Stages
• Infection of the alveolar macrophages or orpharynx .
• Viraemia and virus infection of macrophages and dendritic cells. .
• Spread to most epithelial tissues and skin.
• Opportunistic bacteria cause pyogenic discharges and diarrhoea.
• Hyperkeratosis of the pads (hardpad) and nose, skin rash.
• Late infection of neurones. Demyelination. Incoordination or muscle tremors which may progress to paralysis and coma or to convulsions.
• Death. Recovered animals may have a persistent or spasmodic chorea.
Clinical Signs
• Systemic Disease:
• It usually starts with cold-like symptoms from following 8 to 14 days of the introduction of the agent. In affected animals according to the order of
occurrence frequency; pneumonia, conjunctivitis, dark nasal discharge, diarrhea, coughing and vomiting could be seen. Other findings, lethargy, enlarged lymph glands, weight loss, loss of appetite.
• Systemic disease can sometimes be followed by other forms of disease;
- CNS Disease
- Ocular Disease
- Skin Disease
- Fetal disease
Clinical Signs
CNS Disease;
• CNS signs include circling, head tilt, nystagmus, paresis to paralysis, and focal to generalized seizures.
• Localized involuntary twitching of a muscle or group of muscles (myoclonus, chorea, flexor spasm, hyperkinesia) and convulsions
characterized by salivation and, often, chewing movements of the jaw (“chewing-gum fits”) are considered classic neurologic signs.
• Emerging viral strains may be associated with greater neurotropism;
increased morbidity and mortality from neurologic complications has
been observed.
• These symptoms may continue until day 21 after systemic disease. The disease is progressive and if worsens the prognosis is not good.
• IMPORTANT 30% of CNS disease occurs without systemic symptoms.
head tilt spasms
