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106 Cards in this Set

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  • Back
What is the virus that causes Foot and Mouth Disease (FMD) and name the family of viruses?
Aphthovirus and it is apart of the family of Picornaviridae
What are the clinical signs associated with FMD?
pyrexia, anorexia, lamness, excessive salivation, vesicles on the mucosal membranes and coronary bands, bruxisim, stomping, lip smacking, chronic mastitis
What species are susceptible to FMD?
ALL cloven hooved animals!
FYI: Equine do not get FMD, but humans can (40 cases since 1921)
How is FMD transmitted?
The most prevalent route is aersolsilization of the virus; however can also be spread by indirect or direct contact via fomites; ingestion of contaminated animal products (meat, bone, milk, cheese); contaminated hormones
What are the different types of hosts with FMD?
Pigs- amplifying hosts (large amounts of virus)
sheep and goats- maintenance hosts (mild clincal signs)
cows- indicators (first to show clinical signs of disease, most severe clinical signs)
Is there a vaccine for FMD and if so what is the clinical implication of?
Cows that have been vacinated or have recovered can become healthy carriers of the disease for upto 6-24 months.
The vaccine must match the type of virus and be as close as possible to the subtype.
no universal vaccine
How many serovars are there for FMDV?
There are 7 serovars and over 60 subtypes.
What are the serovars of FMD?
A, O, C, Asia 1, SAT1, SAT2, SAT3
(Southern African Territories)
How do you diagnose FMD?
clinical signs, labratory testing (ELISA, Complement Fixation, Viral Isolation)
How is FMD eradicated and controlled?
Controlled via vaccination, test and slaughter, disinfection (sodium hydroxide, sodium carbonate, citric acid, virkon-S), vaccination around the border to provide a buffer zone, large scale vaccination and with or without slaughter; stop movement, destroy carcasses, disinfect vehicles leaving the area, educate.
What are the post-mortem lesions assoicated with FMD?
single or multiple vesicles/bullae from 2mm to 10cm in diameter. Once vesicles rupture, red, eroded areas of ulcers will be noted, may be covered with a gray fibrinous coating, loss of vesiclular fluid through the epidermis may lead to "dry" lesions (appear necrotic), coronitis may be seen on the hooves and pigs may slough their claws in severe cases, gray or yellow streaking on myocardium (tigger heart)
what is the morbidity and mortality of FMD?
morbidity 100%
mortality 1-40% (higher in young or outbreak situations)
What serotype historically has been associated with Eruope?
A, O, and C
What serotype is associated with South America?
A, O, and C
At pH is FMD inactivated?
pH below 6.5 or above 11.
How is FMD introduced into a free area?
direct/indirect contact, spread of aerosol from infected animals (requires proper humidity and temperature), bulk milk trucks, humans, contaminated garbage feed as food (meat, milk, blood, glands, bones, cheese, etc.), contaminated objects (hands, footwear, clothing), artificial insemination, and contaminated biologicals such as hormones
Why are pigs considered amplifying hosts FMD?
Because they shed 30 to 100 more times virus in aerosals than sheep or cattle.
Why do cattle show clinical signs first with FMD?
It is theorized that they are exposed to much more virus due to higher pulmonary tidal volume
What is the incubation period for FMD?
after experimental exposure: signs may develop as early as 12 hours but usually interval is 24 to 48 hours.
susceptible animals in contact with infected animals: develop in about 3 to 5 days
Pigs fed garbage (cuts in their oral cavity) develop clinical signs in 1-3 days.
What marks the peak transmission time of FMD?
Rupture of the vesicles. Can occur with in hours to 1-2 days.
What are the common sequelae of FMD?
secondary infection-mouth, nose, feet
Hoof deformation
low milk products
unthriftiness- failure to gain weight
breeding problems
Panting- pituitary damage
Diabetes mellitus
What samples should be taken to test for FMD?
serum, vesicular fluid, epithelium covering a vesicle, flaps of epithelial tissue still attached, esophageal-pharyngeal (OP) fluid from convalescent cattle, sheep, or goats, NECROPSY: epithelial lesions, lymph nodes, thyroid, adrenal gland, kidney, and heart.
How long are FMD vaccines effective?
aluminum hydroxid vaccine decreases rapidly in 4-6 months; double emulsion oil vaccine can protect for upto a year
Where does aphthovirus tend to survive within the host?
lymph nodes, and bone marrow at neutral pH, but is destroyed in muscle when pH is less than 6.0, ie. after rigor mortis
How is the US protecting itself from becoming a non-free area for FMD?
Their is a temporary restriction on the importation of live ruminants and swine and their products from all European Union member states (all infected areas as well). Prohibition of agricultural products or other items that could harbor FMDV, vigilant border checks (luggage, packages, disinfecting planes (airforce etc) public education campaigns, signs at airports, industry alerts to livestock owners and veterinarians.
What are the two other major vesicular diseases that presents as FMD?
vesicular stomatitis (can affect horses), swine vesicular disease (only affects pigs)
What are the differential diagnoses that present similiar to FMD?
Vesicular stomatitis, swine vesicular disease, fot rot, BVDV, Malignant Catarrhal fever, rinderpest in cattle, bluetounge, parapox-virus, peste des petitis ruminants and bovine herpes mammilitis, IBR, bovine papular stomatitis
What type of virus is aphthovirus?
it is a single-stranded positive sense RNA virus
What is the only two viruses within the genus aphthovirus?
equine rhinitis
foot and mouth disease
What are the only two countries that are not considered enzootic for FMD?
North America, and Australia
What are the main differences of FMDV and the other picornaviridae viruses?
the lack of a surface canyon, or pit, which has been shown to be the receptor binding site for the entero- and cardioviruses.
FMDV capsid is dissociated at pHs below 6.5; the reason is thought to be due to cluster of His residues at the interface between VP2 and VP3 which become protonated at low pH, weakening the capsid through electrostatic repulsion, leads to differences in the mechanism of its uncoating upon infection and probably plays a role in the targeting of the virus to specific tissues and organs in susceptible hosts.
What is the coreceptor used by type O subspecies 1 (FMDV)?
utilizes the glycosaminoglycan heparan sulfate (HS) as a coreceptor.
What is the cellular recognition site of FMD VP1 and shown to be apart of which family?
tripeptide (Arg-Gly-Asp) referred to as RGD, fibronectin receptor in the large family of transmembrane glycoprotein receptors.
What are transmembrane glycoprotein receptors?
aka integrins, type 1 membrane glycoproteins, consisting of two subunits (alpha and beta) which are noncovalently bound at the cell surface.
What are integrins (transmembrane glycoprotein receptors) involved in?
cell adhesion, cell migration, thrombosis, and lyphocyte interactions.
where does synthesis of RNA virus occur in regards to FMDV?
membranous replication complex; which is derived from membranes of the endoplasmic reticulum and golig and contains viral NS proteins encoded by both the P2 and P3 regions.
During the viral replication cycle of FMDV elicits a certain immune response that than can be differentiated from an animal exposed with the vaccine?
proteases and RNA polymerases expressed during the viral replicative cycle
How is FMDV distinguished from other picornaviruses?
by the lack of a surface canyon, or pit, which has been shown to be the receptor binding site for the entero- and cardioviruses
What is the reason that FMDV dissociates at a pH of less than 6.5?
It is believed to be do to a cluster of His residues at the interface between VP2 and VP3 which become protonated at low pH, weakening the capsid through electrostatic repulsion
What is the receptor that type O virus (FMD) utilizes?
glycosaminoglycan heparan sulfate (HS) as a coreceptor
What type of immune response is elicited by FMDV?
humoral response, and is apparent within 7-14 days with IgG1 being more prevelant than IgG2 in cattle; macrophages may play a role in clearing virus, may also be neutralization
What will be seen in most cases of FMDV in regards to the CBC?
lymphopenia two days post infection involving CD4+, CD8+, CD4+/CD8+ T cells and does not appear to be related to infection or apoptosis but may be due to lymphocyte trafficking (T cells play a protective role for the virus and the reduction of both T cell numbers and function enhances viral pathogenesis by allowing the virus to spread wihtin the host, which equals increased numbers being shed)
What interleukins are responsible for the activation of macrophages?
IL-6, IL-8, IL-12
What is the family and genus of Rinderpest (cattle plaque)?
paramyxoviridae; morbillivirus
there is only one known stran of RPV
What are the clinical signs assoicated with Rinderpest?
sudden onset of fever, depression, and anorexia, nose is dry and mm are congested, oral erosions appear where necrotic foci have sloughed purulent lacrimation occurs , diarrhea is severe and maybe bloody, dehydration and emaciation often lead to death
What are the primary differential diagnoses for rinderpest?
BVDV, MCF, arsenic poisoning, severe coccidiosis, and severe fulminating IBR, vesicular stomatitis
How is rinderpest diagnosed?
virus isolation is most successful in the first days of infection (often before onset of diarrhea); blood should be taken in heparin, the lymph nodes and spleen are reliable sources of virus and in cattle tears and ocular discharges are also reliable sources, lymph node biopsy after day 3 of infection is the most reliable means of diagnosis in living goats.
What is the pathophysiology of rinderpest?
enters through the respiratory mucosa, lymphoid tissue is the primary target of the rinderpest virus, lymphocytes are destroyed in the germinal centers of the lymph node, Peyer's patches, tonsils, splenic corpuscles, and cecal lymphoid tissue, immunosuppression occurs as lymphoid tissue is destroyed, virus also attacks the alimentary tract mucosa, due to loss of mucosa results in diarrhea and emaciation
How is rinderpest prevented or controlled?
only one known strain of PRV and protection after infection usually is lifelong, vaccination of cattle in endemic areas with a live cell culture attenuated virus is an effective means of controlling RP
What type of virus is a morbillivurs (characteristics)?
single-stranded RNA
How is rinderpest transmitted?
transmission is through direct or close indirect contact with infected animals. The virus is shed in nasal and ocular secretions and feces. The most infectious period is from 1-2 days prior to the onset of clinical signs, to 8-9 days after the clinical signs are apparent
What is the incubation period of rinderpest?
3 to 15 days; 4 to 5 days is typical. Virulence, dosage, and route of exposure all affect the incubation period
What are the post-mortem lesions seen with rinderpest?
oral lesions that initially appear as small necrotic foci, which then slough leaving red erosions. These lesions may be present on the gums, lips, hard and soft palate, cheeks, and base of the tongue. Congestion, hemorrhage, and edema can extend into the GI and URT. "Tiger" or "Zebra" striping is often seen in the large intestines due to congestion in the colonic mucosal ridges probably caused by tenesmus. Peyer's patches have necrotic foci, and lymph nodes may be enlarged and edematous. the carcass will most likely be emaciated and dehydrated.
What is the morbitity and mortality of rinderpest?
morbidity rate for rinderpest is high, and mortality rate can be high with virulent strains but varies with milder strains
What is the etiologic agent that is responsible for malignant catarrhal fever?
infection by either of two gamma herpesviruses, alcelaphine herpesvirus-1 (AHV-1), and ovine herpesvirus-2.
What species and what area is OHV-2 found and AVH-1
AHV-1 is carried asymptomatically by wildebeest, and causes MCF in Africa and in zoos throughout the world.
OHV-2 is carried by sheep and causes the disease in most of the world, has not yet been isolated; evidence for its existence is still indirect.
What species are effected by MCF?
wildebeest, wild ruminants in Africa, sheep and goats, Bovinae family, deer
(Bos taurus and Bos indicus are relatively resistant to this infection)
What is the incubation period of MCF?
natural incubation is unknown; experimental is between 9-77 days
What are the clinical signs of malignant catarrhal fever?
wide variety of signs can be seen: sudden death, depression, diarrhea and dysentery, DIC, dyspnea, fever, inappetence, bilateral corneal opoacity, serous discharges from eyes and nose which later become mucopurulent, oral mucosa is hyperemic, open mouth breathing and salivation, skin sometimes ulcerated and hardened scabs may develop on perineum, udder, and teats, horn and hoof coverings may be sloughed, constipation is common, neverous signs etc.
What are the post-moretm lesions found with MCF?
causes epithelial necrosis in the GI, respiratory, and urinary tracts, lymphoproliferation, interstitial infiltration of nonlymphoid tissues by lymphoid cells, and vasculitits.dehydrated, emaciated or normal depending on the severity and type. Muzzle is usually raw, and encrusted, with a serous, mucopurulent, or purulent nasal discharge,hyperemia, edema and small focal erosions may be found on the nasal mucosa,lymph nodes are usually large and edematous,etc...
What is the mortality and morbididty of MCF?
90-100% mortality rate but those that due survive remain carriers, sporadic infections occur (no vaccine) morbidity can be from 28-45%
What are the differential diagnosis assoicated with MCF?
BVD mucosal disease, bluetongue, rinderpest, IBR, vesicular diseases such as foot and mouth disease and vesicular stomatitis, ingestion of caustic materials, and some poisonous plants and mycotoxins
What are the laboratory tests used to diagnose MCF?
PCR, histopathologic demonstration of multisystem lyphoid infiltration, disseminated vasculitits, and degenerative epithelial lesions; serology (ELISA, immunofluorescence, and immunocytochemistry)
What type of hosts are cattled considered in regards to MCF?
What is the pathophysiology behind MCF?
The MCF virus appears to cause proliferation of cytotoxic T lymphocytes. Vasculitis observed with MCF is mediated by lymphoid cell infiltration rather than by virus or immune complexes, lymphocytes and lymphoblasts are found in all affected tissues, wehreas neutrophils and plasma cells are rare, large granular lymphocytes are a subpopulation of T cells that act as NK cells and also as T lymphocyte suppressor cells, indiscriminant killing of normal cells, MHC restriction and macrophages also appear to play a role in the pathogenesis; diagnosis is based on history of exposure, clinical signs, and gross and histologic lesions, rabbit inoculations can also be used
What is the best preventative measure for MCF?
keeping cattle away from sheep in endemic areas
What is the infectious agent is IBR?
it is caused by a herpes virus that may involve the respiratory or reproductive tracts, nervous system, or conjunctiva or may cause wide-spread systemic disease
What are the clinical signs associated with IBR?
conjunctivitis, excessive lacrimation (serous that results in mucopurulent), blepharospasm, URT infections including rhinitis, and dyspnea, pyrexic, and fall in milk yeild, abortion
How is IBR diagnosed?
PCR, viral isolation in cell cultures
What is the pathophysiology of IBR?
results in lymphoid hyperplasia, visible as white plaque (plasma cells and lymphocytes in the conjunctival stroma and may occur histologically); diphthertic membranes develop on the conjunctival surface secondary to conjunctival necrosis
What is the prevention and control of IBR?
vaccination of susceptible animals is the most effective means to prevent and control the disease. there is five types of IBR vaccines.
What is the etiologic agent that causes BVDV?
pestivirus; it is apart of the togaviruses
What is the etiology of bluetongue virus and epizootic hemorrhagic disease?
arthropodborne viral disease, prototypical orbivirus, a genus (or subfamily) within the family Reoviridae (double stranded RNA),
What are the clinical signs of BTV?
reproductive syndromes and bluetongue per se a vasculitic disease of several organ systems; cattle and goats rarely manifest clinical disease; infected sheep commonly do
lamenss and stiffness caused by coronitis and myopathy, diarrhea, early embryonic wastage, excessive salivation, hyperemia and necrosis of the muzzle and a patchy dermatitis, (in sheep oral lesions and ulcers, pulmonary edema)
What is the pathophysiology of BTV?
capable of reproducing in a variety of mammalian cells; in clinical cases the disease appears to be a vasculitis caused by infection of vascular endothelial cells
vasculitis resultls in edema and necrosis of epithelial and mucosal surfaces, cattle may require prior sensitization to the virus, operating through IgE mediated hypersensitivity reaction
What is the host range of EHD and BTV?
BTV: sheep are fully susceptible, all ruminant species but variable expression of clinical disease
EHD: most ruminant species; sheep are poor hosts
What is the biological vector of EHD and BTV?
Culicoides speces (TICK)
What is the incubation period of BTV and EHDV?
BT: sheep usually 7-10 days, however may appear as early as 3-4 days, cattle as early as 4 days postinfection but clinical signs are uncommon.
No information is available on incubation periods for EHDV
What are the clinical signs of BTV in cattle?
usually does not cause any clinical signs
subclinical disease evidenced by leukocyte and lymphocyte subpopulation counts in the peripheral blood and a mild acute eosinophilic dermatitis. pyrexia that is consistent in fluctations of temperature, hyperemia in the buccal cavity and around the cornonary band; vesicular lesions, which lead to ulcerations in the buccal mucosa; errect hair over the cervical and dorsal thoracic areas, similar lesions on the teats of cows, lamness, reproductive failure, fetal death
What are the clinical signs of EHDV in cattle?
rarely causes disease in cattle, however lbaraki virus (an EHDV serotype) has been associated with sporadic outbreaks of severe disease in cattle in Japan. fever, erosive and ulcerative lesions of the oral and esophageal mucosa, stiffness, lameness, and thickened, edematous skin.
What is the etiologic agent associated with vesicular stomatitis?
virus: family Rhabdoviridae; genus Vesiculovirus
large bullet shaped RNA virus
What are three top differentials for vesicular stomatitis?
FMD, swine vesicular disease, and vesicular exanthema
What are the species affected by vesicular stomatitits?
horses, donkeys, mules, cattle, swine, camelids, and humans
sheep and goats are relatively resistant
What is the transmission of Vesicular stomatitis?
incompletely understood; thought to be transmitted via insect vectors, particularly sand flies (Lutzomyia shannoni) and blackflies (family Simuliidae), mosquitoes
once introduced into the herd: direct contact, exposure to fomites with saliva or fluid from ruptured vesicles
humans: contact with vesicular fluid or saliva from infected animals; aerosol transmission in labs, some may be through insect bites
What is the incubation period of vesicular stomatitis?
incubation period is 2 to 8 days; most often, animals become symptomatic in 3 to 5 days
occassionally vesicles develop within 24 hours
incubation period in humans is usually 3 to 4 days, but can be as short as 24 hours or as long as 6 days
What are the clinical sings of vesicular stomatitis?
excessive salivation is often the first symptom
characteristic lesions: blanched, raised vesicles (blisters) that may be found on the lips, nostrils, hooves or teats, and in the mouth
cattle: vesicles are located on the hard palate, lips and gums, and may extend to the nostrils and muzzle; hooves secondary lesions;vesicles eventually result in painful ulcers and erosions can cause anorexia
What are the postmortem lesions of vesicular stomatitis?
necropsy lesions are similar to those in live animals, and may include vesicles, ulcers, erosions, and crusting on the
lips, nostrils, hooves, or teats, and in the mouth;
heart and rumen lesions, which may be seen in foot and mouth diseae, do not occur in cases of vesicular stomatitis
What is the morbidity and mortality of vesicular stomatitis?
morbidity rate is highly variable from 5-90%
mortality: is very low, death is rare in cattle and horses, but higher rates have been seen in some pigs
What are the two serotypes of vesicular stomatitis?
New Jersey and Indiana
What are the main differences between FMD and vesicular stomatitis?
characteristics of VS: horses are affected, sporadic incidence in the herd, distribution of lesions in an animal (small percent have lesions at more than one site of predilection), no rumen lesions, no heart lesions, less severe in young animals, stabled animals usually no affected
What is the clinical sign associated with vesicular stomatitis in man?
frequently occurs and causes influenza-like symptoms but rarely results in vesicles
other vesicular viruses are much more infectious for man (Piry, Isfahan, and Chandipura)
What is vesicular exanthema of swine?
It is an acute febrile disease of swine caused by caliciviruses and characterized by fever and vesicles with subsequent erosions in the mouth and on the snout, feet and teats
What is the etiolgoy of VES?
calicivirus, and has 13 serotypes
closely related to 14 other serotypes of calicivirus found in the San Miquel sea lion virus group
What is the host range of VES?
ONLY pigs
What is the geographical distribution of VES?
Only in the US but has been eradicated
How is VES transmitted?
rapid pig-to-pig spread, and spread from feeding infected pork scraps in uncooked garbage
What is the incubation period for VES?
after natural exposure is 18 to 72 hours
What are the clinical signs of VES?
very similar to FMD, and other vesicular diseases
fever, vesicles in the mouth, on the snout, feet and lameness
Lesions of VES seem to be deeper than FMD and granulation tissue commonly forms especially on the feet
What is the morbidity and mortality rate of VES?
Morbidity is high near 100%, mortality is low
What is the etiology of swine vesicular disease?
porcine enterovirus in the family picornaviridae
What are the affected species of SVD?
pigs are the only species that are naturally infected
humans have been infected while working in a laboratory setting
baby mice can be experimentally infected
What is the transmission of SVD?
transmission occurs via contaminated meat scraps and contact with infected animals or their feces
pigs can excrete the virus from the nose, mouth, and in feces up to 48 hours before clincial signs are seen
What is the incubation period of SVD?
2-7 days following exposure to infected pigs and 2-3 days after the ingestion of contaminated feed
What are the clinical signs associated with SVD?
very similar to FMD and include fever, salivation and lameness
vesciles and erosions can be seen on the snout, mammary glands, coronary band, and interdigital areas
vesicles in oral cavity are rare
What are the post-mortem lesions of SVD?
only post mortem lesions are the vesicles seen in live pigs
What is the morbidity and mortality rates of SVD?
morbidity is lower than FMD and mortality is not a concern