Infectious diseases cram Flashcards
Category A
The U.S. public health system and primary healthcare providers must be prepared to address various biological agents, including pathogens that are rarely seen in the United States. High-priority agents include organisms that pose a risk to national security because they
can be easily disseminated or transmitted from person to person;
result in high mortality rates and have the potential for major public health impact;
might cause public panic and social disruption; and
require special action for public health preparedness.
Agents/Diseases Anthrax (Bacillus anthracis) Botulism (Clostridium botulinum toxin) Plague (Yersinia pestis) Smallpox (variola major) Tularemia (Francisella tularensis) Viral hemorrhagic fevers (filoviruses [e.g., Ebola, Marburg] and arenaviruses [e.g., Lassa, Machupo])
Category B
Second highest priority agents include those that
are moderately easy to disseminate;
result in moderate morbidity rates and low mortality rates; and
require specific enhancements of CDC’s diagnostic capacity and enhanced disease surveillance.
Agents/Diseases
Brucellosis (Brucella species)
Epsilon toxin of Clostridium perfringens
Food safety threats (e.g., Salmonella species, Escherichia coli O157:H7, Shigella)
Glanders (Burkholderia mallei)
Melioidosis (Burkholderia pseudomallei)
Psittacosis (Chlamydia psittaci)
Q fever (Coxiella burnetii)
Ricin toxin from Ricinus communis (castor beans)
Staphylococcal enterotoxin B
Typhus fever (Rickettsia prowazekii)
Viral encephalitis (alphaviruses [e.g., Venezuelan equine encephalitis, eastern equine encephalitis, western equine encephalitis])
Water safety threats (e.g., Vibrio cholerae, Cryptosporidium parvum)
Category C
Third highest priority agents include emerging pathogens that could be engineered for mass dissemination in the future because of
availability;
ease of production and dissemination; and
potential for high morbidity and mortality rates and major health impact.
Agents
Emerging infectious diseases such as Nipah virus and hantavirus
Review of Transboundary Animal Diseases (AKA Foreign Animal Diseases) – Feb 2012
African Horse Sickness
infectious, not contagious insect transmitted
High mortality 70-95%
clinical signs characterized by edema of subqu, intermuscular, and lung tissue
genus Orbivirus, family Reoviridae (similar to blue tongue)
horses most susceptible, mules less so
donkeys, zebras very resistant, very important reservoir
dogs can contact fatal form if eat infected horse carcass
humans can be infected with field strains, has been reported to cause encephalitis and retinitis
transmitted biologically by midges (culicoides), not sure if US species of culicoides can transmit,
minor role of transmission by biting flies
peracute form-pulmonary, sudden respiratory death, frothy nasal discharge
Cardiac form-supraorbital edema due to heart failure
mixed form and horse sickness (mildest form, febrile, overlooked in outbreaks)
if recover life long immunity
post mortem-most suggestive clinical sign is edema around the nucal ligament (only other disease in horses that causes this is botulism)
Vaccine available,
usually introduced via a viremic asymptomatic donkey or zebra, why minimum 60 day quarantine
control-vector control (stabling, insecticides), test and slaughter, or vaccination
Akabane
infectious disease of bovine, caprine, ovine fetuses (interuterine infection)
transmitted by culicoides and mosquitoes
adults not affected clinically
arbovirus, genus Orthobunyavirus family bunyaviridae
no illness in humans
calves affected third trimester
sheep/goats 28-50 days gestation
causes still births, dummy babies, arthrogryposis, hydranencephaly, parturition problems due
to joint problems
vaccine available (inactivated and live attenuated), main way to control
Avian Flu
negative sense single strand RNA
orthomyxoviridae (16 H and 9 N)
aquatic wild species usually responsible for introduction to poultry
large amounts virus shed in feces and respiratory secretions
asymptomatic to decreased egg production/misshapen soft eggs to respiratory disease (swollen
sinuses, matted eyelids, nasal discharge to sudden death)
control best with eradication = inclusion/exclusion biosecurity; diagnostics/surveillance;
elimination of infected animals; increase host resistance; education of personnel in AI control
problems with vaccination=must match vaccine and subtype circulating; must be injected; and identification of infected animals in vaccinated population requires special procedures
http://www.aphis.usda.gov/newsroom/hot_issues/avian_influenza/avian_influenza.shtml
Babesiosis (Piroplasmosis, tick fever, redwater)
protozoan intra erthrocytic tick born parasite
characterized by intracellular hemolysis
host specific
bovine=bigemia and bovis transmitted by Boophilus ticks
equine=caballi and equi (theileria equi)
can be transmitted by veterinary instruments
clinical signs of anemia, hemoglobinuria (not horses)
control=tick control, vaccination, chemophophy, chemotherapy (imidocarb)
Blue Tongue
acute insect transmitted noncontagious disease
Orbivirus, reoviridae
transmitted by Culicoides
fever, hyperemia of mm, salivation, edema of head, foot lesions (hemorrhages at coronary bands)
the large African carnivores can be infected
post mortem lesions consistent with vascular injury
prevent/control=complicated, not contagious, transmitted by insects
vaccine for prevention of outbreaks and to control incursions of virus, but cause fetal infection and teratogenesis
Borna Virus
progressive menigopolioencephalitis
single stranded RNA virus
family bornaviridae
equine, cattle, goats, rabbits in Germany, Austria, Switzerland
possible cause of psychiatric disease in humans
unknown transmission, wild rodents most likely natural reservoir
low incidence
clinical signs correlate to inflammation of the brain=alterations in behavior, eating arrests with
chewing movements (pipe smoking)
immune mediate disease, no treatment, have tried amatadine sulfate
Bovine Ephemeral Fever
Non contagious arthropod borne viral disease of cattle and water buffalo
single stranded RNA virus, family Rhabdoviridae
no threat t humans
transmission by arthropods not demonstrated, but circumstantial evidence for arthropods
overwhelming (mosquitoes, culicoides)
mortality low
clinical signs progress as follows: fever = lameness, stiffness, mucoid nasal discharge,
periorbital/submandibular edema, sternal recumbancy = recovery = sequelae (abortion,
paralysis)
worse recovery in lactating cows, bulls in good shape, fat steers
if recover immune for life
vaccines available, need booster annually
treatable with anti-inflammatory meds, can also treat the hypocalcemia and dehydration
vaccination only useful preventable measure
BSE
chronic non-febrile neurodegenerative disease of CNS
- scrapie in sheep/goats; chronic wasting in elk, deer, moose; FSE cats; TME mink
- misfolded prion protein
- BSE absence of horizontal transmission (not the case with CWD)
- transmitted via contaminated feed stuffs (contain CNS material of infected animals)
- not sure if spontaneous BSE can occur
- limited involvement of Peyers Patch
- hyperreactivity and aggression
- current firewall plan: feed ban, import controls, and surveillance
Capripoxviruses
-contains sheep pox, goat pox, lumpy skin
-sheep/goats pox affect all breeds of domestic and wild sheep and goats
-clinical signs=fever, macules/papules, and necrotic lesions in skin (bovine=nodules on skin, mm, internal organs)
-orthopoxviruses
-doesn’t affect people
-aerosol transmission in close contact
-acute disease is death
-epi of sheep/goat pox similar to epi of human small pox, most transmission occurs from
severely infected individuals during stages when ulcerated papules are present (no transmission
during prepapular stage)
-lumpy skin of cows=predominantly spread by insects, mechanical transmissions
-if recover live long immunity
-vaccines available
-prevent in endemic areas by vaccine, prevention in free countries by prohibiting importation of
live sheep, goats, cattle
Contagious Agalactia
-mycoplasma agalactia
-goats more susceptible than sheep
-spreads by ingestion of feed, water, or milk contaminated with the organism
-mastitis then fibrosis, polyarthritis (especially carpus/tarsus); keratoconjunctivitis in 50%)
-vaccine available but can be shed in milk and prevents clinical disease but not
infection/shedding of virulent organism
-prevent via good sanitation and prevent introduction of infected animals
-early AB therapy prognosis is good (not if arthritis or keratoconjunctivitis)
-eradication with slaughter of all infected
Contagious Bovine Pleuropneumonia
- mycoplasma mycoides
- cattle, buffalo
- spread by inhalation of droplets from infected coughing animals
- coughing, thoracic pain, increased RR
- unilateral lung involvement
- recovered animals not susceptible to reinfection
- prevention/control=remove susceptible animals; outbreak test, slaughter, quarantine
- treatment not recommended
- vaccine available can cause sloughing reaction
Contagious Caprine Pleuropneumonia
- acute highly contagious
- mycoplasma capriolum
- principle lesion=fibrinous pleuropneumonia with massive lung consolidation
- transmitted through direct contact with infective aerosols
- clinical signs limited to respiratory tract
- early treatment is effective
- vaccines varying success
- control/prevention=import restriction, remove infected animals
Contagious Equine Metritis
Highly contagious venereal disease
Taylorella equigenitalis
susceptible to common disinfectants
clinical signs=mare short cycle, mucopurulent discharge (if carry foal they can be come carriers)
no vaccine
natural clearance, but takes several months
can cure horse with disinfectants and antibiotics
Dourine
- trypanosoma equiperdum
- transmitted by coitus in horses, donkeys, mules
- donkeys are asymptomatic carriers
- similar to syphilis
- can be intermittently infective
- mare can carry foals which are infected in utero or via infected milk
- course of the disease very long (years), usually fatal from nervous system involvement
- variable edema of genital organs
- pathognomonic clinical signs are circular cutaneous plaques (silver dollar plaques)
- nervous disorders after edema, progressive weakness, incoordination, and paralysis
- treatment not recommended, can continue to spread
- control=test and eradication
Duck Viral Hepatitis
- highly contagious, fatal disease of young ducklings (esp Peking <3 weeks old)
- characterized by liver hemorrhages
- picornavirus, RNA very resistant to physical and chemical agents
- transmitted via direct contact and oral/respiratory (no vertical egg transmission)
- mortality up to 100% in <3 week old ducklings
- spasmodic contractions of legs, head drawn backward
- if recover immune, can immunize parentally or egg yolk
- prevention/control=good biosecurity and control with immunizations
East Coast Fever
- bovine theileriosis
- tick transmitted-Rhipecephalus (3 host ticks, no transovarian transmission)
- theileria parva
- characterized by high fever and lymphadenopathy
- cattle and water buffalo affected
- reservoirs are African buffalo and waterbucks
- first clinical sign usually draining lymph node (parotid)
- treatment involves oxytetracycline and vaccines
- control with vaccines and treat with chemical acaricides
Epizootic Lymphangitis
-infectious granulomatous disease of skin, lymph vessesl, and lymph nodes of neck and legs of
Horses
-not spread animal to animal
-histoplasma capsulatium – in tissue yeast, in environment mycelia
-limited to horses, donkeys and occasionally mules
-introduced via open wounds, transmission can occur via flies
-usually initial lesion is painless, cutaneous nodule, infection spreads along lymph vessels
causing cord lesions
-can treat with IV Na Iodide, K Iodide, surgical excision
-some places treatment not permitted=euthanasia
Equine Encephalosis
- equine encephalosis virus (orbivirus, reoviridae)
- transmitted by Culicoides
- only disease of horses (zebras might be reservoir)
- can be subclinical = fever, congestion of mm, and occ neuro dysfunction
- no vaccine, no treatment
- preventing contact with Culicoides most effective
African Swine Fever
-asfivirus, double stranded DNA
-hosts are swine wild and domestic (peccaries and wart hogs are resistant, how maintained in
the environment)
-transmitted by ticks – Ornithodoros (soft ticks) and direct contact
-highly stable, resistant to heat, putrefaction, and high/low pH
-can last 15 years in frozen carcasses, 6 months in cured hams
-peracute, acute, chronic, and inapparent
-sudden death to fever, recumbancy, cyanosis of skin, vomiting, hemorrhagic enteritis, abortions
-chronic skin ulceration with necrosis, weight loss, int fever
-no vaccine no treatment
-prevention=effective trade restrictions and biosecurity
-control=tick control and sanitation (bleach)
Classical Swine Fever (AKA Hog Cholera)
-highly contagious, often fatal
-genus Pestivirus, family Flaviridae (related to BVD, Border Disease)
-enveloped so moderately fragile
-pig only natural host
-transmission most likely pig to pig and feeding infected garbage
-inapparent infected carrier sows=virus crosses the placenta resulting in immunotolerance (just
like BVD)
-acute signs= high fever, conjunctivitis, constipation then diarrhea, skin hemorrhages then
cyanosis (African Swine Fever = NO conjunctivitis)
-chronic signs=chronic diarrhea, button ulcers in cecum and colon, runted and death (can be reservoir)
-piglets=stillbirths, abortions, mummies, weak shakers, posterior ataxia or born healthy and become persistent shedders
-think classical swine fever when=high mortality with hemorrhages, some piglets show posterior ataxia, tonsilar necrosis, and conjunctivitis
-can be easily confused with common domestic swine diseases
-prevention=trade restrictions for live as well as fresh or cured pig meats
-if introduced=quarantine, slaughter with disposal of bedding too
-vaccination only if elimination doesn’t work, have to be able to distinguish vaccinated from
naturally infected (need validated marker vaccine)
Getah
Alphavirus, togaviridae
- transmitted by mosquitoes (may be some direct transmission during an outbreak)
- causes transient febrile illness in horses (swine can show clinical signs)
- characterized by fever, hindlimb edema, and popular rash
- swine are amplifying host (abortion and illness/death of newborn piglets)
- mortality rare
- killed vaccine available
- prevention/control=mosquito control and vaccination
Glanders (AKA Farcy, Malleus)
highly contagious disease of horses, mules, donkeys
- donkeys usually acute form, horses more chronic
- burkholderia mallei
- Significant Human Health Risk (ZOONOTIC)
- has been used as bioterrorism agent
- characterized by nodular lesions of lungs, nasal cavity, and skin; progressive
- can cause disease in dogs and cats that eat infected meat
- transmitted directly by diseased or latently infected animals; spread in close quarters
- horses can recover, but susceptible to recurrence
- no vaccine
- sensitive to many Abs, but due to zoonotic risk euthanasia recommended
- moderately hardy, need to burn/bury contaminated bedding/foodstuffs
Heartwater (AKA Cowdriosis)
-acute noncontagious infectious disease of cattle, sheep, goats, and some antelope species
-ehrlichia ruminatium
-transmitted by ticks – Amblyomma (transstadially and intrastadially)-can persist in the tick for
up to 15 months
-tick vectors present in US, shown experimentally capable of transmitting disease
-characterized by fever, dyspnea, nervous system signs, hydropericardium, hydrothorax, ascites,
and edema of the lungs
-experimentally causes disease in white tailed deer
-can be transmitted naturally vertically and horizontally
-if recover from natural infection immunity 6-18 months
-vaccine available, can treat with tetracycline Abs (treat enough to let some natural immunity
develop
-prevention=prevent introduction of disease carrying ticks
-risk to US = can easily be introduced on birds, imported wildlife, ticks present to transmit and
carry disease, no vaccine approved in the US
Hemorrhagic Septicemia
high mortality
-pasturella multocidea 6B and 6E (Africa and Asia)
-cattle and water buffalos susceptible
-transmission oronasal from exposure to infected animals, carrier animals, or fomites
-clinical signs respiratory distress, frothing at the mouth, recumbancy, edema of submandibular
region, head, neck, brisket
-lesions consistent with severe endotoxic shock
-if survive immune, vaccine available (best way to control)
Hendra Virus
-family paramyxoviridae (same group as Nipah virus)
-characterized by fever, increased respiratory rate, profuse nasal discharge, can cause jaundice
and neuro disease (severe pulmonary edema)
-uniformly fatal
-horses only species naturally infected
-large fruit bats (flying foxes) are reservoirs
-have been 4 cases of human illness, with 2 deaths
-virus shed in bat’s placental fluids, and also urine
-infected horses shed virus in urine, nasal/conjunctival excretions, and feces
-no vaccine available
-classified as BSL 4 virus; ZOONOTIC
-outbreaks in horses controlled by slaughter of infected horses and professional removal of bats
Infectious Salmon Anemia
IE notifiable disease
-infects Atlantic salmon (esp farmed)
-virus is orthomyxovirus
-farmed rainbows, browns can be infected, but not clinically ill
-sea run brown trout thought to be main carriers of ISAV to susceptible populations of Atlantic
Salmon
-transmitted when infected fish come in contact with susceptible salmon
-generally transmitted horizontally
-clinical signs anorexia, darkening of skin, exophthalmia, petechiation of skin
-prevention=biosecurity, health pre-screening of prospective brood and production stock,
elimination of site to site marine transfers of fish, decrease stocking densities, minimize stress,
thorough disinfection of cages between fish
-control=rapid identification of ill/diseased fish with destruction
Japanese Encephalitis
-mosquito born flavivirus
-affects horses, humans, pigs
-horses and humans neurologic disease
-pigs are amplifying host (can cause abortions)
-virus naturally circulates between mosquitoes and wild birds
-ardeid birds (herons, egrets) natural reservoir.
-ZOONOTIC
-HUMAN Disease=25% clinical cases fatal; 50% result in neurologic sequelae including
psychiatric disturbances, ataxia, and catatonia
-horses can have inapparent infections to impaired locomotion, stupor, coma, death
-if survive immunity lifelong
-vaccines available for horses and swine (not in US)
-prevention=elimination of vectors, immunization of horses and swine
Jembrana Disease
- severe acute disease of cattle
- lentivirus
- characterized by fever, lethargy, lymphadenopathy, oral erosions, diarrhea
- clinically disease only in Bali Cattle
- unknown method of transmission
- if survive immune, no vaccine
- recovered animals can carry virus for up to 2 years and be source of infection for other cattle
- control cattle movements
Louping-ill
tick born acute viral disease
-flavivirus
-transmitted by Ixodes ticks
-characterized by fever, neurologic signs, death
-HUMANS can be infected
-sheep primarily infected, but cattle, horses, pigs, goats, dogs llamas can be
-humans can be infected by tick bite, entrance through skin wound, aerosol exposure, ingestion
of contaminated milk
-humans can have flu like illness, encephalitis, poliomyelitis like or hemorrhagic fever
-in sheep infects brainstem, cerebellum=leads to characteristic clinical signs
-vaccine available, natural infection can result in carriers and only partial immunity
-control with vaccination and tick treatment
Malignant Catarrhal Fever
- fatal viral disease of ruminant species
- characterized by fever, rhinitis, depression, bilateral keratoconjunctivitis
- gammaherpesviruses in Rhadinovirus genus (4 cause disease)
- has occurred in 33 ungulate species
- major carrier species are wildebeest, sheep and goats
- wildebeests infected perinatally by horizontal and intrauterine transmission, infected for life
- transmitted mostly by direct contact with nasal and ocular secretions, mechanical vectors and contaminated water might play a role
- hallmark microscopic changes are lymphoproliferative inflammation with vasculitis
- no vaccine available
- prevent contact between carriers and clinically susceptible species best
Nairobi Sheep Disease
- noncontagious tick born viral infection of sheep and goats
- characterized by fever, hemorrhagic gastroenteritis, abortion, and high mortality
- Nairobi sheep disease virus, genus Nairovirus, family bunyaviridae (related to Crimean-Congo Hemorrhagic Fever group)
- sheep and goats natural hosts
- can infect HUMANS self limiting fever back and abdominal pain, headache, vomiting
- tick – Rhipecephalus
- recovery leads to life long immunity
- vaccines available
- control with vaccines and allow stable enzootic state with the virus to occur
Newcastle Disease
acute viral disease of poultry
-avian paramyxovirus 1 (family paramyxoviridae)
-three pathotypes: lentogenic, mesogenic, and velogenic (foreign highly fatal)
-250 species of birds can be infected with this virus
-Can infect HUMANS-usually transient conjunctivitis (ZOONOTIC)
-direct transmission with infective material including fomites (also introduced from carrier birds)
-clinical signs range from mild respiratory/decreased production to acute death and permanent
paralysis and other neuro signs
-vaccine available for low virulence strains
-prevent introduction of carriers/infected birds, biosecurity,
-control=euthanasia, vaccination
Nipah Virus (AKA Barking Pig Syndrome)
-paramyxovirus (newly emerged from Malaysia)
-acute febrile respiratory and or neurologic disease of pigs
-ZOONOTIC
-high fatality in HUMANS (40-75%)
-pigs are amplifying hosts, main source for human infections
-fruit bats (flying foxes) are natural reservoir
-pigs infected from direct contact with bat fluids or tissues, pigs transmit to humans by aerosols
and direct contact with pig secretions
-pigs have fever, cough, and occasionally neuro signs
-no commercial vaccine exists (some experimental ones)
-prevent by keeping bats out of pig rearing systems
-control by mass culling
Peste Des Petits Ruminants
-acute or subacute contagious viral disease of goats and sheep
-characterized by fever, conjunctivitis, erosive stomatitis, gastroenteritis, and pneumonia
-paramyoxoviridae, genus morillivirus (related to canine distemper, rinderpest, measles)
direct transmission from close contact with ocular, nasal, oral secretions and feces, aerosol
transmission too
-no known carrier state
-recovered immune for up to 4 years
-vaccine available (cant distinguish between naturally infected and vaccinated)
-no specific treatment, control secondary bacterial complications
-eradication best if introduced to new area
Rabbit Hemorrhagic Disease
- peracute to acute viral disease of the European rabbit only
- characterized by extensive hepatic necrosis and DIC
- calicivirus
- wild rabbits of Oryctolagus genus are susceptible
- transmission by direct contact with infected animals or indirectly by fomites
- most prominent clinical sign is sudden death after fever
- can have neurologic signs and terminal foamy nasal discharge
- vaccine is available
- prevention of introduction of disease best
Rift Valley Fever
peracute or acute arthropod born viral disease
-characterized by epidemic hepatitis of ruminants
-ZOONOTIC
-HUMANS infected after bite of an infected mosquito or contact with infected animal, causes
acute influenza illness, minority of patients develop ocular lesions, encephalitis or hepatic disease
-family of bunyaviridae, phlebovirus genus
-sheep, goats, cattle, camels all susceptible
-biologic vectors are mosquitoes
-mechanical vectors are biting flies
-lambs, kids under 2 weeks die within 24-96 hours
-can cause abortion storms at any stage of gestation (fetuses autolyzed)
-vaccine available
-control difficult due to sporadic long inter-epizootic periods in endemic countries
-control=restrict movement with trade; vector control; vaccination
Rinderpest
-contagious viral disease of cattle, buffalo, and some wildlife
-characterized by fever, oral erosions, diarrhea, lymphoid necrosis, and high mortality in
susceptible populations
-family paramyoxoviridae, genus morbillivirus (peste des petites, human measles, canine distemper)
-direct transmission with nasal-ocular secretions, indirect fomites (aerosol not sign)
-recovered and vaccinated animals immune for life
-eradicated!!!
Spring Viremia of Carp
-viral disease of coolwater and warmwater finfish
-caused by rhabdovirus
-goldfish, carp
-horizontal transmission shed by infected/diseased fish
-clinical signs exophthalmia, edema, inflammation and hemorrhages of swim bladder, ascites,
and petechial hemorrhages of gills
-no vaccine exists
-prevention with enhanced treatment of water supplies by UV or sand filtration systems and
health status prescreening of fish
-eradication with outbreak
Swine Vesicular Disease
- contagious viral disease of pigs
- enterovirus family picornaviridae
- characterized by fever, vesicular lesions, and subsequent erosions
- HUMANS infected in laboratory settings-similar signs of Coxsackie B5 infections=influenza like
- infection through damaged skin, ingestion or inhalation
- Problem because lesions indistinguishable to FOOT and MOUTH
- no vaccines
- prevent introduction by controlling movements of pigs and no garbage feeding
- control by test and slaughter
Tropical Theileriosis
- tickborne disease – Hyalomma tick
- caused by Theileria annulata
- characterized by anemia, jaundice, ill thrift, dyspnea, hemorrhagic diarrhea
- cattle disease
- animals can be protected by intentional low dosing of sporozoites
- vaccination available
African Trypanosomiasis
-chronic debilitating disease of cattle and other livestock (sheep, goats, pigs, horses, camels,
dogs, cats, monkeys)
-anemia primary disorder (emaciation, loss of productivity, fever)
-trypanosoma congolense, brucei, vivax
-transmitted biologically infected tsetse fly
-wild ruminants harbor agents and are reservoirs
-humans have own trypanosomes that cause sleeping sickness
-evades immune response by sequential shifting of surface glycoproteins
-no vaccine
-major constraint to ruminant livestock production in many areas of Africa
-many drugs available, but resistance problems
-tsetse fly eradication most effective solution
Venezuelan Encephalitis
-zoonotic mosquito viral born disease of horses and humans
-alphavirus togaviridae
-ZOONOTIC
-humans infected mosquito bite or contact with infected horses; causes flu like syndrome with
high fever and frontal headache
-some variants cycle from mosquito to rodent with horses and humans incidental
-horses are amplifiers in another cycle
-unknown origin during interepizootic periods and origin of epizootic VEE
-horses clinical signs are subclinical to staggering, blindness to mortality
-diffuse necrotizing meningoencephalitis
-vaccines available
-control equine movement during epizootics, mosquito control; immunization of equines!
Vesicular Exanthema of Swine
-cause by number of marine dwelling caliciviruses
-characterized by fever, vesicular lesions, and erosions (indistinguishable from FOOT and
MOUTH)
-reservoirs are marine mammals and opaleye fish
-transmission with contact of infected marine mammals or fish or pig to pig through
contaminated meat and contact
-no vaccine
-don’t feed pigs dead marine mammals
-if disease depopulate
Vesicular Stomatitis
-insect tramsmitted acute disease of horses, cattle, and pigs (less frequent in goats/sheep)
-vesiculovirus family rhabdoviridae
-HUMANS can be infected by contact or aerosols=influenza symptoms with fever, headache,
muscle aches, and vesicles in oral cavity
-maintenance cycle poorly understood
-sand flies, culicoides, black flies
-cycles about every 7-10 years in SW US, most likely from Mexico
-transmitted by insect vectors, contact and fomites
-clinical signs fever, vesicles in mouth, coronary bands and teats of lactating animals
-no vaccine in US, is in South America
-similar to FOOT and MOUTH
-prevent with insect control
Wesselbron Disease
acute arthropod viral disease of sheep, cattle, goats
- characterized by abortion and neonatal deaths (can see edema of head, icterus)
- flavivirus family togaviridae
- HUMANS subclinical infections most common, can be flu symptoms
- transmitted by aedine mosquitoes
- vaccine available but associated with reproductive morbidity
- vaccine to control, avoid pregnant animals
Foot and Mouth
-extremely contagious (one of the most contagious diseases know)
-characterized by fever, vesicular lesions, erosions
-high morbidity low mortality
-genus apththovirus family picornaviridae
-seven completely immunological distinct types A O C (European) SAT1 SAT2 SAT3 Asia1
-60 subtypes due to short RNA strand, replicates quickly with no” proof reading” so virus always
evolving and genetics changing (why no good vaccine)
-very susceptible to pH changes
-all cloven hoofed animals susceptible (cattle water buffalo yaks most susceptible)
-sheep/goats mild or inapparent
-amplifying hosts=PIGS
-indicator hots=CATTLE
-maintenance hosts=SHEEP
-wildlife=can be infected, minor role in spread when disease eradicated in domestic animals,
goes away in wildlife
-all secretions/excretions contagious
-transmission direct, indirect with fomites, and feeding contaminated garbage (most common
entry method)
-animals shed the virus up to 4 days before clinical signs
-extremely short incubation period as short as 24-36 hours in outbreaks
-cows can be carriers for up to 3.5 years, pigs only 3-4 weeks (African buffalo up to 5 years)
-clinical signs cattle= fever, drop in milk production, excessive salivation, lameness, recumbency
pigs=same signs, but myocardial infarctions in young
-sheep=look at hard palate wont show many clinical signs
-vaccines available but no cross protection between serotypes (immunity lasts about 6 months)
-difficult to distinguish vaccinated from naturally infected
-vaccinated animals can become carriers when exposed to the virus
-majority of outbreaks caused by feeding legal or illegal imported garbage products
-prevent=control import, garbage feeding regulations; biosecurity; rapid reporting of suspects
-control=eradication? Vaccination? Combinations?
-public perception, disposal issues, wildlife, many issues raised
2003 These are internationally, quarantinable diseases by WHO
Plague, Yellow Fever and Cholera.
WHO is trying to eradicate the following:
Polio and Guinea Worm Disease (dracuncuuliasis)
WHO is trying eliminate
nchocerciasis (River blindness), Leprosy, Chagas disease (American Trypanoniasis) Malaria - cut in half burden by 2010
Anthrax
gram +, rod, spore forming
Increase in drought conditions, alkaline soils, (calcareous soils) “wool sorters disease” “charbon”
Occupational-animal handlers. inhale, ingest, cutaneous forms
Erysipelas
Erysipelothrix rhusiopathiae Gram + rod In soil, water, decay matter Diamond skin disease of swine. Occupational disease-vets, farmers, slaughter house workers.
Glanders “farcy pipes” Burkholderii (Pseudomonas) malleii.
Horses: gram-negative bacillus. Man has seldom been infected, despite frequent and often close contact with infected animals. This may be due to exposure to low concentrations of organisms from infected sites in sick animals and the fact that strains virulent for equids are often less virulent for man.
There are acute and chronic forms of disease in horses and man. The acute forms are more common in mules/donkeys
The acute form is characterized by a high fever, septicemia, respiratory signs and a thick nasal discharge, with death in a few days.
Chronic disease can occur in surviving horses with ulcerating nodules on the skin and nasal cavity, and nodules in the lungs. The chronic form of the disease is more common in horses and causes generalized lymphadenopathy, multiple skin nodules that ulcerate and drain, enlargement and nodularity of regional lymphatics on the extremities and in other areas. These animals are carriers and spread the organism.
Human cases have occurred primarily in veterinarians, horse caretakers, and abattoir workers. The organism spreads to man by invading the nasal, oral, and conjunctival mucous membranes, by inhalation, and by invading abraded or lacerated skin.
Since aerosol spread is efficient, and there is no available vaccine or really dependable therapy, B. mallei has been viewed as a potential BW agent. The disease in Equidae in its natural form poses a minimal threat to military personnel. Mallein test, Eradicated in US.
Johnes disease or paratuberculosis (no RELIABLE efficacious vaccine)
affects both wild and domestic ruminants.
Mycobacterium avian subspecies Paratuberculosis can survive for extended periods in contaminated environments or in manure spread on pasture for over a year.
Contaminated soil and bacteria-laden feces coat the teats and udder of the dam and are nursed by the newborn, and infected animals shed mycobacterium in both milk and colostrum.
Incubation period is very long and clinical symptoms are more common in animals 2 to 4 years of age.
The most common presentation in goats is severe, progressive weight loss leading to emaciation in spite of good nutrition. AGID, ELISA or fecal culture may confirm diagnosis.
Johne’s disease does affect deer and elk, and these species will probably be part of a forthcoming regulatory program.
Phenolics inactivate it b/c of ability to penetrate the lipid-rich cell wall.
Leptospirosis-
Caused by a spirochete and is common worldwide. Flooding after heavy rainfall helps spread the bacteria in the environment.
People get leptospirosis by contact with fresh water (lakes, rivers, and streams), damp soil, or vegetation contaminated by the urine of infected animals.
The important serotypes recognized in livestock in the United States include Leptospira pomona, L. canicola, L. icterohaemorrhagiae, L. grippotyphosa and L. hardjo. Among domestic animals, swine, cattle, dogs, and horses are most frequently affected. Known wildlife hosts include many of the small rodents, raccoons, foxes, opossums, skunks, deer, and moose. Leptospirosis is generally contracted by the direct splashing of urine from infected or carrier animals into the eyes of susceptible animals. It can also be spread through the skin and mucous membranes from contact with water contaminated with leptospires. Transmission may also occur during breeding through residual urine in the genital tract or through infectious semen. The major sources of contamination are swine, cattle, dogs, and wildlife that have recovered from the disease and have become carriers. Cattle and swine are major sources because of the volume of urine and the extent and duration of leptospires in the urine. A significant percentage of human cases are acquired through direct contact with the urine of infected livestock or with contaminated soil or water. Many epidemics of L. pomona have occurred among persons swimming in water contaminated with the urine of infected livestock. The organism may survive up to six months in alkaline water.
Lepto Cattle
May vary in severity from a mild, in apparent infection to an acute infection that may cause death.
Cattle may develop a high fever of 104° to 107°F, depression, loss of appetite, decreased milk production.
Hemoglobinuria, anemia, icterus and bloody milk are also seen. Abortion, frequently the only clinical sign reported, usually occurs two to five weeks after initial infection. The fetus has usually been dead for several days before it is expelled. Most abortions occur in the last three months of pregnancy.
Lepto swine
The disease in swine is largely subclinical except for abortions, which usually occur during the last two to three weeks of pregnancy. Some aborted fetuses may have been dead a short time. Abortion is not delayed as long in swine; therefore, many infected fetuses contain viable leptospires when aborted
Lepto dogs
Canine leptospirosis is widespread in the United States.
Serotypes in vaccine include: L. grippotyphosa and L. pomona and against the older serotypes, L. canicola and L. icterohemorrhagiae
Acutely, a febrile, bacterial disease, with vomiting, muscular stiffness, and nephritis. In severe cases, jaundice and death may occur.
Central nervous system signs may occur with or without other clinical signs, and organisms may be present in the brain tissue for extended periods.
Chronic leptospirosis is primarily associated with chronic kidney degeneration. Shedding of leptospires in the urine may continue for over a year.
Lepto rodents
Wild rat populations in urban and rural areas are frequently infected with L. icterohaemorrhagiae
Lepto diagnosis
Confirm a diagnosis with demonstration of significant levels of antibodies to leptospires in the serums of recovered animals.
Use either plate agglutination test with killed antigens or the microscopic agglutination test, in which living organisms are used as antigens.
May also be diagnosed by demonstrating the organism microscopically in tissues by fluorescent antibody and by isolating leptospires in a culture or in laboratory animals following the injection of infected material.
Leptospires are most readily isolated from blood or milk taken from animals during the acute phase, or from the urine, kidneys, spinal fluid, and brains of recovered animals.
Lepto treatment and prevention
When leptospirosis is diagnosed in swine or cattle during the early phase, further abortion losses may be reduced or prevented by promptly vaccinating the entire herd against serotypes prevalent in the area.
Swine should be vaccinated at 6-month intervals and cattle annually.
Additions to the herd should originate from herds that are free of leptospirosis and antibodies on the basis of a complete herd test.
The vaccine used in infected herds should be identical with the serotype causing the diseases, as there is little or no cross-protection between vaccine serotypes.
The future breeding efficiency of herds that have experienced leptospirosis is usually unaltered.
In fact, their value may be enhanced because they are solidly immune against re-infection with the same serotype.
Annual vaccination is recommended for dogs with a booster given if an outbreak occurs in the area.
Q fever a rickettsial infection caused by Coxiella burnetii.
High potential for bio weapon. Very resistant to desiccation and disintergration.
Extremely infectious: one organism can cause disease. Worldwide distribution. Airborne dissemination over long distances possible.
The incubation period in people is 2 to 4 weeks.
Most infections in man are also subclinical. When people do show symptoms, it is usually characterized by a flu-like illness with fever, chills, headache, respiratory signs, muscle pain and malaise. Serious complications can occur including abortion, endocarditis and hepatitis.
Cattle, sheep, and goats are reservoirs but other kinds of animals can also have this disease.
Most infected animals do not show signs, but the bacteria can be in barnyard dust that contains dried fluids from the births of calves or lambs, manure, or urine.
People usually get Q fever by breathing in this contaminated barnyard dust. An rare occasions, people can get Q fever from drinking contaminated milk or from tick bites.
Avoid contact with placenta, birth products, fetal membranes, and aborted fetuses of sheep, cattle, and goats. Drink only pasteurized milk and milk products. If you work around pregnant sheep and goats, get vaccinated. Interestingly, no rash associated like w/ other ricketsial infections.
Q fever is what the pasteurized temperatures are based on at present: 145 F (68C) for 30 minutes. Or 161F (71C) for 15 seconds. Vaccination is possible but not practiced in this country.
Plague
Yersina pestis gram – nonspore former
Vectorborne: fleas. Aerosol
Epidemically preceded by many rats/small rodents dying
Severity #1 septicemia #2 pneumonic #3 bubonic
Pneumonic form in Western US from cats
High Case fatality rate, survivors spread Dz
Bubonic most common CFR 50-60% if untreated
Tularemia: (Francisella tularensis)
transmission
Tularemia, (rabbit fever or deerfly fever).
Gram-negative organism Francisella tularensis.
Ticks are the most important vectors of F. tularensis, transferring the bacterium between rabbits, hares, and rodents and serving as an interepizootic reservoir.
Horseflies, mosquitoes, sucking lice, and biting flies (deer flies as well) may also serve as vectors.
In endemic areas, transmission to humans and other domestic vertebrates usually occurs via bites from infected arthropods, or the bacterium may enter scratches or knife cuts exposed to infected animal tissues.
Tularemia may also be transmitted by ingestion of infected tissues or contaminated water, and by inhalation of aerosolized particles. Sheep and domestic cats can be a source of infection for man.
However, it can also be aerosolized. Both the inhalation of organisms and drinking contaminated water can cause human infection.
F tularensis is considered a high-priority (category A) agent for bioterrorist use because it meets the following CDC criteria:
can be easily disseminated
results in high mortality rate and has the potential for major public health impact
might cause public panic and social disruption
requires special actions for public health preparedness i.e. drug/vaccine stockpiling
Tularemia: (Francisella tularensis)
incubation and symtpoms
Public health authorities would most likely become aware of an outbreak of unusual respiratory disease in its early stages, but this could be difficult to distinguish from a natural outbreak of community-acquired infection, especially influenza or various atypical pneumonias. Although the majority of individuals with inhalational tularemia develop pneumonia, the initial presentation may be an undifferentiated febrile illness-
The incubation period is typically 3 to 5 days, but may range from 1 to 14 days.
Fever, chills, malaise, myalgia, and vomiting are followed by more specific signs of disease that depend on route of entry: ulceroglandular, glandular, typhoidal, oropharyngeal, oculoglandular, or pulmonary.
All forms of tularemia can progress to pleuropneumonia, meningitis, sepsis, shock, and death.
Ulceroglandular tularemia is the most common form (75 to 85% of reported cases). An ulcer is evident at the site of entry, usually the fingers or hands in cases associated with exposure to rabbits, hares, or rodents. Ulceration progresses to necrosis and lymphadenopathy; lymph nodes may suppurate, ulcerate, and become sclerotic. Signs of glandular tularemia are similar, but no skin ulcer is evident.
Pulmonary tularemia represents about 30% of contracted infections and is caused by inhalation of aerosolized bacteria. Pneumonia in one or both lungs is the typical clinical sign.
Influenza and tularemia share only the epidemiologic characteristic of abrupt onset. The epidemiologic features of inhalational tularemia following use as a biological weapon would include:
Point-source outbreak pattern (outbreak begins at point of attack)
More likely in urban, nonagricultural setting
Unexpected, severe respiratory illness in otherwise healthy persons
No differences in susceptibility by age or sex
tuleremia reservoirs
Tularemia is one of the most infectious pathogenic bacteria known, requiring inoculation or inhalation of as few as 10 organisms to cause disease. It is potential biological weapon because of its extreme infectivity, ease of dissemination, and substantial capacity to cause illness and death.
It is a hardy non-spore forming organism that is capable of surviving for weeks at low temperatures in water, moist soil, hay, straw or decaying animal carcasses.
Natural reservoirs include small mammals such as mice, rats, squirrels, rabbits.
Naturally acquired human infection occurs through: bites of infected arthropods (American Dog Tick: Dermancentor variabilis, Lone Star Tick: Amblyomma Americana and Rocky mountain wood tick; Dermancentor andersoni); mosquitoes, deerflies, handling infectious animal tissues or fluids; direct contact or ingestion of contaminated water, food, or soil; and inhalation of infective aerosols.
Human to human transmission has not been documented.
Depending on how the person is infected, it can cause flu-like symptoms, skin ulcers, swollen eyes and a sore throat. In the natural setting, tularemia is noted to be a predominately rural disease with clinical presentations including ulceroglandular, oculoglandular, pneumonic, typhoidal and septic forms. Tularensis as a weapon, aerosol release would cause the greatest adverse medical and public health consequences. This would result in the abrupt onset of large numbers of cases of acute, non-specific febrile illness beginning 3 to 5 days later with pleuropneumonitis developing in a significant proportion of cases.
Without antibiotic treatment, the clinical course could progress to respiratory failure, shock and death. In pulmonic or septicemic cases of tularemia without antibiotics treatment the mortality rate has been as high as 30-60%. Given the short incubation period of tularemia and incomplete protection of current vaccines against inhalational tularemia, vaccination is not recommended for post-exposure prophylaxis. Given the lack of human-to-human transmission, isolation is not recommended for tularemia patients. Expect a short half-life due to desiccation, solar radiation, and other environmental factors, and a limited risk from secondary dispersal.
Rat Bite Fever-
Streptobacillus monilformis-acute-chills, febrile, arthalgia, maculopapular rash on extremities. Get from rat bite or food contaminated with rat feces.
Whitmore Disease Rodent Glanders Burkholderii pseudomalleii:Melodosis
Inhalational from soils, surface water and venereal in man.
Caseous lesions in lymph nodes. In animals signs are swollen joints, fever, cough, fistulous tracts; in man simulate typhoid fever or TB with empyema, abscesses, osteomyelitis; high case fatality rate.
Contagious Ecthyma (Orf, Soremouth):
contagious pustular dermatitis. Seen in virtually every place in the world that raises sheep and goats. It also has the ability to spread to the hands and arms of people handling infected animals. Caused by a virus from the pox family. The virus is very hardy and virus has been found in dried scabs up to twelve years after they have been shed. Animals that contact the disease usually develop a strong immunity and will not be re-infected for at least one year. Is extremely infectious disease with up to 90 percent of a flock showing signs. Prevention: Vaccinate.
Equine Morbillivirus virus (Hendra Virus)
Hendra virus (HeV) and Nipah virus (NiV) emerged in the last decade of the twentieth century as the causes of outbreaks of respiratory and neurological disease that infected a number of animal species.
In 1994, HeV caused severe respiratory disease and the death of 13 horses and a horse trainer at a stable in Brisbane, Australia.
Between September 1998 and April 1999, after spreading unrecognised as a respiratory or encephalitic infection in Malaysian pigs, NiV appeared in the human population there and was the cause of fatal encephalitis.
Over one million pigs were culled to stop spread of the disease.
HeV has caused the death of four of seven infected people while it has been reported that there have been 400 cases of NiV in humans, with approximately 200 deaths, in Malaysia, Singapore, Bangladesh and India.
Fruit bats (flying foxes) in the genus Pteropus are natural hosts of both viruses.
HeV infection of horses is characterized progressively by high fevers, facial swelling, severe respiratory difficulty and, terminally, copious frothy nasal discharge.
Some horses display neurological signs.
The most common post-mortem observations are dilated pulmonary lymphatics, severe pulmonary oedema and congestion. The underlying lesion is generalised degeneration of small blood vessels in a range of organs.
Syncytial endothelial cells containing viral antigen are common in capillaries and arterioles.
HeV infection of horses is not uniformly fatal and some horses manifesting clinical signs survive infection.
Hendra virus does not appear to be highly contagious among horses, and close contact seems to be necessary for it to spread. Infected horses on pastures have rarely transmitted the virus. However, transmission appears to occur more readily in closed environments such as stables.
Nipah
NiV infection of pigs is highly contagious, but it was not initially identified as a new disease because morbidity and mortality were not marked and clinical signs were not significantly different from other known pig diseases.
Observations made during the outbreak investigation and during experimental infections confirmed that NiV infection of pigs is characterised by fever with respiratory involvement. In animals showing disease, nervous signs have been frequently reported, but many infections are subclinical.
Some infected animals display an unusual barking cough. Abortion is reported in sows. Immunohistochemical lesions are found in either or both the respiratory system (tracheitis and bronchial and interstitial pneumonia) and the brain (meningitis) of infected animals.
Syncytial cells containing viral antigen are seen in small blood vessels, lymphatic vessels and the respiratory epithelium.
Both viruses affect companion animals. HeV causes pulmonary disease in cats similar to that observed in horses. Natural infection of dogs with NiV causes a distemper-like syndrome with a high mortality rates; there is serological evidence that some dogs survive infection. Experimentally NiV causes a similar disease to HeV in cats.
Syncytial endothelial cells containing viral antigen were demonstrated in both HeV and NiV infections in cats and in NiV infection in dogs.
Infection of humans is from animal contact, usually from an amplifier host rather than directly from the natural, reservoir host:
NiV from swine and HeV from horses.
However investigations of outbreaks of human NiV in Bangladesh have indicated infection from Pteropid bats.
Human-to- human transmission has not been seen with HeV or with NiV in Malaysia and Singapore, but human-to-human transmission is suspected in recent outbreaks of NiV in Bangladesh.
HeV and NiV are closely related members of the family Paramyxoviridae. Differences between them and other family members have led to their classification in a new genus, Henipavirus, in the subfamily Paramyxovirinae.
Requirements for vaccines and diagnostic biologicals: There are no vaccines currently available for NiV.
Equine viral arteritis (EVA)
background
Contagious disease of equids caused by equine arteritis virus (EAV), an RNA virus that is found in horse populations in many countries.
While typically not life-threatening to otherwise healthy adult horses, EAV can cause abortion in pregnant mares; uncommonly, death in young foals; and establish a long-term carrier state in breeding stallions.
While various horse breeds appear equally susceptible to EAV, the prevalence of infection can vary widely, with higher seropositivity rates occurring in Standardbreds and Warmbloods.
Historically, outbreaks of EVA have been relatively infrequent. However, the number of confirmed occurrences appears to be increasing, likely attributable to increases in:
1) global movement of horses
2) accessability of carrier stallions
3) utilization of shipped cooled or frozen virus-infective semen
Transmission most frequently occurs through direct contact with virus-infective respiratory secretions leading to widespread dissemination of the virus among susceptible horses in close proximity.
Venereal transmission by infected stallions has a significant role in virus spread on or between breeding farms.
Equine arteritis virus can be very efficiently spread through artificial insemination and the use of fresh-cooled or frozen semen. There is limited evidence that virus can also be transmitted via embryo transfer where the donor mare is bred with infective semen from a carrier stallion. The virus has been shown to remain viable for considerable periods of time in raw, extended or frozen semen held at temperatures equal to or less than 4°C. Indirect transmission, though less significant, can occur through contact with virus-contaminated fomites.
The majority of primary EAV infections are subclinical or asymptomatic. EVA can vary in clinical severity both between and within outbreaks.
EVA cannot be diagnosed based on clinical signs alone, as case presentation is similar to various other infectious and non-infectious equine diseases. Laboratory confirmation is required for diagnosis.
Clinical signs, if they occur, typically develop 3 to 7 days post-infection and are variable but may include any combination or all of the following: fever; depression; anorexia; dependent edema (lower limbs, scrotum and prepuce or mammary glands); localized or generalized urticaria; supra or periorbital edema; conjunctivitis; lacrimal discharge and serous to mucoid nasal discharge. Abortion is a frequent sequel to infection in the unprotected, pregnant mare. When pregnant mares are exposed to the virus very close to term, they may not abort but give birth to a congenitally infected foal, affected with a rapidly progressive and fulminant interstitial pneumonia. Foals within a few months of age, if exposed to EAV can develop a life-threatening pneumonia or pneumoenteritis.
A carrier state can develop following EAV infection in the post-pubertal colt or stallion. The virus can persist in the reproductive tract of stallions for many years and may result in lifelong infection. The carrier stallion is widely accepted as the natural reservoir of EAV and the source of diversity among naturally occurring strains of the virus.
EVA vaccine
Vaccine:
The current licensed vaccine in N. America is a highly attenuated, modified live virus product. It has been shown to be safe and effective in stallions and non-pregnant mares. Mild post-vaccinal febrile reactions with transient lymphopenia have been observed in a small percentage of first-time vaccinated horses.
Primary vaccination provides clinical protection against EVA but does not prevent re-infection and limited replication of challenge virus. However, in first-time vaccinates, the frequency, duration, and amount of vaccine virus that is shed via the respiratory tract is significantly less than that observed with natural infection.
Vaccination in the face of an EVA outbreak has been successful in controlling further spread of the virus within 7 to 10 days.
Immunization with the MLV vaccine stimulates a rapid protective response which in turn restricts development of the cell-associated viremia and viral shedding via the respiratory tract in horses naturally exposed to infection.
As a consequence, the amount of EAV in circulation is greatly decreased, limiting further spread of the virus.
Vaccination Schedules:
In planning a vaccination program against EVA, it is important to consult with state and/or federal animal health officials to ensure that any such program is in compliance with the state’s control program for EVA, if one exists.
The indications for vaccination against EVA have been:
1) To protect stallions against infection and subsequent development of the carrier state.
2) To immunize seronegative mares before being bred with EAV-infective semen.
3) To curtail outbreaks in non-breeding populations.
Note: It is not possible to differentiate vaccine-induced antibody response from that due to natural infection. It is strongly recommended that prior to vaccination, serum from all first-time vaccinates be tested and confirmed negative for antibodies to EAV by a USDA-approved laboratory . Mares intended for export should be similarly tested.
EVA
Outbreak Mitigation
Non-breeding population: Vaccination is an effective strategy in containing outbreaks, particularly in congregated groups of horses where isolation may be problematic. Serologic testing, as described above, should be performed on intact males and females that may be intended for future breeding purposes and/or export.
Breeding population: Outbreaks of EVA can be complex and can have far reaching implications. Vaccination is a component of outbreak management but should be performed only under the direct supervision of a veterinarian. (Link to AAEP infectious disease guidelines)
Foot and mouth background
Picornavirus
Killed by acid or bases
Cattle, pigs, cloven hoofed—NOT horses
Swine and other cloven-hoofed ruminants.
The US has been free of FMD since 1929.
Dx ELISA- antigen detection.
Pigs serve as amplifiers of the disease, being veritable virus factories. It can be so clinically mild in sheep and goats as to miss it completely.
The disease is characterized by fever and blister like lesions on the tongue, mouth, teats, and between the claws. Many affected animals recover, but causes severe losses in the production of meat and milk.
The virus has a remarkable capacity for remaining viable in carcasses, in animal byproducts, in water, in such materials as straw and bedding, and even in pastures. Animals, people, or materials that bring the virus into physical contact with susceptible animals can spread FMD viruses.
An outbreak can occur when: People wearing contaminated clothes or footwear or using contaminated equipment pass the virus. Contaminated vehicles, facilities are used to hold susceptible animals. Raw or improperly cooked garbage containing infected meat or animal products is fed to susceptible animals. Susceptible animals are exposed to materials such as hay, water, feedstuffs, hides, or biologics contaminated with the virus. A cow can be infected by semen from an infected bull.
FMD differentials
Differential Diagnoses:
VS, bluetongue, BVD and foot rot in cattle and VES of swine and SVD in pigs.
A single infected animal or one contaminated sausage could carry the virus to American livestock.
Deer and wildlife populations rapidly could become infected and remain a reservoir for the virus.
