Term
| What type of infectious disease has the greatest economic impact in the equine industry? |
|
Definition
viral diseases <-- because they're sooo infectious
**** vs. bacterial diseases that tend to be opportunistic and therefore less contagious |
|
|
Term
| What is the most contagious bacterial disease in horses, and therefore the most compelling reason for implementing biosecurity measures in riding/boarding establishments? |
|
Definition
| strangles (Strep. equi var. equi) |
|
|
Term
| What are the most significant protozoal diseases of horses? |
|
Definition
| blood parasites + Equine protozoal myelitis (should be a DDX in EVERY neurologic horse) |
|
|
Term
| What is the most common fungal disease of horses in MN? What organ system is most commonly affected? |
|
Definition
Aspergilus (remember fungal diseases vary by geographic region)
commonly affects respiratory tract (opportunistic) |
|
|
Term
| When is ancillary testing for infectious diseases required? |
|
Definition
| If you suspect a reportable, zoonotic, or highly contagious disease |
|
|
Term
| What are four methods of preventing or reducing incidence or spread of infectious diseases? |
|
Definition
avoid exposure
vaccination
reduce vectors
address sources of poor immunocompetence (ex. FPT foals)
client/community education (regarding above concepts) |
|
|
Term
| Which infectious diseases present with non-specific signs and do not always cause fever in affected horses? |
|
Definition
| Equine infectious anemia Equine viral arteritis (may have respiratory signs) Anaplasma (may have neuro signs) Babesia Anthrax Lyme disease (may have neuro signs) |
|
|
Term
| What is commonly the pathophysiologic mechanism behind development of edema with concurrent infectious disease? |
|
Definition
often edema develops secondary to vasculitis
*** may not necessarily be due to the infectious agent (ex. CHF, hypoalbuminemia secondary to increased loss (renal, GI) or decreased production (liver, malnutrition), lymphatic obstruction, or cellulitis) |
|
|
Term
| What are two common sites for identifying petechia (secondary to vasculitis) in horses? |
|
Definition
| mucus membranes and inside ears |
|
|
Term
| What is a common etiology of edema secondary to toxin ingestion in horses (in MN)? |
|
Definition
|
|
Term
| What are six differentials for equine disease with peripheral edema? |
|
Definition
| EIA, EVA,Anaplasma, Purpura hemorrhagica, Lyme, Pigeon fever |
|
|
Term
| What is the etiologic agent of EIA and what are the implications of infection? |
|
Definition
Caused by a retrovirus
No Tx or vaccine, once infected animals will remain infected for life --> generally recommend euthanasia, esp. if animals are acutely ill
*** REPORTABLE disease |
|
|
Term
| What is the underlying pathophysiology associated with clinical signs of EIA? |
|
Definition
|
|
Term
| What are the three syndromes associated with EIA infection? |
|
Definition
Inapparent infection (subtle CBC changes: increased globulins + lymphopenia)
Acute disease: within 30 days of exposure, FEVER + THROMBOCYTOPENIA +/- multi-systemic signs (ataxia, abortion, epistaxis, edema)
Subacute/chronic disease: cyclic recrudescence with fever, weight loss, edema, increasingly severe anemia +/- epistaxis, thrombocytopenia, hyperglobulinemia/hypoalbuminemia <-- negative acute phase response) |
|
|
Term
|
Definition
Coggins test (AGID) <-- may be negative in acute disease phase as animal must be infected for 2-4 weeks before becoming seropositive
*** additionally foals may test false positive secondary to passive transfer of maternal antibodies (wait to test foals until 6-8.5 months of age) |
|
|
Term
| What organs are grossly enlarged in animals infected with EIA that are necropsied during active infection or recrudesnce of chronic infection? |
|
Definition
| enlarged LN, spleen and liver |
|
|
Term
| What is the vector that transmits EIA? |
|
Definition
biting flies act as mechanical vectors
**** most important to limit vector exposure to patient during acute febrile period (virus is most abundant --> greatest risk of transmission) |
|
|
Term
| What is the etiologic agent of EVA and what are the implications of infection? |
|
Definition
single stranded RNA arterivirus
Most concerned about infection in stallions because carrier state is associated with high levels of testosterone and virus is shed in semen --> can cause abortions but infection is generally asymptomatic or associated with mild clinical signs (fever, edema, uticaria) |
|
|
Term
| Is there a vaccine for EIA? |
|
Definition
|
|
Term
| Is there a vaccine for EVA? |
|
Definition
Yes :)
**** beware of false positives on serum titers in vaccinated animals |
|
|
Term
| What is the most common clinical presentation of EVA? |
|
Definition
|
|
Term
| What three organ systems can be affected by EVA? |
|
Definition
Respiratory: rhinitis, dyspnea and coughing (less commonly appreciated)
Reproductive: abortion in mares in mid gestation (3-10 months) or weak born foals **** mare may be assymptomatic and infection has no impact on future fertility***** PI in stallions (30-60% of infected individuals)
Skin: edema (esp. periorbital) + uticaria
*** remember, most common presentation of EVA is ASYMPTOMATIC |
|
|
Term
| Where does the arterivirus responsible for EVA persist in carrier stallions? |
|
Definition
virus persists in the ampulla of the vas deferens <-- this is testosterone dependent
virus is shed in the semen (and is resistant to freezing)
**** virus is shed in ALL bodily fluids/secretions |
|
|
Term
| How are abortions caused by EVA different from those caused by EHV-1? |
|
Definition
EVA affects mid-gestational mares (3-10months) and fetus is generally autolyzed
EHV-1 affects mares in last trimester of gestation and fetus is generally fresh |
|
|
Term
|
Definition
paired serology
*** if titer < 1:4 in a stallion the individual is likely a carrier (sheds virus in semen) |
|
|
Term
| What two breeds have an extremely high rate of positive EVA serologies? |
|
Definition
standardbreds (70-90% +)
austrian warmbloods (93% +) |
|
|
Term
| How long is immunity following natural exposure to EVA? |
|
Definition
|
|
Term
| How is the MLV EVA vaccine used to help control the disease? |
|
Definition
vaccination DOES NOT stop transmission of virus but does help control outbreaks by reducing the viral load and decreasing the severity of clinical disease <-- only use in animals with high risk of infection
**** isolate vaccinated animals for >21 days as they will shed vaccine virus during this time. Additionally, vaccinated animals will be positive on serology |
|
|
Term
| What is the best way to prevent EVA transmission? |
|
Definition
Avoid exposure by screening all 1st year stallions with serology ( titers > 1:4 = carrier)
Test all stallions yearly and breed only to EVA negative individuals |
|
|
Term
| What foreign animal disease strongly resembles EVA but is associated with very high mortality? |
|
Definition
| African Horse Sickness *** presents with periorbital swelling + nasal discharge and pulmonary edema |
|
|
Term
| How can you diagnose equine ehrlichiosis (aka. anaplasma) in horses that have been recently infected? |
|
Definition
| identification of morula in PMN on blood smear |
|
|
Term
| What drug is used to treat equine ehrlichiosis/anaplasma? |
|
Definition
oxytetracycline IV
*** Can use doxycycline PO but more expensive + risk of developing diarrhea as a side effect |
|
|
Term
| What clinical signs are associated with equine ehrlichiosis/anaplasma? |
|
Definition
fever (1-12 days w/tx)
limb edema
petechia
*** remember other infectious diseases that present with fever + edema include EIA, EVA, babesia, purpura, and pigeon fever |
|
|
Term
| How do you diagnose equine ehrlichiosis/anaplasma? |
|
Definition
morula within PMNs if recently infected
IFA on buffy coat cells (paired titers)
CBC: lymphopenia -> neutropenia, mild anemia + thrombocytopenia
PCR (available from UC davis)
*** in endemic areas you may identify seropositive animals that are asymptomatic |
|
|
Term
| What is the best way to prevent equine ehrlichiosis/anaplasma? |
|
Definition
|
|
Term
| Is there a vaccine available for equine ehrlichiosis/anaplasma? |
|
Definition
NO
*** best prevention through minimizing exposure to ticks |
|
|
Term
| What is the etiology of purpura hemorrhagica? |
|
Definition
immune mediated vasculitis most commonly secondary to infection by or vaccination for Strep. equi var equi (Strangles)
**** has also been reported in assocaited with strep. zooepidemicus, influenza, EHV-1, and pigeon fever |
|
|
Term
| What immunoglobulins are responsible for formation of ab-ag complexes that deposite in small vessels during the course of purpura hemorrhagica? |
|
Definition
IgA and IgM
*** may occur at time of infection or vaccination but most occur 2-3 weeks later, may also occur following subclinical infection (strep. equi var equi) |
|
|
Term
| What clinical signs are most commonly associated with purpura hemorrhagica? |
|
Definition
Very painful!
edema (head, extremities, ventrum), petechial hemorrhages, +/- uticaria, dyspnea (secondary to pulmonary edema), collic and acute rhabdomyolysis (secondary to thromboemboli)
**** DDX: EIA, EVA, babesia, ehrlichia/anaplasma, pigeon fever |
|
|
Term
| What is the deffinative diagnosis for purpura hemorrhagica? |
|
Definition
serum ELISA for Strep M protein titers
*** usually clinical signs + history of strangles exposure/vax is adequate for Dx |
|
|
Term
| How can you treat purpura hemorrhagica? |
|
Definition
Corticosteroids
penicillin if active strangles infection (reduce Ag for immune complex formation)
+/- heparin (reduce risk of DIC), plasma/hetastarch (reduce edema formation), NSAIDS/butorphanol (pain managment) |
|
|
Term
| How can you prevent purpura? |
|
Definition
AVOID EXPOSURE! strict isolation of all vaccinated and active strangles infections
*** no vaccines can prevent strangles, and strangles vaccines can trigger purpura or IMTP |
|
|
Term
| What is the most common presentation of lyme disease in horses? |
|
Definition
subclinical
*** may also present with fever, mandibular lymphadenopathy, polyarthritis |
|
|
Term
| How do you diagnose lyme disease? |
|
Definition
serology (4x change in titer)
if animal presents with arthritis you can culture synovial tissue or fluid (requires special media) |
|
|
Term
| What is the ideal treatment for lyme disease in horses? |
|
Definition
oxytetracyline IV
*** can also use high dose penecillin IM or doxy PO($$$$$ and limited oral bioavilability) |
|
|
Term
| What is the best way to prevent lyme disease? |
|
Definition
limit exposure to ticks
*** same prevention strategy as ehrlichiosis/anaplasma |
|
|
Term
| What is the etiologic agent of pigeon fever? |
|
Definition
| corynebacterium pseudotuberclosis (different strain from the agent of CLA in small ruminants) |
|
|
Term
| What geographic regions are more commonly associated with pigeon fever? |
|
Definition
drought areas, esp. in california and pacific NW
*** rare in MN |
|
|
Term
| Although clinical signs associated with pigeon fever are quite variable, what are the two most common presentations? |
|
Definition
most commonly presents ulcerative lymphangitis and cellulitis (edema of distal limbs, pectorals, and ventral abdomen)
or
deep muscle abscesses (very thick walled, usually associated with chest, ventrum, limbs, inguinal or LN but rarely (<5% of cases) can involve internal organs |
|
|
Term
| How is pigeon fever transmitted? |
|
Definition
biting insects act as mechanical vectors
*** although pus associated with abscesses is not likely contagious from horse to horse it should be fastidiously cleaned to limit environmental contamination and vector transmission |
|
|
Term
| How do you diagnose pigeon fever? |
|
Definition
identification of deep muscle abcsesses on ultrasound
culture of corynebacterium pseudotuberculosis from pus
*** if suspect internal/occult abscesses (<5% of cases) serum hemagglutination test is an option |
|
|
Term
| What is the treatment for pigeon fever? What is the prognosis? |
|
Definition
lance and drain abscesses if possible
after lancing long term antibiotics (penicillin, erythromycin +/- in combo with rifampin to increase tissue penetration) <-- if you give Ab prior to lancing you will prolong clinical course of disease (like strangles)
prognosis is good for simple abscesses but guarded if internal organs are involved |
|
|
Term
| How can you control pigeon fever? |
|
Definition
control biting insect vectors and fastidiously clean any draining abscesses in affected animals
*** occurence of disease is indicative of endemic soil habitation by the organism (corynebacterium pseudotuberclosis) |
|
|
Term
| What organ systems are generally affected by herpes viruses? |
|
Definition
| respiratory, eyes, oral cavity, genitalia |
|
|
Term
| What are the three types of alpha herpesviruses in horses and what are their major clinical presentations? |
|
Definition
| EHV-1: abortion and neurologic disease EHV-4: respiratory disease EHV-3: coital exanthema |
|
|
Term
| What are the two types of gamma herpesviruses in horses and what are their major clinical presentations? |
|
Definition
| EHV-2: oral + esophageal ulcers in foals, often latent infections EHV-5: multinodular pulmonary fibrosis *** both EHV-2 and EHV-5 have been isolated from many clinically normal horses so their role in disease is not currently well defined |
|
|
Term
| What are the two most important respiratory diseases in horses? |
|
Definition
equine influenza (more severe respiratory clinical signs)
equine herpes virus |
|
|
Term
| What is the most important microbial cause of abortion in horses? |
|
Definition
|
|
Term
| What is the most contagious etiology of neurologic disease in horses? |
|
Definition
|
|
Term
| How is herpesvirus rhinopneumonitis transmitted? |
|
Definition
aerosol, direct contact, fomites
*** transmission is very rapid in housed horses, and young animals are especially suceptible |
|
|
Term
| What two types of herpes viruses are implicated in cases of rhinopneumonitis in horses? |
|
Definition
EHV-4
EHV-1 <-- greater concern because also associated with abortion and neurologic disease |
|
|
Term
| What clinical signs and length of clinical disease are associated with herpesvirus rhinopneumonitis? |
|
Definition
fever (often biphasic per day), nasal discharge (serous to mucoid) +/- relatively mild cough/pharyngitis/tracheitis normally recover within 2-3 weeks if no complications
*** less severe than clinical signs associated with influenza |
|
|
Term
| What type of equine herpesvirus is almost always implicated in cases of abortion? It is associated with what clinical signs? |
|
Definition
almost always EHV-1
mares in last 4 months of pregnancy abort without any impending signs of disease
*** fetus is usually expelled fresh and with intact placenta and amniotic membrane. If foal is born alive prognosis is poor <-- generally succumb to progressive bacterial pneumonia |
|
|
Term
| Although EHV-1 is the most common cause of infectious abortion in horses, what are some other differential diagnoses? |
|
Definition
EVA
Mare reproductive loss syndrome
placental infection
lepto |
|
|
Term
| What type of herpesvirus is associated with equine herpes myeloencephalopathy? |
|
Definition
EHV-1 <-- associated with a genetic mutation in DNA polymerase (162x more likely to develop neurologic disease)
**** herpes myeloencephalopathy is associated with a greater degree of viremia than other herpes associated disease conditions, and viremia coincides with the development of clinical signs (very useful for Dx) |
|
|
Term
| What is the prognosis for equine herpes myeloencephalopathy? |
|
Definition
| rapid progression to recumbancy is associated with poor prognosis. If patient can be maintained standing with supportive care gradual return to complete recovery is possible but may take months |
|
|
Term
| What are four factors that complicate a diagnosis of herpesvirus infection? |
|
Definition
latently infected animals will be negative on serology
subclinically infected animals can act as sources of infection but are challenging to identify
Herpes virus can infect animals that have high antibody titers
Clinical signs of disease are non-specific |
|
|
Term
| How can you diagnose herpes virus? |
|
Definition
Most effective tests are virus isolation from nasal swabs, whole blood, or tissue (LN, placenta, fetus, CNS) or PCR (get results quicker)
can also do paired serology (4x increase in titer over 7-21 days) |
|
|
Term
| What is the most important mode of herpes virus transmission and what measures can you take to control transmission? |
|
Definition
viral shedding through respiratory secretions is most important mode of transmission
Best way to limit transmission is to ISOLATE cases (>35ft separation) and exposed individuals (monitor BID for development of a fever)
Clean environment (virus persists in organic material, aborted fetus is especially high in virus particles) |
|
|
Term
| T/F natural immunity to herpesviruses is long lived |
|
Definition
FALSE!
*** animals may develop new infections 3-6 months after clearing an initial infection. |
|
|
Term
| Does vaccination in the face of a herpes outbreak help minimize morbidity and severity of clinical signs? |
|
Definition
| No, it's not ideal to vaccinate animals that have already been exposed |
|
|
Term
| T/F recrudescence of clinical signs in animals with persistent herpesvirus infections are associated with stress |
|
Definition
|
|
Term
| What diseases/symptoms are associated with leptospirosis infection in horses? |
|
Definition
abortion and recurrent uveitis, rarely renal disease in adult horses
*** in foals renal, hepatic, and pulmonary lesions, prognosis is grave |
|
|
Term
| Why is leptospirosis difficult to control through vaccination in horses? |
|
Definition
many serogroups and serovars can cause disease in horses
*** L. bratislava may be host adapted to horses |
|
|
Term
| How can you diagnose leptospirosis infection in horses? |
|
Definition
serology - check for all serovars, single high titer is sufficient for Dx
can also culture a midstream urine sample (ensure that patient is not on diuretics) <-- often false negative, organism is hard to grow |
|
|
Term
| How do you treat leptospirosis? |
|
Definition
High dose of IV potassium penicillin QID 2-3 wks
*** if infection is associated with abortion do serology on other pregnant mares and consider treating those with high titers (1:6400) to reduce incidence of abortion |
|
|
Term
| How can you prevent leptospirosis infections? |
|
Definition
| disinfect environment (esp. sites of foaling and urination) and try to mantain animals away from disease reservoirs (wildlife and cattle) |
|
|
Term
| What type of environments are generally associated with anthrax? |
|
Definition
| alkaline soil, areas that get flooded (allows large numbers of spores to accumulate on ground surfaces in low lying areas) followed by a long dry spring with cases peaking during the hot summer months |
|
|
Term
| What are the three clinical forms of anthrax? |
|
Definition
cutaneous: associated with insect bites and skin wounds --> localized plaque-like lesions, SQ swelling in dependent areas (ex. throat) + high fever --> best prognosis of the three forms
Pulmonary: inhalation of spores --> hemorrhagic mediastinitis --> rapidly fatal
Gastrointestinal: ingestion of spores --> septicemia, enteritis, bleeding from mucus membranes --> high mortality |
|
|
Term
| How do you diagnose anthrax? |
|
Definition
collect peripheral blood in a CLOSED vacutainer --> gram stain, ELISA, FA
**** DO NOT render carcass or do a necropsy if you suspect anthrax --> this will disperse spores and is extremely dangerous to people |
|
|
Term
| How can you treat anthrax? |
|
Definition
if caught early may be amenable to tx (in goats-Penicillin or tetracycline) but animals are often found dead
segregate affected animals to minimize environmental contamination
*** REPORTABLE ZOONOTIC disease |
|
|
Term
| How can you dispose of a carcass with suspected anthrax? |
|
Definition
| complete incineration, bury ashes at least 6 feet underground |
|
|
Term
| Is there a vaccine for anthrax? |
|
Definition
YES
*** need state vet permission to use, and only recommended for use in endemic areas. Generally only used in cattle (associated with injection site reactions in horses) |
|
|
Term
| What is the most common manifestation of brucellosis in horses? |
|
Definition
Fistulous Withers (aka supraspinous bursitis)
*** also associated with poll evil (atlantal bursitis) |
|
|
Term
| How can you prevent brucellosis infection in horses? |
|
Definition
limit horse and cattle commingling
isolate affected animals and minimize environmental contamination, fomite transmission (tack, brushes) and control mechanical vectors (flies) |
|
|
Term
| What is the etiologic agent of vesicular stomatitis, and what clinical signs are associated with the disease? |
|
Definition
caused by a rhabdovirus and associated with fever (generally brief), oral and coronary band ulcerations
*** dz is self limiting and resolves in 1-5 wks (hoof lesions may take longer) |
|
|
Term
| How do you diagnose vesicular stomatitis? |
|
Definition
| serology, PCR, or virus isolation |
|
|
Term
| What is the etiologic agent of infection bovine rhinotracheitis (IBR)? |
|
Definition
BHV-1
*** goats, pigs, and wild ruminants can become infected but are not the natural host for BHV-1 and therefore are unlikely sources of infection |
|
|
Term
| What clinical syndromes are associated with BHV-1 infection in cattle? |
|
Definition
infectious bovine rhinotracheitis (IBR)
conjunctivitis (extension of infection of oral cavity via lacrimal duct, often occurs in conjunction with respiratory disease)
genital form: infectious pustular vulvovaginitis and balanoposthitis (lesions can coalesce to form large necrotic plaques in severe cases)
abortion (secondary to viremia in dam, often occurs late term)
neonatal systemic form (respiratory and GI systems, usually fatal) <-- occurs in calves infected in utero (late gestation) or immediately after birth generally in association with herd outbreaks of respiratory disease and abortion |
|
|
Term
| What type of disease is associated with BHV-5? |
|
Definition
meningoencephalitis <- BHV-5 spreads to the brain via the trigeminal nerve, almost always affects calves <6 months of age
**** vs. EHV-1 causes myeloencephalopathy in horses |
|
|
Term
| What tissues are generally implicated in cases of latent herpesvirus infections in cattle? |
|
Definition
neurons (trigeminal ganglia), lymphoid tissue, and site of primary infection (ex. genital lesions)
*** latently infected animals shed virus without displaying any clinical signs |
|
|
Term
| What are the principal resevoirs for infection of BHV-1? |
|
Definition
| adult cattle (either recently infected or PI) |
|
|
Term
| How is BHV-1 transmitted? |
|
Definition
| shed in respiratory, ocular and genital secretions and transmitted via inhalation, ingestion or venereal |
|
|
Term
| What clinical signs other than fever, tachypnea, and cough are commonly associated with the respiratory form of BHV-1 infection? |
|
Definition
| nasal lesions: hyperemia (aka "red nose"), necrosis and crusting secondary to mucosal ulceration (aka "gold leaf lesion" when involving inner surfaces of nares) |
|
|
Term
| T/F vaccination of a pregnant cow with MLV herpesvirus vaccine can induce abortion |
|
Definition
TRUE
*** retained placentas are common in association with BHV-1 infection |
|
|
Term
| What necropsy findings are associated with encephalitic form of BHV-5 infection? |
|
Definition
intranuclear inclusion bodies on histologic exam of cerebral cortex
** encephalitic form sporatically affects calves <6 months of age |
|
|
Term
| How can you diagnose herpes virus in cattle? |
|
Definition
IHC of aborted fetus or post mortem tissues (tests for viral antigen)
serology (paired samples, 4x rise in titer)
**** remember in horses Dx herpes virus ideally with PCR or virus isolation (nasal swab, post mortem tissues, whole blood/buffy coat) but can also used paired serology |
|
|
Term
| Why is herd vaccination against BHV-1 so important? |
|
Definition
natural immunity (post infection) DOES NOT prevent re-infection or recrudescene and passive immunity from collostrum provides protection against medium challenge for only 4-6 months
*** vaccination will control clinical respiratory disease and abortion but WILL NOT prevent infection |
|
|
Term
| What type of BHV-1 vaccine is safe to use in pregnant animals and does not experience interference from maternal immunity in calves? |
|
Definition
MLV intranasal vaccine --> protective immunity occurs more quickly than MLV IM vaccines
**** virus in intranasal vaccines will only replicate at lower than core body temp present in the nostrils and therefore do not pose any risk of viremia and abortion in pregnant animals |
|
|
Term
| Which species are the natural hosts for blue tongue? Which species develop clinical disease? |
|
Definition
Cattle are natural hosts and act as a source of infection (subclinical with prolonged viremia and decreased reproductive efficiency)
Clinical disease associated with bluetongue is largely restricted to sheep although all ruminants are susceptible to infection |
|
|
Term
| How is bluetongue transmitted? |
|
Definition
the virus naturally cycles between cattle and insect biological (ie. viral replication occurs) vectors (mosquitoes, ticks, flies, and midges)
---> primary vector is culicoides spp. (midges) so disease distribution mirrors geographic distribution of this vector
*** rarely the disease may also be transmitted venereally (shed in semen) as well as transplacentally |
|
|
Term
| What is the pathogenesis of bluetongue infection in sheep? |
|
Definition
| virus replicates in endothelial cells throughout the body --> widespread vasculitis --> edema (esp. face) and necrosis of epithelial and mucosal surfaces throughout the body |
|
|
Term
| What are the primary lesions associated with bluetongue disease in sheep? |
|
Definition
facial edema
oral lesions (petechea, erosions/ulcers)
ulcerative coronitis and laminitis
generalized myopathy
**** tongue cyanosis is actually quite uncommon |
|
|
Term
| What are three DDx for oral lesions in sheep? |
|
Definition
bluetongue
contagious ecthyma (ORF)
Foot and mouth |
|
|
Term
| What is the most important impact of bluetongue infection in cattle? |
|
Definition
| decreased reproductive efficiency: early embryonic death, abortions, still births, congenital birth defects |
|
|
Term
| How do you diagnose bluetongue? |
|
Definition
virus isolation is most definitive (blood collected from febrile animals or post-mortem tissue)
can also do PCR (detect viral RNA) or serology |
|
|
Term
| How do control measures for bluetongue differ in endemic and non-endemic regions? |
|
Definition
prevent disease in non-endemic regions by restricting importation (only accept seronegative animals)
In endemic regions, control vectors and vaccinated ewes and rams with a MLV at least 2 weeks prior to breeding (if you administer the vaccine closer to the breeding date there is a risk of teratogenesis associated with the vaccine) |
|
|
Term
| What are the two types of malignant catarrhal fever? |
|
Definition
African form (wildebeest are reservoir hosts, eitologic agent is alcelaphine herpesvirus 1 and 2)
North American and European form (sheep are reservoir hosts, etiologic agent is ovine herpesvirus 1)
*** NO clinical disease in reservoir hosts! |
|
|
Term
| T/F malignant catarrhal fever occurs sporatically in cattle, but although morbidity is low infection is ALWAYS fatal |
|
Definition
TRUE
**** fatal disease occurs in cattle and cervids |
|
|
Term
| What is the pathognomonic histological lesion associated with malignant catarrhal fever in cattle? |
|
Definition
widespread necrotic vasculitis (esp. epithelial and encephalitic) with lymphocytic cuffing of affected blood vessels
*** also associated with symmetrical lymphadenopathy (non-specific) secondary to viral replication within lymphoid tissues |
|
|
Term
| What are the major clinical signs associated with malignant catarrhal fever? |
|
Definition
corneal edema and erosive cutaneous lesions (secondary to vasculitis)
copious mucopurulent nasal discharge
generalized symmetrical lymphadenopathy (viral replication within lymphoid tissue)
progressive neurologic signs --> death |
|
|
Term
| How do you diagnose malignant catarrhal fever? |
|
Definition
pathognomic histologic lesions (necrotizing vasculitis with lymphocytic cuffing) PCR (OHV-1)
serology- ELISA (OHV-1 and AHV-1 antibodies cross react)
*** remember OHV is associated with north american/european form <--- sheep reservoir
AHV is associated with african form <-- wildebeast reservoir |
|
|
Term
| What is the treatment for malignant catarrhal fever? |
|
Definition
NO TX
symptomatic until diagnosis --> euthanasia |
|
|
Term
| What form of lymphoma and signalment is associated with BLV infection? |
|
Definition
Enzootic lymphosarcoma, disease occurs in adult animals, multiple cases develop within a herd over time
***Vs. sporatic forms (juvenile, thymic, and skin) that affect individual animals and are not of viral origin |
|
|
Term
| What clinical signs are associated with juvenile sporatic lymphosarcoma? |
|
Definition
| occur in cattle <1yr old, present with generalized bilaterally symmetrical lymphadenopathy, weight loss/poor growth and anemia |
|
|
Term
| T/F in adult cattle with sponatneous cutaneous form of lymphosarcoma, lesions may regress and recur and the disease may progress to a generalized/disseminated form |
|
Definition
TRUE
generalized lymphosarcoma secondary to cutaneous lymphosarcoma appears similar to enzootic (BLV associated) form |
|
|
Term
| T/F despite high prevelence of BLV infection, there is little economic significance associated with infection |
|
Definition
TRUE
*** only 1-5% of animals infected with BLV will develop enzootic lymphosarcoma and subclinically infected animals do not have decreased production |
|
|
Term
|
Definition
horizontal transmission by direct contact with infected blood lymphocytes (partuition, blood sucking insects, iatrogenic (rectal sleeves, needles etc.))
and vertical (transplacental and colostrum/milk) |
|
|
Term
| T/F persistant mature lymphocytosis in cattle that are seropositive for BLV represents a preleukemic state, these animals will invariablly go on to develop lymphosarcoma |
|
Definition
FALSE
**** many infected animals >4yrs of age display marked mature lymphocytosis but very few of these animals go on to develop lymphosarcoma (<5%) |
|
|
Term
| What are the most consistent lesions associated with enzootic lymphosarcoma in cattle (BLV)? |
|
Definition
external and internal lymphadenopathy
(tumors may be fluctant, warm and painful on palpation <-- can r/o abscess with FNA)
*** tumors may also infiltrate lumbar spinal canal --> pressure necrosis of spinal cord results in posterior paresis/paralysis (so lymphosarcoma should always be a DDx for downer cows) |
|
|
Term
| What is the most accurate method for diagnosing enzootic lymphosarcoma? |
|
Definition
Dx lymphoma with wedge biopsies of peripheral lymphnodes
can r/o enzootic lymphosarcoma with negative serology titers for BLV (AGID or ELISA with serum or milk)
**** positive titers are not diagnostically useful as many animals infected with BLV DO NOT go on to develop lymphosarcoma (<5%) |
|
|
Term
| What are three methods of controlling BLV transmission (with the goal to eliminate infection from a herd)? |
|
Definition
test and cull seropositive cattle (not always economical/practical, esp. with large population if infected animals)
Test and segregate infected animals into a separate facility (requires frequent serologic testing and may take years to eliminate infection from a herd)
Test an implement corrective management measures (ex. pasturize colostrum, single use rectal sleeves etc.) <-- also requires frequent serologic testing and may take years to eliminate infection from a herd
**** because BLV infection DOESN'T affect production it is generally more economically feasible to implement the last two strategies |
|
|
Term
| What is the most prevelant biotype of BVD virus? |
|
Definition
Noncytopathic
**** responsible for ALL clinical syndromes associated with BVD infection other than mucosal disease (in PI animals), accounts for 90% of isolates, and crosses the placenta to establish PI animals (maintain and spread virus within populations of cattle) |
|
|
Term
| What syndrome is associated with the cytopathic biotype of BVD virus? |
|
Definition
mucosal disease in PI animals
*** thought to arise from a mutation in the non-cytopathic biotype --> induce rapidly fatal disease in host |
|
|
Term
|
Definition
| vertical transplacental infection (50-125 days of gestation) results in PI animals --> PI animals continuously shed virus in ALL bodily fluids/secretions (acutely infected animals also shed) --> horizontal transmission primarily through ingestion or inhalation |
|
|
Term
| What is the pathogenesis of BVD infection in non-PI immunocompetent animals? |
|
Definition
primary viral replication in respiratory epithelium and tonsils --> virus disseminates to epithelial and lymphoid tissues throughout the body --> diarrhea (GI epithelium affected), immunosuppresion (increased susceptibility to secondary bacterial infections), and infertility
**** subclinical or mild infection is most common in non-PI immunocompetent animals |
|
|
Term
| What is the consequence of transplacental infection of BVD between 50-125 days of gestation? |
|
Definition
PI animal
**** immune system is developing at this time so viral antigens are programmed into the system as "self" (ie. immunotolerance) |
|
|
Term
| What is the consequence of transplacental infection of BVD between 125-150 days of gestation? |
|
Definition
congenital abnormalities (esp. cerebellar hypoplasia and occular defects)
*** most likely secondary to immunoinflammatory response to BVD that interferes with fetal organogenesis |
|
|
Term
| What is the consequence of transplacental infection of BVD between 150-270 days of gestation? |
|
Definition
| congenital infection --> late term abortions, still births, or live birth of a seropositive calf (predisposed to developing severe illnesses and associated with lower fertility rates than non-infected heifers) |
|
|
Term
| T/F animals that are persistently infected with BVDV typically develop fatal mucosal disease and die between 6 months to 2 years of age |
|
Definition
TRUE
**** remember, mucosal disease only occurs in PI animals and is associated with spontaneous mutation of the non-cytopathic biotype resulting in development of a cytopathic biotype and fatal disease (profuse watery diarrhea, oral and interdigital erosions) |
|
|
Term
| What clinical signs are associated with mucosal disease in animals with PI BVD? |
|
Definition
profuse watery diarrhea, oral erosions, interdigital/coronal erosions, and severe neutropenia
*** incidences of mucosal disease are generally sporatic but epizootics may occur (associated with acute outbreak of BVD during 50-125 days of gestation so that all calves are born affected by the same strain of virus) |
|
|
Term
| What condition is generally associated with infection of non-cytopathic type II BVD? |
|
Definition
hemorrhagic disease, characterized by thrombocytopenia (<25,000/ul), bloody diarrhea, hyphema, and epistaxis
AND
acute BVD infection of seronegative non-PI cattle (profuse watery diarrhea, often occurs as outbreaks in herds with inadequate vaccination programs) |
|
|
Term
| How can you differentiate acute BVD infection from mucosal disease? |
|
Definition
test for BVD antibodies and monitor neutrophil count (neutropenia is associated with mucosal disease while neutrophilia is associated with acute infection)
*** remember, PI animals are immunotolerant to BVDV so they will NOT develop any antibodies |
|
|
Term
| What necropsy findings are generally associated with BVD infection? |
|
Definition
GI erosions (esp. linear erosions of the distal 1/3 of the esophagus and peyers patches on the antimesentaric side of the jejunum)
secondary bacterial diseases associated with immunosuppresion (esp. fibrinous necrotizing lobar pleuropneumonia) |
|
|
Term
| T/F single titers for BVD are of little value when trying to identify BVD as the causative agent of disease, unless compaired to non-affected individuals on the same farm |
|
Definition
TRUE
*** high prevelance of infection (70-90% of animals are seropositive) with most infections resulting in subclinical or mild disease means that the presence of seropositive animals can only be considered evidence of causation if affected animals have higher titers than unaffected animals on the same farm |
|
|
Term
| How can you identify animals with persistent BVD infection? |
|
Definition
IHC or antigen-capture ELISA of ear notch
**** acutely infected animals do not have a high enough viral load to show up positive using ear notch tissue samples
*** however, post-mortem gut tissue of acutely infected animals will be positive on IHC or antigen-capture ELISA |
|
|
Term
| What are the three most important principles for control of BVD infection? |
|
Definition
Identify and eliminate PI animals from herd (ear notch AG-capture ELISA/PCR, all PI animals should be CULLED)
Limit further introduction of BVD into the herd with biosecurity measures (test all incoming stock, minimize contact with wildlife reservoirs (ex. dear), minimize insect vectors and iatrogenic/fomite transmission
VACCINATE!!!! MLV are most efficacious, for breeding animals vaccinate annually prior to breeding (prevent viremia during gestation and therefore prevents development of PI calves) **** vaccination will NOT reduce incidence of mucosal disease |
|
|
Term
| What are the two most important leptospirosis serovars in cattle? |
|
Definition
L. interrogans serovar pomona (cattle are incidental hosts --> acute, severe disease)
L. borgpetersenii var. hardjobovis (host adapted --> chronic insidious disease and PI in renal tissue) |
|
|
Term
| What is the most important source of infection and mode of transmission for leptospirosis in cattle? |
|
Definition
urine is most important source of infection (L. hardjo persists in renal tissue for months) --> bacteria enter the body via cutaneous and mucosal abrasions or direct penetration of moist skin
*** venereal and transplacental infection is rare but possible |
|
|
Term
| What organ is the site of rapid proliferation following cutaneous or mucosal penetration by leptosirosis organisms? |
|
Definition
|
|
Term
| What is the pathogenesis of disease associated with leptospirosis infection in cattle? |
|
Definition
septicemia and bacterial toxins cause vasculitis, hepatic necrosis, renal tubular damage, and agalactica.
In young calves (<6 months) hemolysin toxin causes intravascular hemolysis, hemolytic anemia, and hemoglobinuria |
|
|
Term
| What organ is associated with persistant infection of leptospirosis in cattle? |
|
Definition
kidney
*** as humoral immune system kicks into action in response to septicemia the bacteria localize within the renal parenchyma causing interstitial nephritis with persistent shedding of organisms in the urine |
|
|
Term
| In addition to signs of septicemia and intravascular hemolysis, what other organ system is commonly affected in small ruminants with leptospirosis? |
|
Definition
|
|
Term
| How do you diagnose leptospirosis in ruminants? |
|
Definition
microscopic agglutination test with paired acute and convalescent serology titers
*** dark-field microscopic examination of urine is possible for diagnosis of infection in acute phase and prior to treatment |
|
|
Term
| What is the treatment for acute infection and elimination of carrier status for animals infected with leptospirosis? |
|
Definition
ceftiofur or oxytetracycline for acute stages (if tx early can prevent irreversible liver and kidney damage, hemolytic anemia, establishment of carrier status, and subsequent abortion) <-- may require additional supportive care (transfusion, IV fluids etc.)
eliminate carrier status with single high dose of long active oxytetracycline |
|
|
Term
| How can you minimize leptospirosis infection in cattle? |
|
Definition
| Minimize exposure to wildlife reservoirs and contaminated water sources Vaccinate (multiple serovar bacterin vaccines - must be boostered every 6-12 months depending on exposure) + urine screening + long acting oxytetracycline (eliminate carriers) |
|
|
Term
| T/F Histophilus somni (gram - rod) can be isolated from urogenital and respiratory tracts of normal cattle |
|
Definition
|
|
Term
| T/F although there is very little antigenic variation between strains of histophilus somni there is variation in respect to virulence and primary organ system affected between strains |
|
Definition
TRUE
*** H. somni is associated with a wide variety of clinical syndromes including pneumonia, endometritis, pericarditis, vasculitis + TME, polyarthritis, and septicemia |
|
|
Term
| What signalment of animals are primarily affected by H. somni infection? |
|
Definition
young feedlot cattle (4-12 months), low morbidity but high mortality
*** primary risk factors are stress and mixing of animals from multiple different sources |
|
|
Term
| How is H. somni transmitted? |
|
Definition
| inhalation, ingestion, and venereal |
|
|
Term
| What is the pathogenesis of initial infection by H. somni? |
|
Definition
| colonization of mucus membrane surfaces (esp. respiratory and urogenital) -> organism may localize in many different organ systems including lower respiratory tract (pneumonia), septicemia, and CNE (TME) -> main action of H. somni at site of localization involves inducution of vasculitis and subsequent ischemic necrosis of tissues supplied by affected vasculature |
|
|
Term
| How is H. somni diagnosed? |
|
Definition
usually diagnosed on necropsy (often associated with extensive fibrinous inflammation)
antemortem diagnosis can be made via bacterial culture of blood, CSF, urine, snyovial fluid OR paired serology |
|
|
Term
| How can you treat H. somni infection in cattle (young, feedlot)? |
|
Definition
| isolate affected animals, organism is suscpetible to most antibiotics (often use ceftiofur or florfenicol) but treatment often fails unless disease is recognized early |
|
|
Term
| How can you prevent infection by H. somni in feedlot cattle? |
|
Definition
feed supplemental antibiotics in the first 60 days of the feeding period reduces disease incidence
*** mataphylaxis with long acting antibiotics has no effect on disease incidence |
|
|
Term
| What is the etiologic agent of caseous lymphadenitis? |
|
Definition
corynebacterium pseudotuberculosis - easily identified gram positive coccobacillus
***** ZOONOTIC |
|
|
Term
| How is CLA transmitted between animals? |
|
Definition
| organisms shed in pus can pursist in the environment for long periods of time --> enters niave animals through cutaneous wounds (ex. shearing), mucus membranes, or inhalation |
|
|
Term
| What two syndromes can develop secondary to infection of goats and sheep by corynebacterium pseudotuberculosis? |
|
Definition
External form: firm to fluctuant non-painful peripheral lymphadenopathy with gradual hairloss over the swellings <-- more common in goats
Internal form: usually associated with aerosolization and inhalation --> abscess formation in internal lymph nodes and visceral organs and commonly presents as weight loss + signs associated with failure of affected organ systems <-- more common in sheep
**** abscesses associated with corynebacterium pseudotuberculosis have thick outer walls and thick, non-odiferous pus |
|
|
Term
|
Definition
Gram stain (corynebacterium pseudotuberculosis is a gram - coccobacillus)
culture pus from abscesses (take sample from outer rim (higher oxygen tension) of abscess to ensure live organisms and positive culture)
SHI serum test can be used to monitor exposure of incoming animals when trying to establish a CLA-free herd (titers > 1:256 are generally associated with internal form of disease) |
|
|
Term
| What are the treatment options for animals with CLA? |
|
Definition
isolate ALL suspected cases
you can lance and flush abcesses but no treatment will eliminate infection, for flocks with low incidence of disease CULLING may be the best option |
|
|
Term
| Is there a vaccine for CLA? |
|
Definition
YES --> reduces morbidity but does NOT prevent infection, vaccinated animals may be positive on SHI test (but high titers will persist longer in naturally infected animals)
*** recommended for use in endemic herds, serious liability issues when used in off label species |
|
|
Term
| What is the etiologic agent of caprine arthritis encephalitis (CAEV) and what is the most common result of infection? |
|
Definition
goat specific lentivirus --> primarily causes subclinical infection + decreased milk production
*** prolonged prepatent period --> clinical disease manifests as progressive polyarthritis and mastitis in adults and progressive pelvic limb paresis/paralysis in kids |
|
|
Term
|
Definition
most important mode of transmission is horizontal via direct contact with body fluids, also venereal (semen) and potentially fomites
vertical transmission occurs secondary to ingestion of infected colostrum/milk and direct contact with body fluids between doe and kids |
|
|
Term
| How does immunity (ie. immune status of the patient) and disease challenge contribute to development of disease in the patient? |
|
Definition
| If a patient is faced with a strong disease challenge clinical disease may occur despite strong immunity...while an immunocompromised patient may develop clinical disease even with a low disease challenge |
|
|
Term
| What regulatory agencies monitor and license veterinary vaccine products? |
|
Definition
USDA, APHIS, CVB (center for veterinary biologics)
*** ensure that produces are pure, safe, potent (ie. good for entire stated shelf life) and efficacious |
|
|
Term
| What element of disease protection is described in the preventable fraction? |
|
Definition
| preventable fraction describes the severity of the disease challenge |
|
|
Term
| What terms must be present for a vaccine to be granted conditional licensure (good for 1 yr)? |
|
Definition
medical need with no other products currently on the market, demonstrated to be pure, potent, and safe
BUT
indication of efficacy is not complete
ex. west nile vaccine |
|
|
Term
| What are the four main claims you will find on a vaccine label? |
|
Definition
Prevention of infection: very rare, product must prevent all colonization and replication in challenged vaccinated animals
Prevention of disease: highly effective at preventing disease in challenged vaccinated animals, confidence interval must be at least 80% (ex. Rabies)
Aid in disease prevention <-- most common
Aid in disease control: shown to alleviate disease severity, reduce disease duration, or delay disease onset |
|
|
Term
| What are the core equine vaccines? |
|
Definition
clostridium
tetanus
Rabies
EEE/WEE
WNL |
|
|
Term
| What is the function of an adjuvant? |
|
Definition
| adjuvants stimulate inflammation to enhance antigen presentation and also act to improve antigen stability in killed vaccines |
|
|
Term
| What are some advantages and disadvantages to using killed vaccines? |
|
Definition
use heat, chemical, or radiation treatment to kill the virus/bacteria --> no potential for reversion to virulence and therefore safe to use in pregnant and immunocompromised animals
because organism is killed requires a large amount of antigenic material and an adjuvant to stimulate immune response --> associated with vaccine reactions and higher cost of production. Killed vaccines require boostering for optimum protection |
|
|
Term
| What is the difference between a toxoid vaccine and anti-toxin? |
|
Definition
toxoid vaccines are chemically inactivated bacterial toxins --> highly effective for prophylaxis prior to exposure and induce active immune response (ex. tetanus toxoid vaccine)
Anti-toxin is a blood product - in the case of tetanus anti-toxin, derived from hyperimmune equine serum and confers immediate passive immunity for a short duration (there is a risk of developing serum sickness) <-- use anti-toxin in animals with potential exposure and unknown vaccine history |
|
|
Term
| What are some advantages and disadvantages to using a MLV vaccine? |
|
Definition
virus is grown on cells of non-target species so that it evolves greater virulence for these non-target species cells and looses the capacity to infect the target species.
Because these vaccines do not require adjuvants they are generally less expensive to produce and are associated with fewer adverse reactions. They also induce a more robust immune response that killed vaccines and do not need to be boostered as frequently.
Although reversion to virulence in target species is unlikely it is a risk associated with MLV vaccines. These vaccines are not as safe to use in pregnant or immunocompromised animals and have a short shelf life after reconstitution (~1hr) |
|
|
Term
| What are some advantages and disadvantages to using a subunit vaccine? |
|
Definition
safety is similar to killed vaccines (safe in pregnant and immunocompromised) and induces a very focused immune response to a specific antigen
often requires adjuvant (more expensive to produce and associated with increased adverse reactions) |
|
|
Term
| What is the best site for administering vaccines in horses? |
|
Definition
neck (between base of nuchal ligament, slope of shoulder, and above cervical vertebrae)
**** can also administer in semi-membranosis and tendonosis and pectoral muscles |
|
|
Term
| How should you store and administer vaccines? |
|
Definition
Refrigeration is good
Freezing, heating and mixing (esp. MLV w/ killed <-- adjuvant will kill MLV vaccine) are BAD |
|
|
Term
| What is the treatment for any animal diagnosed with CAEV? |
|
Definition
humane euthanasia (esp. kid form <- leukoencephalomyelitis)
palliative tx with NSAIDs can be considered for adult polyarthritis form
**** NO effective therapy to clear infection and NO effective vaccines |
|
|
Term
| What type of WBC is most commonly elevated in small ruminants with CAEV? |
|
Definition
lymphocytes --->
kid leukoencephalomyelitis (increased monocytes and lymphocytes in CSF cytology and CNS tissue histology)
polyarthritis (1,000-20,000 lymphocytes on cytology of synovial fluid)
mastitis (lymphoid follicles around ducts) |
|
|
Term
| T/F a positive result from a CAEV ELISA definitively diagnoses CAEV as the cause of clinical disease in that patient |
|
Definition
FALSE
**** positive ELISA only indicates infection, concurrent non-related disease could account for observed clinical signs
*** diagnosis of CAEV requires integration of serologic test with cytology (lymphocytosis), histopathology, herd history, and lack of response to therapy |
|
|
Term
| Is there a vaccine for CAEV? |
|
Definition
NO
*** and no effective therapy either |
|
|
Term
| Given the lack of an effective vaccine or therapy for CAEV, what control measures can be taken to reduce disease incidence and transmission? |
|
Definition
Attend all kiddings and remove kids from doe immediately following partuition (spread through direct contact) --> feed kids heat treated or pasturized colostrum
Maintain CAEV positive animals in a separate facility from CAEV negative, and milk negative animals first
Routinely test all adult animals every 6-12 months with CAEV ELISA |
|
|
Term
| What is the etiologic agent of ovine progressive pneumonia virus (OPPV) and what two clinical syndromes are associated with infection? |
|
Definition
lentivirus -->
most common manifestation of infection is interstitial viral pneumonia w/ cachexia and lymphocytic mastitis
less commonly manifests as progressive proliferative arthritis and nonsuppurative encephalitis |
|
|
Term
| What is the major route of transmission for OPPV? |
|
Definition
horizontal transmission via direct contact and aerosolized saliva from infected sheep
*** VS. CAEV --> primary route of transmission is through milk/colostrum + horizontal transmission also occurs |
|
|
Term
| What clinical signs are associated with OPPV infection? |
|
Definition
hardbag (diffusely firm udder, bilaterally symmetrical, scant milk is produced but appears normal)
dyspnea (lungs are grossly enlarged with rib impressions on necropsy, often secondary bacterial pneumonia)
cachexia (r/o HOT complex, internal CLA, johne's etc.) |
|
|
Term
| How can you diagnose OPPV? |
|
Definition
gold standard is immunoprecipitation
Serology (AGID or ELISA) and histopathology of lung or mammary biopsy are more commonly used in the field |
|
|
Term
| What are the three options for controlling OPPV? |
|
Definition
depopulate and restock with OPPV free animals
test and cull seropositive animals (~6-12 months)
Test and separate managing OPPV free and OPPV infected animals as two separate flocks. Remove lambs from positive ewes at birth and continue monitoring OPPV negative flock for any incidence of disease |
|
|
Term
| List these species in order to vulnerability to anthrax: goats, sheep, horses, cattle |
|
Definition
| cattle and sheep > goats and horses |
|
|
Term
| What the the cause of most pathology associated with clostridial infections in small ruminants? |
|
Definition
exotoxins
*** many clostridial diseases can be effectively prevented with immunization against major bacterial toxins |
|
|
Term
| T/F Clostridial organisms are part of normal GI flora, and dormant spores of often present in many body tissues (liver, spleen, skeletal muscle) |
|
Definition
TRUE
*** culture of clostridial organisms from a necropsy specimine do NOT indicate clostridium as causative disease agent, C. novyi is most common cadaverous clostridial species |
|
|
Term
| What is the etiologic agent of pulpy kidney disease in feedlot lambs? |
|
Definition
Clostridium perfringens type D
** component of normal intestinal microflora |
|
|
Term
| What is the pathogenesis of pulpy kidney disease? |
|
Definition
| unvaccinated ewes and lambs on lush pasture or high concentrate diet --> rumen acidosis with transloation of C. perfringens type D into circulation --> production of epsilon toxin (necrotizing and neurotoxic) --> peracute disease, often present with sudden death but may display ataxia, stargazing, seizures and progressive depression -> coma |
|
|
Term
| What are some differential diagnoses for pulpy kidney disease/enterotoxemia/overeating? |
|
Definition
Polioencephalomalacia
Pneumonic Pasteurellosis
Systemic Pasteurellosis
Acidosis (grain overload)
Nematodirosis |
|
|
Term
| What is the most common gross lesion appreciable on goats that have died secondary to enterotoxemia/pulpy kidney disease? |
|
Definition
fibrinohemorrhagic enterocolitis (dark purple intestine, appreciable from serosal surfaces)
**** VS. lambs, more commonly have CNS lesions, focal symmetrical encephalomalacia |
|
|
Term
| T/F the best way to prevent clostridial disease is vaccination |
|
Definition
TRUE
*** vaccination in the face of an outbreak is helpful for these diseases. Immunity from vaccination is not long lived, recommend twice yearly booster. |
|
|
Term
| What is the etiology and pathogenesis of necrohemorrhagic enteritis in young beef cattle and lambs? |
|
Definition
| ingestion of C. perfringens type C or A from the environment -> lack of proteases in neonatal GI tract allow for rapid reproduction and production of beta toxin --> induces necrosis of abomasal and intestinal epithelium --> hemorrhagic diarrhea |
|
|
Term
| What are some common denominators in patients that develop enteric clostridial overgrowth? |
|
Definition
| overfeeding + anything that slows gut motility ---> clostridial overgrowth and production of toxins ---> clinical disease |
|
|
Term
| What is the etiologic agent and clinical appearance of an animal with tetanus? |
|
Definition
Clostridium tetani enters the body through cutaneous wounds -> muscle rigidity and hyperesthesia progressing to respiratory arrest
*** Prevent through vaccination! |
|
|
Term
| What etiologic agents are associated with clostridial myonecrosis (blackleg, malignant edema, gas gangrene)? |
|
Definition
Clostridium chauvoei, C. septicum, C. sordellii and mixed infections
*** spores are ingested and remain dormant in skeletal muscle until some episode creates a region of localized anarobiosis (ex. bruising, shearing, IM injections etc.) resulting in sporulation and active infection |
|
|
Term
| How do you diagnose clostridial myonecrosis (blackleg, malignant edema, gas gangrene)? |
|
Definition
crepitating muscle in a live animal
gram stain, FA, or culture (anaerobic) of aspirated exudate or muscle tissue biopsy |
|
|
Term
| How can you treat clostridial myonecrosis in horses and valuable cattle? |
|
Definition
extensively debride wounds (to expose anaerobic organism to air)
can administer anti-toxins if specific clostridial species is identified
IV penecillin, NSAIDs, and analgesics |
|
|
Term
| What is the etiologic agent and pathogenesis of bacillary hemoglobinuria? |
|
Definition
toxins of Clostridium hemolyticum (novyi type D)
spores are ingested during grazing --> absorbed in intestine and transported to the liver where they persist within kupffer cells (hepatic macrophages) for long periods of time in an incative state as long has normal tissue perfusion and oxygenation is maintained |
|
|
Term
| How does liver fluke migration initiate sporulation and production of toxins by C. hemolyticum spores in the case of bacillary hemoglobinuria in cattle, and C. novyi in the case of Black disease in sheep? |
|
Definition
| liver fluke migration causes localized anaerobiosis allowing spores to germinate and produce toxins (beta, eta, theta <-- bacillary hemoglobinuria) |
|
|
Term
| What three toxins are produced by C. hemolyticum in the case of bacillary hemoglobinuria? |
|
Definition
beta toxin (necrotizing and hemolytic)
eta toxin (tropomyosinase)
theta toxin (lipase) |
|
|
Term
| What history and clinical signs are strongly suggestive of bacillary hemoglobinuria? |
|
Definition
| endemic area with history of liver fluke infestation, herd vaccination for clostridium is overdue or non-existent, previously healthy animals found suddenly dead with bleeding at mucus membranes |
|
|
Term
| What is the pathognomonic lesion associated with bacillary hemoglobinuria on necropsy? |
|
Definition
| lesions of coagulation necrosis with a zone of hyperemia at interface with viable liver tissue |
|
|
Term
| What three prevention techniques can be used to reduce the incidence of bacillary hemoglobinuria in ruminants? |
|
Definition
burn,bury, or remove carcasses (reduce environmental contamination)
vaccinate
implement liver fluke control measures |
|
|
Term
| What disease in sheep is very similar to bacillary hemoglobinuria in cattle? What is the etiologic agent? |
|
Definition
Black disease, caused by C. novyi type B
vs. bacillary hemoglobinuria <-- caused by C. hemolyticum novyi type D
*** both cause regions of coagulation necrosis surrounded by zones of hyperemia in the liver and are associated with liver fluke migration |
|
|
Term
| T/F there are vaccines for clostridial diseases |
|
Definition
TRUE
*** they are cheap and effective, for the love of god please vaccinate you cheapskate |
|
|
Term
| What disease syndromes are associated with mycoplasma infections in cattle? |
|
Definition
| abortion, keratoconjunctivits, mastitis, pneumonia, ottitis media/interna and polyarthritis |
|
|
Term
| Which mycoplasma species are cattle specific? Of these which is most pathogenic? |
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Definition
| M. dispar and M. bovis are both cattle specific, M. bovis is most pathogenic --> mastitis, ottitis, pneumonia/arthritis |
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Term
| What are the most common routes of transmission of mycoplasma bovis (TB)? |
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Definition
| contamination of milking devices is most common route of transmission but also ingestion of mastitic milk by calves, direct nose to nose contact and aerosol |
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Term
| T/F although mycoplasma is commonly isolated in association with other respiratory pathogens (M. haemolytica, P. multocida, H. somni, IBR, BVDV) respiratory disease has been induced both naturally and experimentally with only M. bovis infection |
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Definition
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Term
| What is the pathogenesis of disease associated with mycoplasma infection in cattle? |
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Definition
organism damages respiratory epithelium + impaires function of pulmonary macrophages, B and T lymphocytes --> predisposes affected animals to secondary bacterial infections
Mycoplasma bovis has an inflammatory toxin that activates complement and increases vascular permiability -> hematogenous spread to joints and local spread from tonsils to inner ear |
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Term
| What is the mechanism of marked neutrophilia and weight loss associated with Mycobacterium bovis infection? |
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Definition
| organisms induce a strong TNF response |
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Term
| What are the three common clinical syndromes associated with Mycoplasma bovis infection? |
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Definition
| Pneumonia and polyarthritis in dairy calves: often associated with ingestion of mastitic milk, horizontal transmission is also possible Pneumonia and polyarthritis in feedlot calves: associated with weather and management stresses, large rotary joints are most frequently affected and result in poor weight gain or weight loss Ottitis media/interna: affects beef and esp. dairy calves. Ingestion or horizontal spread with tonsilar colonization --> local extension of infection to inner ear results in cranial nerve damage, lacrimation, and drainage from external ear in association with pneumonia and conjunctivtis |
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Term
| What postmortem lesions are associated with mycoplasma bovis infection? |
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Definition
Cranioventral lung consolidation, miliary to large pulmonary abcessation with lymphocytic infiltrate on histopath
fibrinosuppurative synovitis
purulent ottitis media/interna |
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Term
| How can you diagnose mycoplasma bovis? |
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Definition
positive culture of M. bovis from joint or lung (positive culture of mycoplasma sp. from lung or nasal swab is NOT diagnostic)
paired serology for herd assessment
PCR and IHC are also options |
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Term
| What drugs are used to treat Mycoplasma bovis infection in cattle? |
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Definition
| tulathromycin and florfenicol metaphylxis for high risk animals are effective at limiting M. bovis replication and disease |
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Term
| What mechanisms can be used to help control Mycoplasma bovis infections? |
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Definition
| Best means of control is to buy disease free cattle from reputable sources Vaccines are available but strain variation makes commercial vaccines less efficacious than autogenous vaccines metaphylaxis for at risk animals |
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Term
| What is the etiologic agent of Bang's disease/undulant fever? |
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Definition
Brucella abortis
Bang's disease causes abortions in cattle, undulant fever causes severe flu-like symptoms in humans |
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Term
| How is B. abortis transmitted to people? to cattle? |
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Definition
to people --> unpasturized milk or direct contact with placental tissues, vaginal secretions, blood, or urine to
cattle --> usually ingestion of aborted tissues or infected milk (calves) but venereal transmission is also possible through both natural service or artificial insemination |
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Term
| What is the pathogenesis of B. abortis infection in cattle? |
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Definition
| organism enters through mucus membranes of oral cavity, conjunctiva, nasal cavity, or cutaneous wounds (or ingestion of infected milk in calves) --> proliferation in regional LN --> bacteremia which eventually localizes to uterus, udder, and associated LN --> inflammation of uterus and placenta causes fetal death and abortion (usually in last trimester), retained placenta/metritis is common *** often infected cattle have no obvious clinical signs |
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Term
| How do you diagnose and treat B. abortis in cattle? |
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Definition
Dx: serology using blood from cow or peritoneal fluid from aborted fetus. Can also culture fetus, placenta, or milk
Tx is NOT allowed due to eradication program (but long acting oxytetracycline is effective) |
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Term
| What two surveillance procedures are in place for the brucellosis eradication program? |
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Definition
Market cattle identification: serologic testing at stockyards and slaughter
Brucellosis ring test: tests bulk milk from dairy herds 2-4x yearly (positive sample is identified by blue ring (blue stained antigen is added to the milk) at milk/cream interface |
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Term
| T/F there is a vaccine for Brucella abortis |
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Definition
| TRUE vaccine is administered only to female cattle and vaccinated animals are identified with USDA ear tag and tattoo in right ear *** vaccinated animals do NOT test positive on serology |
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Term
| What is the result of a positive responder to either the MCI or BRT serveillance tests for brucellosis? |
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Definition
quarantine all infected or exposed animals
test all animals in the herd and cull infected or depopulate
test all herds in a 1 mile radius from positive herd and all herds that have received animals from infected herd
must have 3 consecutive negative herd tests to be considered brucella free (30 days, 6 months, 24 months) |
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Term
| T/F people can contract anthrax and brucellosis from eating undercooked meat |
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Definition
FALSE
you can get anthrax from eating undercooked meat (but you shouldn't be rendering anthrax suspects anyway) but you cannot contract brucellosis from undercooked meat (transmission via ingestion of unpasturized milk products or direct contact with infected fetus/placenta) |
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Term
| What is the etiologic agent of bovine tuberculosis and what microbial characteristics does this organism display? |
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Definition
Mycobacterium bovis (broadest host range and most infectious of all mycobacterium sp.)
intracellular gram positive acid fast rod, survives in macrophages --> granulometous inflammation, long incubation period and can survive in the environment for months |
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Term
| How is mycobacterium bovis transmitted? |
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Definition
organism is shed in respiratory secretions, milk, and manure
disease is spread primarily via direct contact and ingestion, transmission is enhanced by crowding and stress |
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Term
| What is the pathogenesis of bovine tuberculosis? |
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Definition
| primary complex-lesion occurs at point of infection (pulmonary or intestinal LN) --> calcification of primary focus within 2 wks --> lesion progresses to granuloma with necrotic center --> organism spreads to adjacent LN (if associated with blood vessels organisms may be shed into circulation resulting in metastatic granulometous foci that disrupt organ function) |
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Term
| What clinical signs are associated with bovine tuberculosis? |
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Definition
Most cases are assymptomatic despite advanced disease
other common presentations include respiratory form (dyspnea, cough) and generalized form (hematogenous dissemination, signs are associated with specific organ dysfunction secondary to infiltrating granulometous lesions, often cachexia and fluctuating pyrexia) |
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Term
| How do you diagnose bovine tuberculosis? |
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Definition
Caudal tail fold test (intradermal injection of purified tuberculin protein derivative into right caudal tail fold --> same person must read test [visual inspection and palpation] in 72 hours)
report individuals as Negative or Suspect (NOT reactor <-- only for comparative cervical test)
**** need to test all suspect individuals with comparative cervical test |
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Term
| Why is the comparative cervical test a more specific test than caudal tail fold test for identifying individuals infected with mycobacterium bovis? |
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Definition
exposure to other mycobacterium sp., anthelmintics and vaccines can all induce a false positive response to the caudal tail fold test.
Animals identified as suspect on CFT must be tested within 10 days by a state or USDA vet using the comparative cervical test which response to intradermal injection of M. avium (johne's) and M. bovis and will allow for differentiaion between exposure to avian TB, johne's vaccination, cutaneous TB and non TB organisms (ex. nocardia)
*** report animals a Negative, Suspect (retest in 60 days) or Reactor (necropsy <- confirm Dx with culture or PCR of affected tissues) |
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Term
| What is the treatment for bovine tuberculosis? |
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Definition
| TX is NOT allowed due to eradication program (but isonicotinic acid hydrazide is effective in some cases) |
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Term
| What is the consequence of a confirmed bovine tuberculosis reactor on necropsy? |
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Definition
| herd of origin is quarantined and must either depopulate or pass two consecutive herd tests 60 days apart followed by a third check in 6 months <-- herds are accredited free when all animals over 24 months of age pass to consecutive annual tests |
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