Term
| What is the etiologic agent of plague? |
|
Definition
| Yerseinia pestis <-- sensitive to desiccation and heat but may persist in the environment (within organic material, ie. carcasses) for years if maintained at cold or freezing temperatures |
|
|
Term
| how is plague transmitted? |
|
Definition
rodents are naturally resistant and act as a reservoir, the bacteria is transmitted by fleas. Dogs tend to have subclinical to mild infection and can serve as a secondary reservoir but cats are highly susceptible (respond to infection like people)
*** cats (esp.) and dogs, can also be exposed though ingestion of infected rodents bypassing the flea vector. Also possible to transmit the bacteria through mucus membrane/broken skin contact or droplets (pneumonic plague <-- WORST PROGNOSIS!!!) |
|
|
Term
| Where in the US in plague a concern? |
|
Definition
SW (new mexico, arizona, utah, colorado) <-- semi arid, cooler climates adjacent to deserts + year-round rodent flea activity
*** always ask travel history when evaluating a sick pet!!! |
|
|
Term
| When should you consider plague as a differential diagnosis? |
|
Definition
| ANY febrile cat travel to, or living in an endemic area (SW USA - arizona, new mexico, utah, colorado) |
|
|
Term
| What are the three clinical forms of plague? Prognosis and presentation? |
|
Definition
bubonic <-- most common, best prognosis, presents as pyrexia, and lymphadenopathy with abscessation and drainage
septicemic <- rapidly fatal due to septic shock (1-2 days), may be concurrent with bubonic form, most common organ implicated in cat are the lungs
Pneumonic <- worst prognosis, primary droplet transmission or secondary extension from bubonic or hematogenous forms |
|
|
Term
| How do you diagnose plague? |
|
Definition
suspicion based on signalment (geography (SW US), fever +/- lymphadenopathy, exposure to rodents)
FNA of affected tissue yields a monomorphic population of gram negative "safetey pin" organisms
can also submit purulent material for culture, do paired serology, and r/o pneumonic form with thoracic rads
*** always begin antimicrobial therapy before diagnosis is confirmed if you suspect plague based off signalment. Expedient treatment is best hope for recovery. |
|
|
Term
| How do you treat bubonic plague? |
|
Definition
isolate for 48-72 hours (longer in pneumonic) and use protective gloves, gowns and face masks.
eliminate any fleas if found, lance abscessed lymph nodes and flush with nolvasan --> dispose as dangerous medical waste
systemic antibiotics (cholramphenicol *esp. if CNS involvement* or aminoglycosides *caution with renal disease* treat for a minimum of 3 weeks, and well past resolution of clinical signs. For exposed animals 1 week of prophylactic tetracycline is effective.
clean all in contact surfaces with routine disinfectants
*** Yersinia is sensitive to beta-lactam antibiotics in vitro but RESISTANT in vivo - do not use for tx of patient! |
|
|
Term
| How can you prevent animals from contracting plague? |
|
Definition
flea control, eliminate contact with rodents (burrows and/or carcasses), expedient identification of potential cases with appropriate action (isolation and disinfection of fomites)
**** vaccines are ineffective, none are currently approved for use |
|
|
Term
| If you diagnose a pet with plague what public health risks exist for the owners? |
|
Definition
| The owners may have been exposed (remember Yersinia is transmited through fleas, mucus membrane/broken skin, and droplet (pneumonic)) ---> plague is highly contagious and mortality with tx in humans is still 15-22%, so all potentially exposed individuals must contact their physician for evaluation |
|
|
Term
| What is the eitologic agent of leptospirosis? |
|
Definition
Leptospira interogans --> many serovars with different primary host species can affect dogs (incidental hosts -> increased severity of disease, reduced duration of shedding) and clinical signs and prognosis do depend on the specific serovar, however treatment is the same regardless
** cats will seroconvert (ie. positive antibody titers) but tend to have subclinical self limiting infections |
|
|
Term
| How is leptospirosis transmitted? |
|
Definition
major mode of transmission is URINE (organism persists within renal tubules), either directly or via contact with contaminated beddind, food, or water sources
if the patient is septicemic lepto can also be transmitted venereally, transplacentally, via bite wounds, and ingestion of infected material/tissue |
|
|
Term
| What is the optimum time for leptospirosis infections to develop in the upper midwest? |
|
Definition
| late summer, early fall <-- associated with high rainfall and temperate ambient temperature |
|
|
Term
| What is the pathogenesis of lesions caused by leptospirosis? |
|
Definition
the bacteria can penetrate intact mucous membranes or abraided/macerated skin -->
7 day incubation period -->
replication and persistence within renal tubular epithelial cells with shedding in the urine 2 weeks post infection +/- hepatic necrosis depending on the specific serovar that is implicated in the infection (esp. icterohemorrhagia and pomona, and younger dogs tend to have more hepatic involvement) |
|
|
Term
| T/F any dog with hepatic dysfunction or fibrosis should be tested for leptospirosis |
|
Definition
TRUE
*** icterohemorrhagiae and pomona are most commonly implicated serovars with hepatic involvement |
|
|
Term
| What is the most common presentation of a patient with leptospirosis? |
|
Definition
fever
ARF and/or hepatitis with icterus
+/- secondary vasculitis ("lepto lungs" ie. pulmonary hemorrhage and edema, primary hemostatic defects (petechial hemorrhages, bleeding mucus membranes) and risk of DIC) |
|
|
Term
| What is the most consistent hemogram finding associated with leptospirosis? |
|
Definition
thrombocytopenia
*** secondary to vasculitis |
|
|
Term
| What imaging findings are consistent with leptospirosis? |
|
Definition
abd ultrasound --> renomegally with dilated renal pelves and increased cortical echogenicity
thoracic rads --> nodular interstitial to alveolar lung pattern "lepto lungs" secondary to vasculitis with pulmonary hemorrhage and edema |
|
|
Term
| How do you definitively diagnose leptospirosis? |
|
Definition
Dx via microscopic agglutination test (MAT) paired titers (may be negative up to 10 days post infection) or PCR
*** remember, vaccination will affect serology results- interpret elevated titers in light of vaccination history |
|
|
Term
| How do you treat leptospirosis? |
|
Definition
acute disease --> parentral ampicillin (stops active organ injury and infection, stops urinary shedding but only when being giving ie. "on board")
Dx carriers with urine PCR and tx with doxycycline BID for 2 weeks |
|
|
Term
| What is the prognosis for patients with leptospirosis? |
|
Definition
| with expedient diagnosis and treatment most will survive. Severity of disease depends on serovar however, and although patients may survive acute disease process 50% will develop chronic renal disease and potentially chronic hepatitis. |
|
|
Term
| How can you prevent leptospirosis? |
|
Definition
There is a vaccine that protects against 4 serovars and is recommended for use in endemic areas. It is a killed bacterine vaccine and therefore is associated with more vaccine reactions than MLV --> have patients hang out at the clinic for 30 min after getting the vaccine to monitor for adverse reactions
also advise owners to identify and clean potentially urine contaminated areas at home |
|
|
Term
| What is the etiologic agent responsible for lyme disease? How is this disease transmitted? |
|
Definition
| Borelia burgdorferi <-- cannot survive as free living organisms, require transmission between vertebrate reservoirs and ixodid tick vectors |
|
|
Term
| What is the etiologic agent responsible for lyme disease? How is this disease transmitted? |
|
Definition
| Borelia burgdorferi <-- cannot survive as free living organisms, require transmission between vertebrate reservoirs and ixodid tick vectors |
|
|
Term
| T/F Lyme disease cannot be transmitted from dog to dog |
|
Definition
TRUE
*** requires ixodid ticks as a vector for transmission. Dogs are not likely a source of human infection because once the tick has fed on the dog long enough to transmit the disease it will not take another blood meal, and ticks cannot survive very long indoors. Rather, a dog with Lyme disease indicates that human may have been exposed to ticks carrying the organism. |
|
|
Term
| What bacterial diseases can be transmited by the ixodid tick? |
|
Definition
Rickettsia helvitica
Anaplasma phagocytophilum
Babesia sp.
Borrelia sp.
**** Borrelia and Anaplasma coinfections are common |
|
|
Term
| What is the physiologic mechanism by which the Borellia organisms are transmitted during the course of a blood meal by an ixodid tick? Why does this matter? |
|
Definition
OspA is a protein that keeps the Borrelia organisms attached to the tick's gut epithelium. When the tick commences feeding OpsA is down regulated and a different protein OpsC is expressed. OpsC facilitates attachment of the Borrelia organisms to the tick's salivary glands and to the host's tissues
**** the time it takes to downregulate OspA and upregulate OspC explains why a tick must be attached for ~53 hours to actually transmit the Borrelia organisms. |
|
|
Term
| If you find a tick on your dog, does it mean that your dog probably has Lyme disease? |
|
Definition
NO.
Only 50% of ticks in endemic areas are infected, and most ticks are removed before the organisms are transmitted (must be attached for ~53 hours)
factors increasing your dog's risk of infection --> number of ticks attached and host immunity (even if the organisms are transmitted most infections are subclinical. Immunocompromised --> increased risk of developing clinical disease) |
|
|
Term
| What characteristics permit Borrelia to persist and allow chronic infections to develop? |
|
Definition
| the organism persists in connective tissue, joints, and nervous tissue, and can modify its outer surface proteins and shape (ie. transform from motile spirochetes into sessile spheres in the presence of an adverse environment ie. doxycycline) <-- in this form the organism can survive without nutrition for long periods of time, the animal will not be clinically sick but will be positive on PCR |
|
|
Term
| What is the pathophysiologic mechanism of the clinical signs associated with Lyme disease? |
|
Definition
Host antibodies directed against the Borrelia organism bind to host proteins inciting inflammation (--> fever) and release of cytokines that instigate tissue damage (ex. IL-8 upregulation in joints --> suppurative polyarthritis)
*** when patients are clinical serology will be positive |
|
|
Term
| What is the most common etiology of acute onset polyarthritis? |
|
Definition
Lyme Borreliosis
*** often present with fever as well, remember, serology will be positive in dogs that are clinically sick |
|
|
Term
| If recrudescence of Lyme borreliosis is not common following treatment(*** remember, the bacteria can morph into an inactive sessile form which can result in positive PCR but no clinical disease), why might patients that are positive for Lyme present with chronic polyartritis and lameness? |
|
Definition
| although inciting cause of the polyarthritis (ie. Borrelia spirochetes) is no longer present it is possible for clinically transient inflammation to instigate progressive DJD resulting in chronic joint pathology |
|
|
Term
| Although fever and polyarthritis are by far and away the most common presentation of Lyme Borreliosis, what is the pathophysiology of renal lesions associated with this disease? |
|
Definition
Antibody complex deposition results in development of a protein losing nephropathy. Patients may present as ARF or progressive renal disease; however, any presentation of renal disease associated with Lyme Borreliosis is a negative prognostic indicator and often fatal.
*** other uncommon manifestations of Lyme borreliosis include meningitis, rheumatoid arthritis, and myocardial lesions resulting in arrhythmias (ie. conduction system is normal) |
|
|
Term
| T/F Lyme Borreliosis can cause clinical disease and dogs and cats |
|
Definition
FALSE!!!
although cats can be seropositive no natural exposure has resulted in development of clinical disease in cats. Similar story with cats and leptospirosis (seropositive, asymptomatic to mild self limiting disease)
*** remember, this is opposite of Plague, where dogs are seropositive but with mild disease and cats are exquisitely sensitive to infection |
|
|
Term
| How can you document natural exposure to Borrelia burgdorferi (ie. differentiate from vaccination)? |
|
Definition
measure C6 peptide on serology (SNAP or quantitative titer +/- western blot). C6 peptide is ONLY expressed by Borrelia during upregulation of OspC protein
*** Remember, OspC is associated with attachement of the organisms to the tick's salivary glands and the host tissue, thereby facilitating transmission |
|
|
Term
| T/F although we can confirm natural exposure to Borrelia (vs. vaccine) using C6 peptide serology we cannot confirm that clinical disease is the result of exposure based on serology |
|
Definition
TRUE
*** remember, serology will be positive before clinical signs are evident (3-5 weeks post infection) and will remain positive for LONG periods of time following active infection. If you have a dog with fever and polyarthritis AND positive serology this warrants treatment; however, positive serology alone is NOT a good enough reason to put the dog on doxycycline |
|
|
Term
| What medication is used to treat Lyme Borreliosis and how can you assess your response to therapy? |
|
Definition
Doxycycline (also covers other tick borne diseases which is good because coinfection is likely, esp. with anaplasmosis) +/- NSAIDS or anti-inflammatory doses of glucocorticoids
assess response to therapy via resolution of clinical signs (fever + polyarthritis) plus paired titers (remember, serology remains positive for a long time after resolution of clinical disease, but titers will be much higher during active infection) |
|
|
Term
| Which drugs are NOT effective against Lyme Borreliosis? |
|
Definition
| aminoglycosides and quinolones |
|
|
Term
| What is the best way to prevent ALL tick borne disease? |
|
Definition
Tick control....duh
p.s. Lyme vaccine has questionable efficacy |
|
|
Term
| What are the two species of anaplasma that can cause clinical disease in dogs? |
|
Definition
A. phagocytophilum (resides in neutrophils and occasionally eosinophils)--> canine granulocytic anaplasmosis
A. platys (resides in platelets) --> thrombocytopenia
*** remember, these organisms were recently reclassified as anaplasam from erlichia.... |
|
|
Term
| How long must an ixodid tick be attached to transmit anaplasmosis? |
|
Definition
minimum of 24 hours
*** as opposed to Lyme Borreliosis ~58 hrs, remember, have to upregulate OspC protein for transmission to occur |
|
|
Term
| What are the clinical signs associated with canine granulocytic anaplasmosis? |
|
Definition
non-specific (ie. fever, anorexia, lethargy)
polyarthritis and other musculoskeletal pain is reported, but more common with Lyme borreliosis than anaplasma (remember, coinfections of tickborne diseases are common so test for BOTH) |
|
|
Term
| What clinical signs are associated with infectious canine cyclic thrombocytopenia (ie. anaplasma platys)? |
|
Definition
as the name suggests....cyclic thrombocytopenia (usually occurs within 1-2 week intervals with decreasing severity in each subsequent episode). Degree of thrombocytopenia is generally not severe enough to disrupt normal hemostasis
*** many A. platys infections are subclinical |
|
|
Term
| What is the most specific diagnostic test for active anaplasmosis infection? |
|
Definition
identification of morulas within granulocytes (a. phagocytophilum) or platelets (a. platys) on blood smear
*** however this is not a super sensitive test (ie. you might not appreciate morulas in many infected patients) so a positive serology in association with appropriate clinical signs and response to therapy can be sufficient for diagnosis |
|
|
Term
| T/F serology cannot be used to distinguish between exposure to A. phagocytophilum vs. A. platys |
|
Definition
TRUE-ish
there is considerable cross-reactivity between these two species (ie. SNAP test will not distinguish between these two). However, they can usually be differentiated using quantitative titers ---> A. phagocytophilum usually presents with acute infection (much higher titers) while A. platys is usually diagnosed during the chronic phase (much lower titers) |
|
|
Term
| What is the etiologic agent and vector involved in transmission of Rocky Mountain Spotted fever? |
|
Definition
Rickettsia rickettsii --> transmitted by dermacentor ticks
*** most common in SE US |
|
|
Term
| What body "system" is primarily affected by Rocky mountain spotted fever? |
|
Definition
endothelium --> when damaged results in vasculitis, edema, thrombosis, and infarctive necrosis. Poorly localized pain may be the only presenting clinical sign.
*** need to Dx and treat early to prevent shock, DIC, and multi-organ failure |
|
|
Term
| What is the key to a successful outcome when treating rocky mountain spotted fever? |
|
Definition
| Diagnose and treat EARLY!!! |
|
|
Term
| How can you diagnose rocky mountain spotted fever? |
|
Definition
suggestive presentation (tick exposure, geographic location (esp. SE US), fever and poorly localized pain)
thrombocytopenia on hemogram
definitive dx: serology, PCR, or tissue DFA |
|
|
Term
| Which of the tick transmitted diseases has a zoonotic potential to be transmitted to humans from dogs? |
|
Definition
rocky mountain spotted fever
**** the organism is present in the blood stream for 5-14 days, during this time contact with infected BOOD does pose a risk of zoonotic transmission to humans |
|
|
Term
| What is the main vector for transmission of erlichiosis? |
|
Definition
| brown dog tick +/- lone star tick |
|
|
Term
| What are the most commonly seen atypical bacterial infections in dogs? |
|
Definition
Actinomyces (respiratory and oropharyngeal commensal) and nocardia (ubiquitous in soil) <-- both are filamentous bacteria that produce sulfur granules and cause pathology only in immunocompromised/compromised mucosal barrier defense patients
**** stain with acid-fast to distinguish actinomyces from nocardia |
|
|
Term
| What is the typical clinical presentation of a patient with actinomyces/nocardia infection? |
|
Definition
| fever + pleural effusion, abscesses, and bite wound infections |
|
|
Term
| How do you diagnose and treat actionmyces/nocardia infections? |
|
Definition
Dx on cytology (both are hard to grow on culture)
tx: beta-lactams (nocardia may need sulfas) normally need to tx for weeks to months + surgical drainage of any effusions or abscesses |
|
|
Term
| Although actinomyces and nocardia have a similar clinical presentation they have different prognoses, which disease is associated with a good prognosis? |
|
Definition
Actinomyces is associated with a good prognosis
90% of dogs and 50% of cats diagnosed with nocardia were either euthanized or died |
|
|
Term
| What are the two types of mycobacterium infections in dogs and how does their mode of transmission differ? |
|
Definition
tuberculous (ex. M. bovis) --> transmitted mainly through inhalation but also by cutaneous or fecal-oral route
non-tuberculous (M. avium, jhonnes) --> transmission mainly through oral route (infected carcasses, feces, or soil) |
|
|
Term
| How does the clinical presentation of tuberculous mycobacterial infections differ in dogs vs. cats? |
|
Definition
dogs --> primarily respiratory signs
cats --> primarily GI
Although lesions in both species are associated with granulometous inflammation the different organ trophisms are a result of different mycobacterial species infecting dogs and cats |
|
|
Term
| How does the clinical presentation of non-tuberculous mycobacterial infections differ in dogs vs. cats? |
|
Definition
dogs -> disseminated visceral granulometous dz (vomiting and weight loss)
cats --> SQ granulomas associated with regional lymphadenopathy (although disseminated dz is possible) |
|
|
Term
| How do you diagnose and treat mycobacteria? |
|
Definition
dx: cytology (FNA or rectal scrape)/histopathology of granulometous lesions
tx:combination therapy (ie. rifampin +) however tx is prolonged (months to years) which raises concerns about development of antibiotic resistant strains |
|
|
Term
| Chlamydophila felis are intracellular parasites similar to bacteria. In which cells do they persist, and how can they be transmitted from host to host? |
|
Definition
persist in ocular, respiratory, GI, and urogenital mucosal cells
transmission occurs during partuition, direct contact or aerosol |
|
|
Term
| What is the clinical presentation of chlamydophila feis? |
|
Definition
| conjunctivitis and upper respiratory disease in cats (esp. kittens) --> active shedding for 2-7 months 1 week post ocular inoculation |
|
|
Term
| How do you diagnose and treat chlamydophila felis? |
|
Definition
dx: culture or PCR of conjunctival, rectal and/or vaginal swabs
tx: 3-4 weeks of doxycycline or clavamox. MLV is available, it may minimize shedding although it doesn't prevent clinical disease <-- only recommended for high risk settings like catteries |
|
|
Term
| Which of the hemotrophic mycoplasmas cause the most significant clinical disease in small animals? |
|
Definition
Mycopasma heamofelis --> cyclic hemolytic anemia and fever
**** M. haemominutum only causes clinical signs if coinfection w/ M. haemofelis. M. haemocanis and hematoparvum only cause clinical signs in splenectomized dogs |
|
|
Term
| How do you diagnose and treat hemotrophic mycoplasmas? |
|
Definition
dx: PCR is much more sensitive than identifying organisms on blood smear but is expensive and results are not reported back quickly --> often need to tx empirically
tx: doxycycline or enrofloxacin, in severely anemic animals prednisolone can be used to decrease erythrophagocytosis |
|
|
Term
| What is the reservoir host for Bartonella henselae? What is the incidental host? |
|
Definition
reservoir host --> cats = asymptomatic
incidental host --> humans = cat scratch fever (lymphadenopathy) |
|
|
Term
| How is bartonellosis transmitted? |
|
Definition
via arthropods
ex. fleas transmit feline bartonellosis (B. henselae) |
|
|
Term
| How does canine bartonellosis present? |
|
Definition
B. vinsonii -> vegetative endocarditis, pyogranulometous lymphadenitis, sialadenitis, uveitis etc.
B. henselae --> peliosis hepatis (large blood filled cavities dispersed throughout the liver) |
|
|
Term
| What three drugs can be used to treat canine bartonellosis? |
|
Definition
azithromycin, doxycycline, entrofloxacin
*** positive serology or PCR may not be correlated with clinical disease |
|
|
Term
| T/F many dogs are asymptomatic carriers of salmonella and campylobacter and can serve as reservoirs for the disease |
|
Definition
|
|
Term
| Which of the atypical bacterial infections are anthropozoonosis (ie. humans can infect animals)? |
|
Definition
| salmonella and campylobacter |
|
|
Term
| What characteristic appearance do campylobacter organisms have on cytology (of fecal smear)? |
|
Definition
|
|
Term
| What are the host species for tularemia and how are dogs and cats infected? |
|
Definition
host species are rabbits and rodents
cats (most susceptible to clinical infection) and dogs are exposed through predatory behavior (ie. consumption of infected meat)
*** can also be transmitted via bite wounds, ticks (biologic vectors), biting flies (mechanical vectors) and ingestion of contaminated soil |
|
|
Term
| What are the clinical signs associated with tularemia in cats (remember, dogs are relatively resistant to infection)? |
|
Definition
| multifocal granulometous inflammation and necrosis --> fever, lymphadenopathy, hepato-splenomegally, panleukopenia, oral ulcers |
|
|
Term
| T/F an effective treatment for tularemia is not well elucidated for veterinary species |
|
Definition
TRUE
*** streptomycine or gentamicin is recommended in people. May consider doxycycline, chloramphenicol or enrofloxacin as an alternative to aminoglycosides |
|
|
Term
| If a little cat was biting your nose what four infectious diseases should you worry about contracting? |
|
Definition
actionmycosis (pleural effusion, abscesses, bite wound infections)
bartonellosis (cat scratch fever --> lymphadenopathy, fever, endocarditis, uveitis)
chlamydiosis (conjunctivitis/URI)
tularemia (multifocal granulomas + necrosis) |
|
|
Term
| Although clinical signs associated with canine ehrlichiosis vary depending on the species involved, which three clinical signs are most consistently appreciated in the acute phase of the disease? |
|
Definition
| fever, thrombocytopenia and leukopenia (10-20 days post infection) ***other clinical signs that can present include CNS signs and ocular hemorrhage. Very similar in clinical presentation to Rocky Mountain Spotted Fever (differentiate on serology) |
|
|
Term
| What two signs are most commonly appreciated in dogs with chronic ehrlichiosis? |
|
Definition
hemorrhage (associated with thrombocytopenia)
anemia (looks like IMHA, some are even Coomb's positive) |
|
|
Term
| What findings might you see on a blood smear of a patient infected with ehrlichia canis or chaffeensis? How might these findings differ if your patient was infected with ehrlichia eqingii? |
|
Definition
E. canis and cheffeensis --> morulae in monocytes
E. ewingii --> morulae in neutrophils |
|
|
Term
| What chemistry finding would indicate active ehrlichiosis infection and therefor justify treatment? |
|
Definition
hyperglobulinemia (polyclonal or monoclonal <-- don't confuse with lymphoma or multiple myeloma)
+/- hypoalbuminemia (negative acute phase response or potentially associated with protein loosing nephropathy) |
|
|
Term
| How can you diagnose ehrichiosis? |
|
Definition
antibody serology (IFA or ELISA) or PCR (only positive when patients are bacteremic) +/- morulae on blood smear
*** different species of ehrilchia cross-react on serology but will not cross react with other tick borne disease (Rickettsia, Babesia, Anaplasma) |
|
|
Term
| How do you treat ehrlichiosis and how can you confirm effective clearance of the organism? |
|
Definition
tx --> doxycycline (quinolones will cause clinical and lab value improvement but will NOT clear infection)
After effective tx SNAP test may remain positive for years, if hyperglobulinemia progressively declines and PCR is negative (ie. r/o re-infection, Ab are not protective), you can assume tx has been successful |
|
|
Term
| Which species of ehrlichia can cause severe disease in humans (meningoencephaitis, ARF, acute respiratory failure)? |
|
Definition
| E. chaffeensis (remember, morulea in monocytes) |
|
|
Term
| T/F although cats can become infected with ehrlichia and develop morulae within lymphocytes, monocytes, ad granulocytes, clinical disease associated with ehrlichia infection is not a major concern |
|
Definition
TRUE
**** so of all the tick borne diseases, none of them are a big deal in cats....Plauge however kils cats but doesn't affect dogs too bad |
|
|
Term
| What are the three methods of developing clinical disease due to botulism? |
|
Definition
Ingestion of pre-formed botulinum toxin in spoiled food is most common
contamination of deep puncture wounds with production of the botulinum toxin as the spores become vegetative in the anaerobic environment (pretty uncommon)
neonatal (not recognized in dogs and cats) |
|
|
Term
| What is the pathophysiology of botulism toxicity? |
|
Definition
| the toxin binds with high affinity to nerve cell membranes and is internalized --> inside the axon terminal the toxin cleaves SNARE proteins (proteins that mediate exocytosis of synaptic vesicles) --> the result is diminished release of acetylcholine at the synaptic cleft --> flaccid paralysis and keratoconjunctivitis sicca (these patients are cognitively BAR) |
|
|
Term
| What is the prognosis for botulism? |
|
Definition
with good nursing care for the duration of the illness (14-24 days) prognosis is good and complete recovery is expected
*** complications resulting in a poorer prognosis include secondary infection (ex. aspiration pneumonia) and respiratory failure (paralysis of diaphragm, intercostals etc.) |
|
|
Term
| How can you definitively diagnose botulism? |
|
Definition
| identify botulinum toxin in serum, feces, vomit, or food sample (ie. you see your dog eating a carcass....he develops flaccid paralysis and you go take a sample of that carcass for analysis) |
|
|
Term
| How can you treat botulism? |
|
Definition
if early in the course of the disease induce vomiting (reduce intestinal absorption of the toxin) and give anti-toxin (only effective before the toxin is internalized by the neurons)
otherwise supportive care (padded cage, physical therapy, lubricate eyes, urine and fecal evacuation +/- ventilatory support)
Antibiotic therapy is only warranted for secondary infections (ex. aspiration pneumonia) |
|
|
Term
| What toxin and pathogenesis is responsible for the clinical signs associated with tetanus? |
|
Definition
| C. tetanus organisms germinate in puncture wounds (anaerobic) and produce tetanospamin toxin --> binds to peripheral nerves and travels retrograde to CNS --> cleaves SNARE proteins necessary for the release of GABBA (inhibitory neurotransmittor) --> loss of inhibitory signals results in spastic paralysis |
|
|
Term
| T/F although the most common presentation of a dog with tetanus is a young dog with an infected wound or surgical incision, not all wounds will appear infected, and small puncture wounds may heal making it difficult to locate the source of infection |
|
Definition
TRUE
*** one way to localize the source of infection is to ask the owner where the clinical signs first appear |
|
|
Term
| Why is definitive diagnosis of tetanus challenging? |
|
Definition
identification of tetanospamin toxin is extremely rare, organism is hard to culture (30% positive), and inciting wound is not always easily appreciable
*** dx based of history and clinical signs |
|
|
Term
| What is the treatment for tetanus? |
|
Definition
neutralize any circulating toxin with anti-toxin (equine or human --> risk of anaphylaxis)
Minimize production of new toxin by cleaning the wound and giving antibiotics (metronidazole or Pen G IV)
supportive care (quiet dark room, monitor for hyperthermia, arrhythmias, blood pressure, and ventilation) |
|
|
Term
| What is the prognosis for a dog that is being treated for tetanus? |
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Definition
| prognosis is good if they survive the acute presentation of clinical signs but prolonged hospitaization is often necessary and clients may be discouraged because they tend to get worse before they get better. |
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Term
| How does clinical presentation of tetanus differ in cats vs. dogs? |
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Definition
cats tend to get localized tetanus associated with large grossly contaminated wounds
dogs are more likely to have generalized tetanus and wounds may be difficult to identify (small healed puncture wounds, grass awns etc.) |
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Term
| Where does the word vaccine come from? |
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Definition
the latin word for cow (vacca)
*** b/c cow milkers got cow pox and were spared a horrible small pox death, I knew I should have gone into food animal medicine.... |
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Term
| An ideal vaccine would stimulate what elements of the immune system? |
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Definition
| both humoral (antibodies) and cell mediated (killer T, monocytes etc.) |
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Term
| What are the pros and cons associated with killed vaccines (ex. canine rabies)? |
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Definition
pros: no potential to cause disease (ie. safe to use in immunosuppressed, pregnant etc.)
cons: do not stimulate as strong or long lasting immune response (ie. as opposed to MLV) and are associated with increased adverse reactions (because need to include adjuvants and high antigen burdens to stimulate an adequate immune response) |
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Term
| What are the pros and cons associated with MLV (ex. DAP2, FVRCP)? |
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Definition
pros: rapid onset and sustained protection, better ability to stimulate cell mediated immunity and mucosal IgA (ex. intransal vaccines)
cons: potential for reversion to virulence or disease associated with contamination during manufacturing process |
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Term
| What are the pros and con associated with recombinant vaccines (ex. feline rabies)? |
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Definition
pros: safe immunogenic DNA (safe as killed vaccines) +/- some ability to overcome maternal antibody interference
cons: efficacy and duration of immunity is not currently established |
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Term
| T/F NO vaccine is 100% safe or 100% effective |
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Definition
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Term
| What are the criteria used to determine core vaccines for dogs and cats? |
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Definition
severity of the disease (needs to be associated with significant morbidity and mortality)
highly transmissible to other animals (ie. contagious)
zoonotic potential (ie. Rabies)
Widespread distribution (ie. ubiquitous diseases that ALL animals are likely to be exposed to) |
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Term
| What are the core vaccines for dogs? |
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Definition
distemper, parvo, adenovirus-2 (MLV)
rabies (killed) |
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Term
| What are the core vaccines for cats? |
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Definition
| panleukopenia, herpesvirus-1, calicivirus, and rabies |
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Term
| T/F only cats testing negative for feline leukemia virus should receive the vaccine |
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Definition
TRUE
**** recommended to booster annualy for high risk individuals (ie. unsupervised outdoor cat, or living with an FelV+ cat) |
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Term
| What are some of the problems with using serum antibody titers to determine necessity of re-boostering patients? |
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Definition
no standard methodology resulting a wide variety in quality of results between different labs
animals may not be protected against the disease despite having adequate titers (only way to know is to challenge) |
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Term
| What are three reasons that a patient might have a negative serum antibody titer after being vaccinated? |
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Definition
maternal interference
poor host response to vaccine antigens
poorly immunogenic vaccine (ie. reconstituted too early, left in the sun, mixed with another product etc.) |
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Term
| Although the etiology of systemic lupus erythematosis is not completely ellucidated what are some of the current thoughts how this disease develops? |
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Definition
| genetics + loss of self tolerance (many potential mechanisms for this, ex. release of anatomically sequestered antigens - ie. occular; exposure to exogenous antigens that mimick endogenous antigens - ie. strep infections; expression of cytokines that alter antigen presentation etc.) |
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Term
| What is the main pathogenic mechanism associated with systemic lupus erythematous? |
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Definition
| immune complex deposition (type III hypersensitivity reaction) |
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Term
| What are the most common clinical manifestations of systemic lupus erythematous? |
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Definition
fever, polyarthritis, protinuric renal disease, skin lesions, hematologic abnormalities (ex. hemolytic anemia, thrombocytopenia, leukopenia, splenomegaly)
consider lupus if you see intermittent acute presentations involving a combination of at least 3 of these organ systems |
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Term
| How can you differentiate skin lesions associated with systemic lupus erythematous from canine discoid lupus? |
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Definition
Dx via skin biopsy as well as lack of systemic signs (ie. only skin is effected)
*** discoid lupus as a good prognosis vs. SLE which has a poor prognosis |
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Term
| What is the test that can be used to diagnose SLE, what are some of its limitations? |
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Definition
ANA = antinuclear antibody test
this test is not specific (ie. most patients with a positive ANA DO NOT have SLE) and there is no diagnostic cut-off values for confirming the disease (ie. high titers are correlated with disease severity in general, but you can't say, a titer over this number is definitely SLE positive)
*** also drugs and bacterial/protozoal infections can cause false positive ANA (always look for infections and resolve before ordering this test) |
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Term
| How can you diagnose SLE? |
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Definition
definitive --> 4 or more (of 11) criteria occuring consecutively or simultaneously in intermittend acute episodes
probable= at least 3 criteria are met
*** criteria are clinical signs + positive ANA |
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Term
| What is the cornerstone of therapy for systemic lupus erythematous? |
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Definition
immunosuppresion
corticosteroids +/- azathiprine, cyclophasphamide, vincristine, levamisole <--- might want to add on the other immunosuppresive drugs to lower the dose of corticosteroids required (associated with negative side effects)
**** monitor response to therapy via resolution of clinical signs and lower ANA titers |
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