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390 Cards in this Set
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What is the typical amount of time that it takes for a hospital acquired infection to present itself?
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a. Generally over 48 hours |
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What is an endemic infection?
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Results from a patient’s own flora (not from the environment) b. Secondary to breach of normal anatomical barriers, debilitation from illness, or inplant source |
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What is an epidemic infection
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a. When a sick patient causes nearby patients to become contaminated 4. |
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Which is more common and harder to treat, epidemic or endemic
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a. Endemic 5. |
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What is the single most effective way to reduce endemic infections
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a. Handwashing 6. |
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What is the most important step in preventing a hospital acquired infection
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a. Decreased colonization 7. |
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What are the four categories of infections traditionally seen
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a. Pneumonia b. Surgical site infections c. Catheter related infections d. Urinary tract infection 8. |
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What is the most common type of infection and why
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a. UTI b. Changes to normal urinary habits, increased resistance seen with antimicrobial prophylaxis c. Culture of catheter tip is not recommended d. Low morbidity and mortality 9. |
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Which infection is associated with the highest level of morbidity and mortality
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a. Pneumonia 10. |
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What are six risk factors shown to increase risk of pneumonia
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a. ET intubation b. NG tube c. Positive pressure ventilation d. Antacids e. Neurological injry or surgery f. Propofol use 11. |
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What has been shown to increase risk of surgical site infection
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a. Anesthesia over 90-120 minutes 12. |
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What is recommended for treatment with cefazolin perioperatively
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a. Do not use closer than 1 hour before surgery b. Use every 2 hours while in surgery 13. |
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What is the definition of pharmacokinetics
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a. Drug exposure, area under the curve, maximum plasma concentration, time the antimicrobial concentration exceeds a defined threshold 14. |
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What is the definition of pharmacodynamics
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a. Potency of drug against infecting organism, MIC 15. |
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What is the difference between time and concentration dependent antibiotics
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a. Certain classes of antibiotics like aminoglycosides and fluoroquinolones eradicate bacteria by achieving high concentrations at the binding site. This concept is called concentration-dependent killing, and the pharmacodynamics parameter can be simplified as peak/Minimum Inhibitory Concentration (MIC) ratio (Figure 1).1,2 The best responses occur when the concentrations are ≥ 10 times above the MIC for their target organism at the site of infection. For classes of antibiotics that demonstrate time-dependent killing (e.g., beta-lactams [penicillins, cephalosporings, carbapenems, monobactams], clindamycin, and linezolid), the optimal response occurs when the time that the drug remains above the MIC is ≥ 50% of the dosing interval 16. |
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Which abx are concentration dependent
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a. Fluoroquinolones, aminoglycosides, metronidazole, azithromycin 17. |
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Which abx are time dependent
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a. Penicillins, cephalosporins, most macrolides, lincosamides, tetracyclines, chloramphenicol, potentiated sulfas 18. |
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What is the most common pathogen for UTI’s
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a. E.coli 19. |
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In alkaline urine, you suspect a gram +, cocci, it is likely a
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a. Staph 20. |
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“” gram negative rod
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a. Proteus 21. |
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In acidic urine, you suspect a gram + cocci, it is likely a
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a. Enterococcus 22. |
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In “”, gram – rod
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a. E. Coli 23. |
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What is the only oral drug that has spectrum against pseudomonas
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a. Fluoroquinolone 24. |
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Which antibiotics develop plasmid mediated resistance and are excreted unchanged in the urine, achieving good penetration in the prostate and kidneys
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a. Tetracyclines 25. |
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What infectious organism is most common in Pyoderma
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a. Staph intermedius 26. |
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How does Staph incite inflammation
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a. Protein A is produced by staph and this incites complement cascade 27. |
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What is considered a first line treatment for Pyoderma
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a. Cephalosporins (cefpodoxime is reserved for more complicated infections) 28. |
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What are two other good choices
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a. Macrolides or lincosamides are OK but recurrent organism tend to be resistant b. Clindamycin 29. |
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How long should Pyoderma be treated
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a. 3-6 weeks 30. |
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What organisms are common upper respiratory pathogens in dogs
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a. Bordetella 31. |
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“” cats
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a. Bordetella, mycoplasma, chlamydophila felis 32. |
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Patients with chronic URT should be screened for what
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a. Osteomyelitis 33. |
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Which antibiotic is a good first choice for URT
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a. Doxycycline 34. |
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What organism is common in the lower airways of dog/cat
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a. Bordetella b. Mycoplasma c. Strept zoo d. Pasturella e. E. Coli f. Chlamydophila felis in cats 35. |
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Are prophylactic abx recommended for bone surgery
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a. No proven benefit 36. |
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What organisms are common iatrogenic causes for septic arthritis
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a. Staph aureus and intermedius b. MRSA 37. |
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Fluorquinolones commonly do not treat what species
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a. Streptococcus 38. |
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Septic patients most commonly have what organism
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a. Gram negative organism with E. coli being common 39. |
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What do they get secondarily
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a. Gram + cocci and anaerobes i. Commonly have more than one species ii. Treatment with cefoxitin is a good choice 40. |
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What are the four major ways that glucocorticoids work at the cellular level
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a. Diffuse into the cytoplasm of the cell b. Inactivates pro-inflammatory transcription factors c. Increased production of proteins that inhibit cytokines d. Increased production of lipocortin-1 which inhibits phospholipase A2 41. |
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Which arm of the immune system is likely affected more
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a. Cell mediated 42. |
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What are the likely complications of GC use
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a. Enhanced pathogenic potential of infectious organisms b. Prevention of cell mediated clearance of infectious organisms c. Perpetuate inflammation due to persistence of organism d. Activation of other inflammatory pathways e. Decreased phagocytic and oxidative pathways 43. |
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When are steroids useful
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a. When the infectious organism is know to incite a lot of inflammation b. Low dose steroids generally accepted in treating humans w/ sepsis 44. |
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Why might steroids worsen infectious meningitis
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a. May make BBB less leaky and get a lower penetration of antibiotics into CSF 45. |
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What are the four main Sequelae from SIRS
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a. DIC b. ARDS c. Multiple organ failure d. Relative adrenal insufficiency 46. |
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When treating an infectious disease, what are two guidelines to abide by
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a. Wait until diagnostic testing is finished before starting GC b. Give time after starting antibiotics before starting GC 47. |
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What should one avoid when using GC in infectious diseases
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a. Long acting depots of the drug b. Applying a blanket approach c. Using an inappropriate dose for the goal desired 48. |
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What is a must anytime using GC
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a. Advise owners of potential risks 49. |
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What are 6 main disadvantages to using anti-virals
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a. Cost b. Toxicity c. Limited to DNA viruses mostly d. Most work only in replication phase e. In vitro effects overestimate in vivo effects f. Most are virostatic 50. |
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What are DNA viruses
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a. A DNA virus is a virus that has DNA as its genetic material and replicates using a DNA-dependent DNA polymerase. The nucleic acid is usually double-stranded DNA (dsDNA) but may also be single-stranded DNA (ssDNA). b. Adenoviridae, Asfarviridae, Iridoviridae, Papillomaviridae, Polyomaviridae and Poxviridae 51. |
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Name four categories of anti-virals:
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a. Nucleoside analog (anti-metabolite)b. Retroviral inhibitors c. Interferonsd. Acemannan52. |
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What is the thymidine analog that has the potential of working against the DNA polymerase of the host cell and is known to have systemic toxicity so it is used topically only
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a. Idoxuridine 53. |
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What does this drug treat
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a. Topically treats herpes keratitis b. Can cause corneal ulcers and hepatotoxicity 54. |
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Name two purine analogs
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a. Vidarabine and acyclovir 55. |
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Which of the two is used systemically and in veterinary medicine
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a. Acyclovir-specific b. Vidarabine is nonspecific 56. |
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Which enzyme specifically does acyclovir inhibit
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a. Thymadine kinase (virus must be actively replicating for this to work) 57. |
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What are the side effects of acyclovir
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a. High dosages needed b/c of poor bioavailability b. Hepatotoxicity c. Renal failure- microprecipitates and creates casts d. Bone marrow suppression 58. |
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What is recommended to monitor while using this drug
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a. CBC b. Chemistry 59. |
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What drug is a guanosine analog used in cats and has been shown to be fairly effective at reducing clinical signs in about 7-10 days
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a. Famcyclovir (prodrug of a drug that is not easily metabolized in cats called Pencyclovir) 60. |
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What are the disadvantages to famcyclovir
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a. Unpredictable bioavailability b. Similar side effects seen in acyclovir 61. |
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What is a cyclic amine that has some activity against RNA viruses (inhibits penetration and uncoding of RNA viruses) and used for Influenza in humans
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a. Amantadine 62. |
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What triazole nucleoside has in vitro activity against DNA and RNA viruses
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a. Ribavirin 63. |
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What retroviral inhibitor (reverse transcriptase inhibitor-RNA viruses) is used in feline leukemia cats
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a. AZT –Zidovudine 64. |
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How effective is it
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a. Decreased clinical signs in 3 weeks b. Decreased stomatitis and p27 antigenemia 65. |
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What are the side effects
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a. Myelosuppressive 66. |
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What are interferons
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a. Polypeptides produced in response to foreign particulate matter 67. |
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How do interferons work:
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a. Bind to virally infected cellsb. Stimulates NK cells c. Enhances MHC class II antigensd. Inhibit viral nucleic acid formation and protein sysnthesis e. Prevents infections of new cells68. |
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Which two interferons used most in vet med
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a. Alpha and beta (delta and omega available too) 69. |
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What are the benefits to intererons
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a. Virostatic to DNA and RNA viruses b. Good bioavailability 70. |
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What are disadvantages
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a. Work best if species specific product usedb. Have to be given parenterally |
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Which interferons have shown promise with FIV
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a. Omega and alpha 72. |
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“”” Felv
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a. Omega 73. |
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What is acemannan
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a. Carbohydrate derived from aloe vera plant 74. |
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What properties does it have for anti-virals
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a. Prevents viral replication in cells by glycosylating the virus 75. |
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What has there been successful treatment of with this
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a. Influenza b. Fibrosarcoma c. Felv/FIV 76. |
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What is the disadvantage
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a. Hypersensitivity reaction 77. |
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What antibiotics inhibit the 50s ribosome
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a. Macrolides (erythromycin, azithromycin) b. Lincosamides (clindamycin) c. Chloramphenicol 78. |
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Which antibiotics inhibit the 30s ribosome
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a. Tetracyclines (doxycycline) 79. |
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Which antibiotics are cell wall inhibitors
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a. Penicillins b. Beta lactams c. Cephalosporins d. Carbapenums e. Vancomycin 80. |
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Which antibiotics are cell membrane inhibitors
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a. Polymixin b. Bacitracin c. Colistin 81. |
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What are the eleven antibiotics that are cidal
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a. Penicillins b. Beta lactams c. Cephalosporins d. Aminopenicillins e. Fluoroquinolones f. Aminoglycosides g. Potentiated sulfas h. Metronidazole i. Carbapenums j. Vancomycin k. Rifampin 82. |
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First generation cephalosporins include what
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a. Cephalexin b. Cefazolin c. Cephaphinin d. Cephalothin 83. |
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Second generation cephalosporins include what
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a. Cefoxitin b. Cefamandole c. Cefuroxime d. Cefaclor 84. |
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Third generation “””
85. |
a. Cefovecin b. Ceftazadimec. Ceftiofurd. Cefpodoximee. Cefotaxime |
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What is the MOA of fluoroquinolones
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a. Inhibits DNA gyrase 86. |
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What is the MOA for rifampin
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a. Inhibits RNA polymerase 87. |
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What two types of antibiotics inhibit folic acid synthesis
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a. Sulfonamides-competitive PABA b. Trimethoprim- inhibits dihydrofolate reductase 88. |
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What are beta lactamases
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a. Penicillin binding protein as a result of chromosomal mutations or plasmid mediated resistance 89. |
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How do aminoglycosides cause renal toxicity
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a. They are actively taken up into renal tubular cells with disruption of cellular lysosomes 90. |
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Which of the aminoglycosides are most toxic
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a. Neomycin b. Followed by i. Streptomycin ii. Kenomycin iii. Gentamicin iv. Amikacin v. Tobramycin 91. |
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What is unique about folic acid and bacteria
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a. They must synthesize their own, cannot get from diet like mammals do b. Used for AA synthesis/protein metabolism 92. |
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How is folic acid synthesized
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a. P-amino-benzoic acid (PABA) is combined with Pteridine to make Dihydrofolic acid 93. |
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What is the enzyme used
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a. Dihydropteroate synthetase 94. |
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What is the final step in the pathway
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a. Dihydrofolic acid is reduced to Tetrahydrofolic acid which is then converted to folic acid 95. |
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What is the enzyme that reduces dihydrofolic acid
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a. Dihydropteroate reductase 96. |
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Which of the antibiotics are lipid soluble
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a. TMS b. Chloramphenicol c. Quinolones d. Tetracyclines (tetracycline is water soluble) e. Macrolides 97. |
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Which tick is the brown dog tick
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a. Rhipicephalus sanguines 98. |
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What diseases are carried by the brown dog tick
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a. E. Canis b. Babesia c. Hepatozoonosis d. Canine hemobart. 99. |
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What is the American dog tick called
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a. Dermacentor variabilis 100. |
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What diseases does the American dog tick carry
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a. Cytauxzoonosis b. Tularemia c. RMSF 101. |
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What is the black legged tick (deer tick) called
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a. Ixodes scapularis 102. |
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What disease does this tick carry
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a. RMSF b. Borrelia (lyme disease) c. Ehrlichia equi d. Tularemia 103. |
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What is the lone star tick
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a. Amblyomma americanum 104. |
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What diseases does this tick carry
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a. RMSF b. E. ewingii c. Hepatozoonosis 105. |
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What are the four stages of the tick lifecycle
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a. Egg b. Larvae (6 legs) c. Nymph d. Adult (8 legs) 106. |
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Which anaplasma species cross reacts with ehrlichia ewingii
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a. Anaplasma phagocytophium 107. |
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Which ticks transmit anaplasma phagocytophium
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a. Ixodes 108. |
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How long must these ticks feed to transmit the disease
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a. 24 hours 109. |
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What are the clinical signs
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a. Thrombocytopenia b. Neutropenia c. Vasculitis d. Fever e. Lethargy f. Anorexia g. Rarely, IMHA 110. |
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Which anaplasma species often causes a subclinical cyclic thrombocytopenia
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a. Anaplasma platys 111. |
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These dogs are often coinfected with what
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a. E. canis b. Lyme disease 112. |
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Which tick transmits this disease
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a. Rhipecephalus 113. |
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When are these infections detected in higher numbers
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a. Spring, Summer, fall 114. |
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How does one diagnose anaplasma
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a. PCR-very reliable b. Serology- 4DX c. Blood smear 115. |
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How do you treat anaplasma
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a. Doxycycline for a minimum of 14 days, reinfection is possible for analplasma and ehrlichia 116. |
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Which ehrlichia species is worldwide and considered “canine ehrlichiosis”
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a. Ehrlichia canis 117. |
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Which types of cells does E. canis infect
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a. Monocytes b. Macrophages 118. |
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Which two ehrlichia species are unique to the US, transmitted by Ambylomma Americanum and which one infects people vs. dogs
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a. E. chaffeenis-> Humans b. E. ewingii-> Dogs 119. |
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What is unique about ewingii vs. Canis and Chaffeenis
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a. Infects neutrophils and platelets only vs. monocytes and macrophages 120. |
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Which breed of dog is predisposed to ehrlichiosis
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a. GSD 121. |
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In acute cases of ehrlichiosis, what are the expected clinical signs?
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a. Incubation is about 2-4 weeksb. Then clinical signs develop i. Feverii. Lethargyiii. Anorexiaiv. Myalgia (lameness)v. Petechiaevi. Malaisevii. Thrombocytopenia (60-90%)1. Consumption2. Sequestration3. Malproduction4. Decreased function and migration from migration inhibition factor from lymphocytes122. |
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How long can the subclinical phase last
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a. Weeks to years, no clinical signs b. Organism in the wbc and bone marrow 123. |
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What is expected in the chronic phase
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a. Cyclic i. Lethargy ii. Anorexia iii. Lameness iv. Weight loss v. Vasculitis -> anterior uveitis, neuromuscular disease, CNS signs, GN, polyarthritis, hepatomegaly, splenomegaly 124. |
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What can be seen on routine labwork
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a. Pancytopenia b. _+/- Hyperglobulinemia (can be poly or monoclonal) 125. |
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How can you diagnose ehrlichiosis
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a. PCR is helpful in acute phase if untreated b. Serology is the best screening test w/ convalescent titers i. Not species specific ii. Does not detect E. ewingii iii. Won’t detect antibodies in acute infection, need 7 days 1. ELISA (3, 4DX), positive at 1:160 2. IFA detects surface protein p30-p31 at 1:16 126. |
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How can one speciate
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a. Immunoblotting b. Bloodsmear (poorly sensitive but very specific) 127. |
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How does one treat ehrlichiosis
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a. 28 days of doxycycline b. Chloramphenicol c. NOT Enrofloxacin 128. |
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How long must the Ixodes tick feed before transmitting borrelia burgdorferi
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a. 24-48 hours (~50 hours) 129. |
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How does lyme disease manifest its pathogenesis
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a. Immune complex deposition in skin, joints, kidneys, heart, neurologic system, ocular, lymph nodes 130. |
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Which interleukin is involved in joint immune complex deposition
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a. IL-8 131. |
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What is the major disadvantage between the serologic tests for lyme
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a. Cannot differentiate from vaccine and infection b. Does not matter if doing ELISA or IFA 132. |
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What is the benefit of the PCR
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a. Can detect low numbers of organsims in body fluids and skin but not blood 133. |
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How could someone test for infection vs. vaccine
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a. Western blot i. Osp C= infection 134. |
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How does one treat lyme disease
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a. Doxcycline x 28 days b. Ceftraixone i. 3rd generation cephalosporin that is given parenterally 135. |
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Which organism is what is referred to as Salmon poisoning
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a. Neorickettsia helmintheca 136. |
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What are the two vectors for salmon poisoning
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a. Nanophytes salmincola (fluke) b. Oxytena silicula (snail) 137. |
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How is the organism most commonly transmitted
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a. Dogs that eat uncooked or raw fish 138. |
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What organs are affected by the granulomatous inflammation
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a. GI system b. LN c. Spleen d. Neurologic system 139. |
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What are the typical presenting clinical signs
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a. Enteritis, diarrhea, fever, neurologoic signs 140. |
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What are common differential diagnoses
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a. Salmonella, parvo, prototheca 141. |
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How does one diagnose this
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a. Fecal sedimentation b. PCR c. Aspriate affected organs 142. |
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How does one treat
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a. Praziquantel for the trematode b. Doxycycline 143. |
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How long does the Dermacenter tick need to feed for to transmit RMSF
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a. ~24 hours 144. |
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What are the clinical signs for RMSF (Rickettsi rickettsi)
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a. Fever b. Lameness c. Anorexia d. Vomiting e. Neuro (central vestibular, meningitis) f. Chronically-> splenomegaly, hepatomegaly 145. |
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What cells are primarily affected by RMSF
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a. Endothelial cells 146. |
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What changes would likely be seen on bloodwork of a patient with RMSF
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a. Hypoalbuminemia b. Thrombocytopenia c. Anemia d. Inflammatory leukogram e. Increased liver values f. Azotemia 147. |
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How does one test for RMSF
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a. Serology- IFA is ideal b. Latex agglutination ELISA c. PCR likely false if an early infection 148. |
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How is RMSF treated
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a. Doxycycline for 10-14 days b. Good prognosis 149. |
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What two Rickettsial organisms are most commonly associated with IMHA
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a. Analplasma phagocytophilum b. Babesia 150. |
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What types of changes would you expect to see in the bloodwork of a dog infected with Babesia
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a. Regenerative anemia (intracellularly infects rBC) b. Thrombocytopenia c. Hyperglobulinemia d. Splenomegaly e. Fever (wax and wane) f. Bilirubinemia 151. |
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What is the time frame in which clinical signs develop
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a. 1-3 days 152. |
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What other test is routinely positive
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a. Coomb’s test 153. |
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What four things does a 4DX test for
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a. Dirofilaria immitus b. Borrelia burgdorferi c. Anaplasma spp. d. Ehrlichia canis 154. |
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Which of the babesia organisms is the least virulent
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a. Babesia canis rossi found in greyhounds and transmitted by Rhipicephalus 155. |
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Which is considered the most impactful for canine infetions in recent years
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a. Babesia gibsonii 156. |
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Which breed is overrepresented
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a. Pit Bulls 157. |
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How is it spread
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a. Dog bite b. Transplacentally 158. |
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What are common and uncommon clinical signs with B. gibsonii
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a. Renal failure b. Proteinuria c. Less commonly i. Ascites ii. CNS iii. Cardiopulmonary signs 159. |
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How is B. gibsonii diagnosed
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a. Light microscopy –not sensitive b. Serology- good sensitivity for detecting anti-piroplasma antibodies c. PCR- considered the best test because of the sensitivity 160. |
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What are the treatments
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a. Atovaquone + Azithromycin b. Treat until get 2 negative PCR panels in 30 days 161. |
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What is being used in france for this condition
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a. Vaccine offers partial protection 162. |
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What are the two phases found with cytauxzoonosis
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a. Schizont b. Piroplasm 163. |
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Where are each of these forms found
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a. Schizont is found in the macrophages b. Piroplasm is found in the red blood cells (later in the course of diseae) 164. |
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Which tick transmits cytauxzoonosis
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a. Dermacenter variabilis 165. |
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Which type of species/animals serve as asymptomatic carriers
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a. Wild cats 166. |
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Highest incidence is found with what
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a. Male, outdoor cats 167. |
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Which phase of the organism causes most of the clinical signs
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a. Schizont because infects macrophage and infects every part of the body with macrophages 168. |
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What is the MOA of clinical signs
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a. Occlusion of blood vessels leading to thrombus like mechanical obstruction which causes tissue hypoxia and organ failure 169. |
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When the infected macrophage is infected and ruptures, what happens next
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a. Merozites are released -> how they infect rBC by endocytosis 170. |
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A cat that does not have the schizont phase will likely not have this
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a. Clinical disease 171. |
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If a cat is exposed to the merozite will have what
|
a. Protective immunity 172. |
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How long is the cat sick before show c/s
|
a. 1-2 weeks 173. |
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How long will the cat live without therapy
|
a. Usually dies within 3 weeks of receiving organism 174. |
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What things would someone see on labwork
|
a. Cytopenias (can be lack of production and schizont’s in BM) b. Hyperbilirubinemia c. Hypoalbuminemia d. Tachycardia e. Splenomegaly f. +/- Hepatomegaly g. Generalized pain h. Fever i. Hypothermia sets in 24-48 hours before death 175. |
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How is this frequently diagnosed
|
a. PCR developed recently b. ID organisms on smear, in tissue samples (not sensitive) 176. |
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How is it treated
|
a. Treat for secondary infections b. Atovaquone c. Azithromycin d. Imidicarb diproprionate 177. |
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What type of bacteria is bartonella
|
a. Fastidious gram – bacteria 178. |
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What is the importance of this organism
|
a. Zoonotic, over 20 spp. 179. |
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What are the two main species of canine bartonella spp.
|
a. B. vinsonii b. B. berkhoffi 180. |
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“” feline spp
|
a. B. henselae b. B. clarridgeiae 181. |
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How is bartonella transmitted
|
a. Biting fleas b. Flies that bite c. Keds d. Lice e. Sandflies f. Ticks- Rhipicephalus 182. |
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Where do the organisms preferentially infect the host
|
a. RBC’s and endothelial cells b. Capable of infecting progenitor bone marrow cells 183. |
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What is a common theme about babesia across subspecies
|
a. Widespread or persistent bacteremia in a reservoir host does not induce obvious signs of disease 184. |
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What things routinely facilitate development of clinical disease
|
a. Immunosuppression b. Coinfection c. Pre-existing heart valve malformations 185. |
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What are the traditional clinical signs
|
a. Regional lymphadenopathy, endocarditis, cardiac arrhythmias, polyarthritis, meningitis, encephalitis, hepatitis, dermatologic lesions, epistaxis, mimic immune mediated diseases like SLE, self-limiting fever is common 186. |
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Which heart valve is most likely to be affected
|
a. Aortic valve 187. |
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What are the ideal ways to diagnose this
|
a. PCR and serology combined is best i. Convalescent titers not routinely performed 188. |
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What is unique about the presence of autoantibodies in this disease
|
a. Does not correlate with level of bacteremia 189. |
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What kind of aniamls are most likely to be affected
|
a. Younger animals – most likely to be bactermic for longer 190. |
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What is the best way to treat bartonella
|
a. Flea control b. Humans: doxycycline, erythromycin, rifampin i. Treat for longer if immunocompromised (at least 6 weeks) c. Cats- treating them does not treat bacteremia 191. |
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Mycoplasma lives on the surface of red blood cells and primarily causes hemolytic anemia in what species
|
a. Cats i. Mycoplasma haemofelis ii. M. hemoninutum iii. H. Turicanis 192. |
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Which species of mycoplasma is most common
|
a. M. Haemonintium 193. |
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What are the most common clinical signs
|
a. Hemolytic anemia (usually extravascular), hyperbilirubinemia 194. |
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What will one see on a CBC
|
a. Macrocytic hypochromic anemia +/- spherocytes, +/- agglutination + 195. |
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What infections do these cats have a higher risk of developing
|
a. Felv/FIV 196. |
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How is this diagnosed
|
a. PCR b. Bloodsmear c. No serology exists 197. |
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What is the treatment
|
a. No treatment eliminates infection i. Doxycycline ii. Enrofloxacin/Marbofloxacin (resistance) iii. Imidocarb iv. GC |
)
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Can you treat until get a negative PCR
|
a. No get false neative b/c of release from the organisms from Sequestered sites so need more than 1 199. |
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What is the definitive host for toxoplasmosis
|
a. Cat 200. |
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What is the traditional routes of infection for toxoplasmosis for a cat
|
a. Transplacentally b. Fecal oral 201. |
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What are the 6 major locations for this protozoal parasite
|
a. Eyes b. CNS c. Liver d. Gastrointestinal tract e. Muscle f. Respiratory system 202. |
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What are the three parts of the lifecycle
|
a. Sporozoite b. Tachyzoite (asexual)- blood, lymph c. Bradyzoite (sexual)-Tissue 203. |
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How does the lifecycle for toxoplasmosis go
|
Sporozoites develop in oocysts after 1 to 5 days of exposure to oxygen and appropriate environmental temperature and humidity. Tachyzoites are the rapidly dividing stage of the organism; they disseminate in blood or lymph during active infection and replicate rapidly intracellularly until the cell is destroyed. Tachyzoites can be detected in blood, aspirates, and effusions in some dogs or cats with disseminated disease. Bradyzoites are the slowly dividing, persistent tissue stage that form in the extraintestinal tissues of infected hosts as immune responses attenuate tachyzoite replication. Bradyzoites form readily in the central nervous system (CNS), muscles, and visceral organs. T. gondii bradyzoites can be the source of reactivated acute infection (e.g., during immune suppression by feline immunodeficiency virus [FIV] or high-dose cyclosporine therapy), or they may be associated with some chronic disease manifestations (e.g., uveitis). Infection of warm-blooded vertebrates occurs following ingestion of any of these three life stages of the organism or transplacentally. Cats infected by ingesting T. gondii bradyzoites during carnivorous feeding shed oocysts in feces from 3 to 21 days. Fewer numbers of oocysts are shed for longer time periods if sporulated oocysts are ingested. Sporulated oocysts can survive in the environment for months to years and are resistant to most disinfectants. For dogs, cats, and humans it is believed that bradyzoites persist in tissues for the life of the host, regardless of whether drugs with presumed T. gondii activity are used. 204. |
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What is the infective stage of toxoplasmosis
|
a. Sporulated oocyst (can only be effectively “created” by a cat) i. Can be spread mechanically by other hosts that ingest fecal material from cat 205. |
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How do cats get infected
|
a. Transplacentally b. Ingestion of bradyzoites from tissue of infected animals 206. |
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How often should the litterbox be cleaned to prevent human infection and transmission
|
a. Every 24 hours 207. |
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What are the typical signs of disseminated infection of toxoplasmosis
|
a. GIb. Neuroc. Uveitis d. Icteruse. Nasal/ocular dischargef. Coughg. Increased CK |
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|
What is the gold standard diagnosis
|
a. IgG and IgM serology by IFA (quantitative assessment) b. Can also do ELISA but this is qualitative and only is positive if over 1:64 c. Can also try PCR 209. |
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|
Shedding of the organism from a cat occurs how often
|
a. Once for about 3-21 days after infected for the first time 210. |
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Treatment of toxoplasmosis includes what
|
a. Clindamycin b. TMS -> best for CNS involvement 211. |
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|
How does Neospora compare to toxo for lifecycle
|
a. Similar in that has bradzyoites, tachyzoites, and sporozoites b. Only difference is DH is the dog 212. |
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|
What is likely the most commonly encountered form found in clinical practice
|
a. Transplacentally infected dog 213. |
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|
What are the clinical signs of neospora
|
a. Acute CNS disease-> LMN that can progress to diffuse CNS and rigidity 214. |
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|
What are differential diagnoses for neospora
|
a. Tetanus b. Tick paralysis 215. |
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|
How is it diagnosed
|
a. Gold standard is serology of CSF i. Can also do special stains on tissue ii. CSF samples will show elevated protein and pleocytosis 216. |
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|
How is neospora treated
|
a. Clinda and TMS 217. |
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|
What is the prognosis
|
a. Worse than toxoplasmosis 218. |
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|
What type of bacteria is brucellosis
|
a. Aerobic gram negative coccobacillus 219. |
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|
How hardy is the bacteria
|
a. Not, does not survive long outside of the body 220. |
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|
How does brucella canis reproduce
|
a. Replicates intracellularly in macrophages and evades host immune systems 221. |
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|
Where can the bacteria be found
|
a. Semen b. Vaginal secretions c. LN d. Mucosal linings e. Prostate f. Uterus 222. |
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|
How does the organism evade host immune system
|
a. Contains oxidase which inhibits the bactericidal myeloperoxidase peroxide halide system by releasing 5-guanosine and adenine b. This inhibits TNF, NK cells, and macrophages 223. |
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|
|
What are some of the clinical signs seen in the male
|
a. Infertility b. High morbidity, low mortality c. Sperk leakage d. Fever e. Enlarged scrotum f. Dermatitis g. Painful ejaculate h. Discospondylitis i. Anterior uveitis j. GN k. Meningitis 224. |
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|
What c/s can be seen with females
|
a. Abortions,->45-60 days b. Lethargy, c. Lymphadenopahty 225. |
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|
What do the sperm look like
|
a. Bent tails, agglutinated 226. |
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|
Can see what with bloodwork
|
a. Coomb’s + w/o anemia, hyperglobulinemia, hypoalbuminemia b. LN will show lymphoid hyperplasia c. CNS will show elevated protein 227. |
|
|
|
What is the recommended way to diagnose
|
a. the semiquantitative 2-mercaptoethanol modified RSAT, which substitutes B. canis as the antigen for increased (but not perfect) specificity; the semiquantitative tube agglutination test, in which a titer of 1:200 or greater correlates well with positive blood culture; the indirect fluorescent antibody; the cell wall agar gel immunodiffusion (AGIDcwa); the cytoplasmic agar gel immunodiffusion (AGIDcpa); and the enzyme-linked immunosorbent assay. AGID testing requires trained personnel and special media. Positive serologic results are detected in most dogs within 8 to 12 weeks of infection. Because incubation periods can vary from 2 to 12 weeks, there can be a window of time in which an infected individual may elude serologic diagnosis. Correct interpretation of serologic results is critical to making an accurate diagnosis. Screening serology is sensitive but not specific: a high rate of false positives occurs because surface antigens of B. canis cross-react strongly with antibodies to several other nonpathogenic bacterial species. False-positive rates can be as high as 50% to 60% because of cross-reacting bordetella, pseudomonas b. PCR is most sensitive 228. |
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|
What antibiotic is not recommended
|
a. Enrofloxacin but has been shown to prevent spread and worsening of clinical signs b. Multiple abx are helpful such as aminoglycosides, tetracyclines 229. |
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|
|
What is the important factor about this disease
|
a. It is reportable b. Euthanasia is recommended b/c of zoonotic potential (humans that are immunocompromised) 230. |
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|
|
What is the most globally widespread zoonotic disease
|
a. Leptospirosis 231. |
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|
How is lepto transmitted
|
a. Ingestion of contaminated water 232. |
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|
What are the wildlife reservoirs for Leptospirosis
|
a. Raccoons, rodets, opossums, cattle, swine 233. |
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|
The prevalence of lepto reaches what percent during what time of the year
|
a. 80% during July –December 234. |
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|
What breed is predisposed to Lepto
|
a. GSD 235. |
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|
What are the serovars
|
a. Grippotyphosa- most prevalent canine b. Pomona c. Bratislava d. Autumnalis e. Canicola f. Iceterohemorrhagica 236. |
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|
90% of those infected will have this diseae
|
a. ARF 237. |
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|
|
What percent will have liver failure
|
a. 10-20% 238. What liver enzyme is typically higher with the liver failure |
a. ALP > ALT 239. |
|
|
What other clinical signs might be present
|
a. Uveitis (might be subtle) b. Intussussception c. Pleural and pericardial effusion d. Myelitis e. Meningitis 240. |
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|
What are the three outer membrane proteins
|
a. Lipl32-found on pathogenic strains b. Ompl1+Lipl41-expressed on pathogenic strains and work synergistically to provide protective immunity c. LigA and LigB-immunoglobulin like proteins that conver protective immunity (might be good for vx going forward) 241. |
|
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|
How is lepto diagnosed
|
a. MAT is gold standard (microscopic agglutination test) i. Titers over 1:800 supportive of dx ii. 4 fold increase at 2-4 weeks convers dx 242. |
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|
What are the major disadvantages for MAT
|
a. Vaccine can have high titer and does not distinguish b. Cross reactivity 243. |
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|
What other testing options are available
|
a. PCR- false – if treated w/ abx but fairly sensitive b. IFA of urine or tissue i. Sensitivity is less than PCR ii. False + common 244. |
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|
What is the recommended tx
|
a. Treat for 3-4 weeks i. Doxycycline is recommended to clear carrier state (blood and renal phases) ii. Ampicillin only kills blood phase iii. Quinolones may cross BBB so would use this treat CNS or uveitis 245. |
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|
|
What tick transmits Hepatozoon americanum
|
a. Ambyloma tick (lone star tick) 246. |
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|
How is Hepatozoon transmitted
|
a. Ingestion of the infected tick i. Organism migrates through tissue and muscle through the intestinal wall ii. Cyst formation from sporozoites iii. Get marogony iv. Can also penentrate mononuclear cells 247. |
|
|
|
How do clinical signs develop
|
a. Cysts will rupture and release gametes which cause pyogranulomatous inflammation 248. |
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|
|
What are the clinical signs
|
a. Pain b. Muscle pain c. Ocular discharge-> KCS d. Wieght loss e. Fever f. Osteomyeletis (trouble standing d/t osteoblast activity) g. Hyperesthesia h. Nasal discharge i. Hemorrhagic diarrhea 249. |
|
|
|
What will bloodwork show
|
a. Leukocytosis, profound over 50K b. Hypoglycemia c. Increased CK d. Hypoalbuminemia e. Elevated LE 250. |
|
|
|
How does one test for this
|
a. Serology -> ELISA at OSU (sensitive and specific) b. Muscle biopsy c. PCR 251. |
|
|
|
What long term Sequelae can develop in infected dogs
|
a. Type III hypersensitivity i. Amyloid-> GN, PLN 252. |
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|
How is hepatozoon treated
|
a. Clinda b. TMS c. Pyromethamine in acute disease (14 days) d. Decoquinate for chronic disease e. NSAIDS for muscle pain f. NO TREATMENT ELIMINATES CYST 253. |
|
|
|
What kind of virus is parvovirus
|
a. DNA virus 254. |
|
|
|
What mutations exist to explain the various strains
|
a. At the surface transferrin receptor (tfr) resulting in A, B.C mutations 255. |
|
|
|
What is the pathogenesis of how parvovirus works
|
a. Invades rapidly dividing cells of lymphoid tissues of oropharynx, mesenterin LN, thymus b. Residies in intestinal crypts-epithelial development is disrupted, resulting in blunted villi c. Destroys mitotically active precursors of circulating leukocytes resulting in neutropenia and lymphopenia 256. |
|
|
|
How is parvovirus transmitted
|
a. Fecal oral 257. |
|
|
|
What is the incubation period
|
a. 7-14 days b. Marked viremia in 1-5 days post infection c. Shed in feces for 7-10 days 258. |
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|
|
How long do antibodies last
|
a. 1 year 259. |
|
|
|
How is parvovirus diagnosed
|
a. ELISA fecal – sensitive and specific b. PCR fecal is sensitive and specific and differentiates from vaccine 260. |
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|
What are some reasons for a false negative
|
a. If it has been longer than 10-12 days post infection as antigen is not being shed in feces 261. |
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|
|
What are some reasons for false positive
|
a. Vaccination recently b. Positive for 5-12 days post vaccine 262. |
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|
What virus is the preventative
|
a. Modified live virus 263. |
|
|
|
What is Panleukopenia
|
a. Feline parvovirus 264. |
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|
|
What kind of virus is parvovirus
|
a. Single stranded DNA virus 265. |
|
|
|
What is the pathogenesis of the virus
|
a. Shed by all body secretions b. Needs rapidly dividing cells c. Reduced short cell layers in the cerebellum d. Recovered from hearts of infected cats-> HCM, DCM 266. |
|
|
|
How is it diagnosed
|
a. Fecal ELISA for CPV antigen will pick up virus 24-48 hours post infection b. Serology will detect positive antibodies, convalescent titers 267. |
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|
|
What age are kittens typically presenting with signs
|
a. At 3 mos as maternal antibodies have worn off by then 268. |
|
|
|
What is the treatment of choice
|
a. Supportive b. Early feeding-> Not recommended as it can injure the intestinal epithelium 269. |
|
|
|
What kind of virus is Rabies
|
a. RNA, rhadoviridae 270. |
|
|
|
What animals serve as hosts for Rabies
|
a. Skunks, bats, rabbits, cattle, some felidae 271. |
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|
|
What animals are moderate hosts for Rabies
|
a. Dogs, goats, sheep, horses, non-human primates; cats are more resistant experimentally 272. |
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|
|
How is rabies transmitted
|
a. Saliva from bites, aerosolized from tissues, ingestion of infected tissues b. Virus enters peripheral nerves i. Glycoprotein attaches to neurotoxins-axon terminals through lipoprotein receptors ii. Affects motor and sensory nerves iii. Spreads quickly if bite occurs near areas with high concentration of nerve tissue 273. |
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|
|
The severity of rabies cases depends on what
|
a. Bite site b. Virus variant c. Quantity infected d. Animal that provided the bite 274. |
|
|
|
What are the three phases of rabies and which ones have clinical signs associated
|
a. Prodromal phase (no c/s)- 2-3 days, anxiety, variable fever, behavioral changes, slow PLR b. Furious phase-hyperexcitability, photophobia, restlessness, attacks on inanimate objects c. Paralytic phase-2-3 days, LMN paralysis, bark changes, dropped jaw, hypersalivation, coma, respiratory paralysis 275. |
|
|
|
How is Rabies diagnosed
|
a. IFA of brain tissue b. Microscopic negri bodies (hippocampus in carnivores) (purkinje fibers in herbivores) 276. |
|
|
|
What is the incubation periods for dogs, cats, and humans until neuro signs develop
|
a. Dogs-1-5 (shedding before neuro signs) b. Cats -2-24 weeks post infection c. Humans-3 weeks to 1 year 277. |
|
|
|
What are the rules regarding animal bites and quarantine
|
a. Euthanize or 6 mos quarantine unvaccinated animals b. Vaccinated animals-45 day quarantine 278. |
|
|
|
What type of vaccine is used to prevent
|
a. Inactivated vaccine (MLV caused clinical signs) 279. |
|
|
|
What type of virus is Felv
|
a. An RNA retrovirus b. Oncornevirus 280. |
|
|
|
How is Felv transmitted
|
a. Can be transmitted in utero to kittens b. Saliva/biting/bodily fluids; litterboxes c. Sharing of food bowls provides low means of spreading the virus 281. |
|
|
|
How does the virus provide pathogenesis
|
a. Replicates in bone marrow, salivary glands, respiratory tissues 282. |
|
|
|
What are common risk factors
|
a. Urban b. Male c. Young animal d. Outdoor access 283. |
|
|
|
What are the three types of Felv
|
a. A=Infectious b. B=Associated w/ tumors c. C=Associated with nonregenerative anemia> generated into A for transmission 284. |
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|
|
How does the virus convey immunosuppression
|
a. T lymphocytes affected, loss of helper and CD8 cytotoxic cel b. Decreased IL-2, IL4 285. |
|
|
|
What are the clinical signs associated with felv
|
a. Fading kitten syndrome (thymic atrophy) b. Anemia, lymphoma, leukemia, myeloproliferative disease, leukopenia, thrombocytopenia, immune mediated disease, tumors, neuropathy, reproductive disorders 286. |
|
|
|
How does Felv convey leukemia or lymphoma
|
a. Insertion of Felv genome near myc oncogene-> allows activation and overexpression of that gene 287. |
|
|
|
What other Sequelae are found in cats with Felv
288. |
a. Fibrosarcoma- likely from Felv-A infected catsb. Stomatitis |
|
|
|
How is Felv diagnosed
|
a. ELISA- SNAP test detects the p27 protein b. PCR- reasonable amount of false negative due to mutations of the virus and also latent infections c. Direct IFA-confirmatory 289. |
|
|
|
How is Felv prevented
|
a. Vaccine –gp70 in vaccine b. Identify infected cats and separate in mutlicat households 290. |
|
|
|
Treatment
|
a. None b. Many different immunomodulators have been tried with conflicting results and lack of published controlled studies 291. |
|
|
|
What type of virus is FIV
|
a. Lentivirus, RNA virus 292. |
|
|
|
How is FIV transmitted
|
a. transmission via saliva and blood- common in fighting cats b. Rare in mild and in utero 293. |
|
|
|
What are the expected life expectancies for these infected cats
|
a. 18% die within 2 years of diagnosis (after 5 years estimated infection) b. 50% remain asymptomatic during those 2 years 294. |
|
|
|
What are the clinical signs of the acute phase
|
a. Fever b. Stomatitis c. Lethargy d. Enteritis e. Dermatitis f. Conjunctivitis g. Lymphandeopathy h. Respiratory disease 295. |
|
|
|
What are the two phases of FIV infected cats
|
a. Asymptomatic-can last years b. Symptomatic- reflection of infections, neoplasia, etc. 296. |
|
|
|
What body systems are affected commonly by inflammation
|
a. Mouth-stomatitis b. Eyes-uveitis, chorioretinitis 297. |
|
|
|
What kind of cancer to FIV cats get
|
a. B cell LSA b. SCC 298. |
|
|
|
What affects to the bone marrow
|
a. Anemia b. Leukopenia 299. |
|
|
|
Affects to the kidney
|
a. LUTD 300. |
|
|
|
Affects to the endocrine system
|
a. DM b. Hyperthyroidism 301. |
|
|
|
How is the immune system affected by FIV
|
a. Decreased CD4:CD8 ratio due to decreased CD4 in blood and lymph tissue i. CD4 plays critical role in promoting and maintaining humoral and cell mediated immunity 302. |
|
|
|
How does it affect neurologic system
|
a. ~5% have neuro disease behavioral> motor 303. |
|
|
|
How is FIV diagnosed
|
a. ELSIA- type p24 protein 304. |
|
|
|
What should one do if the test is psotive in a cat under 6 mos of age
|
a. Retest in 6 months as it can be the maternal ab 305. |
|
|
|
If negative, should the cat be retested
|
a. Yes, in 60 days if suspcicious of the disease 306. |
|
|
|
What are three ways to confirm infection
|
a. Flow cytometry b. Virus culture c. Western blot-IFA (gold standard but low sensitivity) 307. |
|
|
|
What is the treatment that is used most frequently
|
a. AZR-blocks lentivirus from reverese transcriptase activity, integrated into the DNA b. Feline omega interferon-+/- efficacy 308. |
|
|
|
Prevention
|
a. Segregeate infected cats if can 309. |
|
|
|
What kind of virus is a distemper virus
|
a. Morbilivirus b. RNA virus –enveloped 310. |
|
|
|
What is the principle host and reservoir for distemper
|
a. Dogs 311. |
|
|
|
What are the two options that occur in infected dogs
|
a. Acute infection and clear b. Acute infection then becomes chronically infected (severe) 312. |
|
|
|
When do most dogs present with distemper
|
a. Between 3-6 months when maternal antibodies wane 313. |
|
|
|
Where does the virus replicate
|
a. Macrophages in the 1st 24 hours 314. |
|
|
|
How is parvovirus spread
|
a. 2-6 days: lymphoid tissues affected b. 10 days: epithelial cells of the respiratory tract, intestinal tract, dermatologic tract c. 20 days: CNS, enamel hypoplasia 315. |
|
|
|
What are the clinical signs seen
|
a. Fever b. Lethargy c. Neutropenia d. Respiratory disease e. Diarrhea f. Hyperkeratosis of foot pads g. Generalized CNS disease 316. |
|
|
|
What kinds of conditions can be seen in large breed dogs
|
a. Osteosclerosis and HOD 317. |
|
|
|
How is it diagnosed
|
a. Serology as early as 6-8 days post infection, IgM b. CSF is best way to diagnose chronic infections -> see inclusion bodies 318. |
|
|
|
What is the treatment
|
a. Supportive 319. |
|
|
|
What is the vaccination protocol
|
a. MLV- do not give pregnant dogs b. May see CNS signs 7-10 days post vaccine 320. |
|
|
|
What type of virus is Canine Influenza
|
a. Orthomyxoviridae b. RNA enveloped virus 321. |
|
|
|
How is the virus transmitted
|
a. Inhalation of aerosolized particles-binds to type II pneumocytes and alveolar macrophages 322. |
|
|
|
How long does the virus stay patent in the environment
|
a. 48 hours 323. |
|
|
|
What are the two portions of the virus that cause its virulence
|
a. Hemagglutin- determines attachment , attaches to sialic acid b. Neuramiridase i. 9 subtypes, cleaves sialic acid and allows newly formed virus to exit 324. |
|
|
|
Is the virus species specific
|
a. No, there is cross species transmission b. Ususally self limiting but not when H3N8 transmitted from horses to dogs 325. |
|
|
|
How much of a concern is this virus
|
a. High mortalitiy and low morbidity b. No true carrier state 326. |
|
|
|
What are the clinical signs
|
a. Fever b. Respiratory disease i. Cough ii. Pneumonia (hemorrhagic pneumonia in greyhounds) iii. Coinfections are common iv. Sneezing w/ purulent debris 327. |
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How is the infection diagnosed
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a. Virus isolation early in the disease b. Highly sensitive-> Virus antigen isolation c. Later in disease-> Virus specific antibodies (good for surveillance) d. RT-PCR-most accurate before clinical signs 328. |
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How is it treated
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a. Supportive b. Antibiotics for secondary infections c. Oxygen d. Fluids e. NO ANTIVIRAL MEDS 329. |
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Is the vaccine worthwhile
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a. Yes, reduces the shedding and severity of clinical signs 330. |
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What is the only way one can diagnose FIP
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a. Tissue histopathology-most likely post mortem 331. |
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What are the hallmark findings of FIP
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a. Phlebitis b. Perivascular granulomas 332. |
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How is FIP diagnosed
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a. Detecting coronavirus antibodies or viral RNA in tissue 333. |
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Is the FIP vaccine helpful
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a. Temperature sensitive mutant that only replicates in the cooler nasal mucosa that is derived from Type II coronavirus 334. |
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What are a majority of cats infected with
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a. Type I coronavirus b. Type II is recombinant from canine coronavirus and is controversial 335. |
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What percentage of FIP positive cats are below 2 years of age
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a. 50% 336. |
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What type of organism is Leishmaniasis
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a. Intracellular protozoal parasite 337. |
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What cells does it prefer
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a. Macrophage 338. |
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Is this zoonotic
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a. Yes 339. |
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What are the reservoir hosts
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a. Domestic and wild dogs 340. |
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What vectors transmit this organism
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a. Sandflies (Phlebotomine sandflies, Lutzomyia shannoni) b. Other insects c. Blood transfusions d. Transplacentally e. Vertical sexual transmission 341. |
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What phase of the life cycle is in the vector
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a. Promastigone 342. |
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“” in the host
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a. Amastigone within the macrophage (after binary fission) 343. |
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What are the clinical signs
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a. Cuteneous forms (means there is a visceral component); skin lesions b. Mucocutaneous -> ocular discharge c. Visceral -> Lymphadenopathy, weight loss, splenomegaly 344. |
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What labwork findings would one see
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a. Hypoalbuminemia b. Thrombocytopenia c. NR anemia d. Azotemia e. Hyperglobulinemia f. Proteinuria 345. |
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How is it diagnosed
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a. Aspriates (amastigotes) b. Imprints from skin lesions c. IFAT w/ 1:64 Titer d. Recombinant immunoassay (antigen)-> rK39 assay 346. |
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What is a benefit of the recombinant immunoassay and IFAT
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a. Distinguishes between chagas 347. |
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What is the treatment
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a. None offer cure b. Meglumine pentamoniate + allopurinol i. Prolonged survival with fewer relapses > 4 years (can cause nephrotoxicity though) c. Amphotericin B 348. |
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Prevention
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a. Prevent sandflies b. Vaccine |
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What is pneumocystosis
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a. Saphrophyte b. Toxonomy is uncertain i. Unicellular –classified as protozoal initially 1. Behaves like a protozoan and responds to treatment ii. Behaves like a yeast with reproductive behavior iii. RNA sequence resembles a fungus 350. |
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How is it transmitted
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a. Aerosolization i. Colonizes lower airway tract ii. Problem when there is immunosuppression 351. |
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What is the life cycle
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a. Occurs in alveolar spaces and adheres to pneumocytes (forms oocytes and trophozoites) b. Not out of respiratory tract normally c. Can have hematogenous or lymphatic spread 352. |
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What is the pathogenesis behind cyanosis
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a. Alveolar capillary blockage and decreased gas exchange 353. |
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What breeds are predisposed
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a. Small breed dogs, young dogs b. Dachshunds 354. |
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How are the patients generally immunocompromised
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a. Impaired B cell function and little to no antibody production b. Defective T cells c. Hypoglobulinemia 355. |
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What other bloodwork findings does one find
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a. Polycythemia from hypoxia b. Thrombocytosis 356. |
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How is it diagnosed
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a. ET wash b. BAL c. Lung aspirate 357. |
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How is it treated
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a. TMS most effective and least toxic, treat for 3 weeks b. Pentamine isethionate-effective but toxic c. Atovaquone d. Oxygen, bronchodilators, GC (anti-inflammatory dose) 358. |
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What kind of virus is a calicivirus
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a. RNA virus with rapid mutations and minimal rates of repair so has increased amount of strains 359. |
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Severity of disease depend on what three factors
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a. Strain of FCV involved b. Infecting dose c. Host immunity 360. |
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What benefit do the vaccines give
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a. Reduce clinical signs b. No effect on infection or shedding 361. |
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What clinical sign are they commonly associated with
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a. Stomatitis b. Polyarthritis c. Lameness 362. |
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Secretions reach what radius when sneezed
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a. 4 feet b. Spread via fomites 363. |
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What is unique about shedding and testing them
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a. Shed for months b. 50% of shedding occurs in 15 days c. Need to wait 2.5mos between tests to determine if shedding has stopped 364. |
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What are poor prognostic factors
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a. Jaundiced b. Dyspnea c. 50% mortality 365. |
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What are the clinical signs
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a. Pyrexia b. Edema c. Crusting/ulceration on i. nose ii. Lips iii. Periocular skin and distal limbs d. Pleural effusion e. Icterus f. V/D 366. |
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How is FCV diagnosed
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a. Virus isolation-oropharyngeal swab b. Culture c. Serology (not recommended b/c of high exposure rate but can run convalescent titers) 367. |
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How should one clear the environment
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a. Bleach will inactivate the virus 368. |
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Intranasal vaccine is available
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a. Yes, killed antigen only 369. |
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What is barrier nursing
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a. Working from least to most infected area b. Sneeze barriers c. Quarantine area 370. |
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What type of virus is herpes virus
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a. DNA virus with 1 serotype (FHV-1) 371. |
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Latent infections are kept wehre
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a. Trigeminal ganglion 372. |
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How long does a cat shed herpes virus after stress
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a. 7-10 days occurs for 1-2 weeks 373. |
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How does L-lysine work
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a. Competes with Arginine in the formation of the herpes virus particle and decreases shedding 374. |
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Pythiosis and lagenidiosis are classified as what type of fungi
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a. Water molds: Oomycetes 375. |
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How do they reproduce
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a. Motile, flagellated zoospores 376. |
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How are they different from other fungi
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a. Lack chitin in cell wall b. Lack ergosterol in cell membrane 377. |
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What type of clinical syndromes do they cause
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a. Eosinophilic pyogranulomatous inflammation 378. |
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How do they appear in tissues
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a. Irregularly, branching sparsely septate hyphae 379. |
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Where is pythium found routinely
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a. SE US b. Often fatal 380. |
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Which types of dogs are mostly affected
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a. Large, young dogs 381. |
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After encountering the mobile zoospore, how does the organism get into the dog
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a. Encyst in damaged skin or GI mucosa 382. |
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What are the two main forms of disease
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a. GI i. Segmented transmural thickening of the GIT 1. Pylorus 2. Proximal duodenum 3. Ileocecal junction ii. Mesenteric lymphadenopathy iii. Mass at root of mesentery b. Cutaneous i. Non healing wounds with draining tracts ii. Regional lymphadenopathy iii. Extension of post surgical recurrence 383. |
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What layers of the GIT are mostly affected
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a. Submucosa and muscularis layers -> may be missed on endoscopic biopsy 384. |
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How is it diagnosed
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a. Identification of hyphae in or near the mass i. Readily seen with GMS stain b. Culture- grown w/in 12-24 hours on right media c. PCR-done on cultured organisms d. ELSIA i. Has high sensitivity and specificity-detects anti Pythiosis antibodies @ LSU and helpful for monitoring therapy too 1. Should drop by 50% in 2-3 months 385. |
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What is the treatment
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a. Aggressive surgery 386. |
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What degree of margins are necessary
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a. 3-4 cm b. Biopsy or remove lymph nodes 387. |
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How common is recurrence
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a. Common so treat for 2-3 months i. Itraconazole and terbinafine (have to use both) 388. |
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Lagenidiosis has how many species
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a. 2 i. Uniformly fatal dermatologic and disseminated dz ii. Chronic ulcerative nodular dermatopathy (less common) 389. |
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What types of lesions are found in the fatal form
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a. Occult lesions in chest or thorax b. Invasion of vessels leading to hemoabdomen and death 390. |
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How is this diagnosed
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a. Cytology or histopath-> hyphae seen on H&E stain, larger than pythiosis b. Serology (cross reactivity w/ pythiosis and other fungal diseases so not recommended often) c. Culture-Best way to diagnose-> differentiates between pythiosis and this 391. |
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What is the treatment
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a. Aggressive surgical resection with wide margins followed by itraconazole and terbinafine |
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