SA Med Exam 3

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SA Med Exam 3
2013-02-26 07:48:21

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  1. What places are rabies free?
    • Antarctica
    • Australia and NZ
    • Taiwan
    • Japan
    • some Caribbean Islands
    • England
    • Ireland
    • parts of Scandinavia
    • Hawaii
  2. What are the characteristics of rabies virus?
    • Rhabdoviridae, Lyssavirus
    • enveloped -ssRNA
  3. What are the major wildlife reservoirs of rabies, and where are each of concern?
    • Dogs: worldwide, esp India
    • Racoons: US east coast (40%) because they are adapted to the urban setting
    • Skunks: US (30%) because they can be chronically infected, shed tons of virus in their saliva and have the furious form
    • Foxes
    • Coyotes
    • Bats: US (20%), cases the most human rabies cases!
  4. What is the incubation period for rabies in animals?
    2-24 weeks, but usually 1-2 months from time of bite
  5. What is the pathogenesis of a rabies infection?
    • bite wound inoculation
    • replication in local myocytes (weeks - months)
    • travels up peripheral nerves to CNS
    • multiplication in CNS -> encephalitis
    • travels out peripheral and CN to salivary glands, skin, mucosal surfaces, gut and most other organs
  6. How long is saliva infective before CS are seen?
    <2 weeks
  7. What are the forms of rabies?
    • Prodromal: 1-3 days, behavior change (esp aggression in cats), licking bite site
    • Furious: excitable, biting at imaginary objects, pica, seizures, coma, death
    • Paralytic: LMN and CN paralysis, causes change in voice and dropped jaw, then get respiratory paralysis and death in 2-4 days
  8. How can rabies be dx ante- and post-mortem?
    • Ante: CS, increase in CK, CSF protein and CSF WBC. Use direct FA
    • Post: Histopath showing Negri bodies (poor sensitivity), direct FA (rapid, highly sensitive, before CS)
  9. What are some ddx for rabies?
    • Toxoplasmosis
    • FIP
    • Distemper
    • WNV
    • Neoplasia
    • Trauma
    • Hepatic encephalopathy
    • Thiamine deficiency
    • Oral and pharyngeal foreign bodies
    • Toxins (e.g. strychnine, lead, organochlorines)
    • Causes of generalized weakness
  10. What are the vaccine recommendations in dogs and cats?
    • Initial vaccine at 4 months of age, boostered 1 year later, then every 3 years after that
    • Killed rabies vx in R rear leg
  11. What is the protocol for unvaccinated pets that are exposed to rabies?
    • Euthanize
    • 6 month quarantine + vaccine at 5 months
  12. What is the protocol for vaccinated pets that are exposed to rabies?
    Revaccinate, then confine for 45 days
  13. What is the protocol for overdue vaccinated pets that are exposed to rabies?
    case by case basis
  14. What is the protocol for humans bitten by a vaccinated pet?
    confine animal for 10 days (they will develop CS that fast if were infective)
  15. What is the protocol for humans bitten by an unvaccinated pet?
    • Euthanize
    • Potential quarantine at shelter
  16. What is the protocol for humans bitten by a stray animal?
  17. What post-exposure measures should you take if you are bitten by a potentially rabid animal?
    • wash wound under pressure with warm water and quat
    • vaccine series (more extensive for unvaccinated humans)
  18. What are the CS of distemper?
    • Mild signs (common): inappetence, fever, serous oculonasal discharge, cough, tachypnea, enamel hypoplasia
    • Severe signs: conjunctivitis, obtundation, anorexia, V, D, severe dehydration, death.
    • Neurologic signs: may be delayed up to 6 weeks. Myoclonus, old dog encephalitis (after recovery from mild/inapparent infection)
  19. What is an important differential for distemper?
    kennel cough
  20. What are the characteristics of distemper virus?
    • enveloped RNA virus
    • Paramyxovirus, Morbillivirus
  21. What is the main source of distemper virus, and when are infections seen?
    • Racoons
    • Most infections subclinical
    • See at weaning in dogs and cats (vaccinated population)
    • Shed in resp secretions, feces and urine for 1-3 months
  22. What is the pathogenesis of distemper infection?
    • Lymphoid tissue: inhaled virus infects URT epi -> replication in macrophages while spreading through lymphatics -> infects tonsils and bronchial nodes -> infects systemic lymhoid tissue in GIT, spleen, MLN, kupffer cells on days 2-6 -> fever and lymphopenia
    • Epi and nervous tissue: hematogenous spread from lymphoid tissue to epi and CNS tissue on days 8-9 -> viral shedding and good-intermediate-poor humoral or response -> virus elimination or persistent -infection-fulminant epi infection -> no CS or CNS / cuteanous / ocular CS or severe GI signs / pneumonia / +- CNS signs
  23. What is the px of distemper infection?
    CNS signs = poor prognosis, could develop at any time
  24. How is distemper infection dx?
    • CS
    • CBC with lymphopenia, neutrophilic leukocytosis, distemper inclusions
    • Thoracic rads for intersitial coalescing to alveolar pattern
    • Serology IgG compared to CSF (differentiate from vaccinated with C coefficient)
    • Conjuctival scrapings to apply IFA to look for inclusions
  25. What is the tx for distemper infection?
    • Treatment is purely supportive
    • Fluid therapy
    • Abx
    • Antiemetics
    • Nebulization and coupage
    • Oxygen
    • Neurologic signs are usually permanent, and may occur later
  26. How is distemper infection prevented?
    • Vaccinate q3-4 weeks from 6-16 weeks (need two doses in pups > 8-10 weeks)
    • Booster at 1 year (then every 3 years)
    • All are MLV except one recombinant
  27. What is infectious canine hepatitis caused by, and what animals does it affect?
    • Usually young puppies
    • Preferentially targets endothelial cells and hepatocytes
    • Caused by canine adenovirus 1 (non-enveloped DNA virus)
    • Probably now extinct in the US
  28. What is the pathophysiology of ICH infection?
    • oronasal exposure
    • infects tonsils
    • infects local LN = viremia 4-8 days
    • systemic spread allows viral shedding in all secretions
    • good, partial or poor ab response
    • recovery with minimal endothelial damage (good), chronic hepatitis (partial), severe hepatic centrilobular necrosis and DIC (poor)
    • all cases have persistent renal tubular infection and shed virus in the urine from day 14 to 6-9 months
  29. What are the CS of ICH infection?
    • Most infections are subclinical
    • Peracute form
    • Acute form is usually 6-10 weeks, or older unvaccinated dogs that show fever, anorexia, depression, TONSILLITIS, hepatomegaly, edema, ascites, C, V, D, hemorrhage
    • CNS signs
    • uveitis and corneal edema (direct viral damage and type 3 hypersensitivity that resolves in 1-2 weeks)
    • glomerular injury (direct viral damage and Ab-Ag complex deposition)
  30. How is ICH dx?
    • CBC: lymphopenia, neutropenia
    • Chem: increased liver enzymes, hypoglycemia, hyperammonemia
    • U/A: bilirubinuria, proteinuria
    • Coag panel:
    • Ascites analysis: yellow - red, high protein
    • Histopathology: intranuclear inclusions in kupffer cells, hepatocytes, glomeruli, renal tubular vascular endothelium
  31. What is the tx for ICH infection?
    Supportive care: IVF, anti-emetics, blood, dextrose, HE txt (lactulose, neomycin, restrict dietary protein)
  32. How is ICH infection prevented?
    • All MLV vaccines against CAV-2
    • Vaccinate at 8-10 and 12-14 weeks of age (if >12 weeks old just booster once)
    • Booster at one year then every 3 years
  33. When do maternal abs wane?
    12-16 weeks
  34. What agents can cause canine upper respiratory tract infections, and what are their characteristics?
    • Bordetella bronchiseptica (g- coccobacillus)
    • K9 Parainfluenza (enveloped RNA or Paramyxoviridae)
    • K9 Herpes
    • K9 adenovirus-2
    • K9 Resp Corona
    • K9 Influenza
    • K9 Distemper
    • Mycoplasma (normal nasopharyngeal flora, can cause LRT disease)
    • Strep equi zooepidemicus
    • Secondary invaders e.g. Pasteurella, Pseudomonas, coliforms
  35. How are URT infections transmitted?
    aerosol, variable shedding for 2 weeks (viral) or >3 months (B. bronchispetica and Mycoplasma)
  36. What are the CS of URT infection?
    • Incubates for 3-10 days
    • paroxysmal C, retching (V), tracheal sensitivity
    • self-limiting
  37. How is canine URT dx?
    • Hx, CS, txt response
    • Thrx rads
    • TTW + C&S
    • PCR
  38. How is canine URT tx?
    • +/- abx (e.g. doxycycline, enro, clavamox) for 4 weeks
    • anti-tussive (e.g. hydrocodone) - but not if bronchopneumonia!
    • supportive (e.g. O2, IVF
  39. How can canine URT infection be prevented?
    • vaccines for Bord, CAV-2, CDV, CPiV, CIV
    • CPiV is MLV (IN, SC)
    • Bord is avirulent live for IN, killed for SC
    • Given SC twice 3-4 weeks apart or one IN, then booster annually and 5 days before boarding
  40. What are the feline URT pathogens?
    • Calici
    • Herpes-1
    • Chlamydia felis
    • B. bronchiseptica
    • Mycoplasma
  41. Which feline URT pathogens survive in the environment?
    FCV > FHV > Chlamydia
  42. How are feline URT infections spread?
    • direct close contact
    • fomites
    • carrier cat
  43. In which animals do you see feline URT infections, and when do you see CS?
    • Incubation period 2-6 days
    • Course 1-3 weeks
    • Most severe signs in very young, elderly, or immunosuppressed cats
  44. What are the characteristics of FCV?
    non-enveloped RNA, but >100 strains
  45. What are the CS of FCV, and what is the px?
    • Conjunctivitis, sneezing, nasal discharge
    • Facial ulceration, edema, coagulopathies, lethargy, fever
    • Limping syndrome
    • High mortality
    • Self-limiting
  46. What are the CS of FHV?
    • Severe oculonasal discharge
    • CNS
    • Reproductive (abortion, resorption, congenital defects)
    • Ulcerative facial and nasal dermatitis
  47. How are the carrier status of FCV and FHV similar and different?
    • FHV: carriers common (80-100% infected cats), virus excreted intermittently, excretion precipitated by stress
    • FCV: carriers common (50% infected cats), virus excreted continuously, long term virus excretion
  48. What are the CS of C. felis, and which animals is it seen in?
    • Conjunctivitis, S, abortion?
    • Younger cats (esp. 9 weeks to 6 months)
    • Course 1-3 months
  49. How is FHV dx?
    • Isolation
    • FA
    • Serology
    • PCR
  50. How is C. felis dx?
    • Isolation
    • PCR
  51. How are B. bronchiseptica and Mycoplasma dx?
    • Culture (special for Mycoplasma, takes weeks)
    • PCR
  52. What is the txt for feline URT infection?
    • IVF, TPN, O2
    • Abx for C. felis (doxy of clavamox for ALL cats for 4 weeks)
    • Topicals for FHV-keratitis
    • Famciclovir
  53. How do you prevent feline URT infections?
    • FHV, FCV have MLV (IN, SC) or killed vx
    • C. felis has MLV and killed vx
    • Bord vx
  54. What animals does Borrelia borgdorferi infect?
    dogs, cattle, humans, horses
  55. What are the vectors for lyme disease?
    • Ixodes scapularis: East coast, midwest
    • Ixodes pacificus: West coast
  56. What is the life cycle of Borrelia burdorferi?
    • Eggs are always uninfected, emerge in spring
    • Larvae feed on infected white footed mouse (Peromyscus leucopus) in the summer
    • Larvae overwinter, reimerge as infected nymph (trans-stadial) in spring
    • Nymph feeds on white footed mouse and deer
    • Adults lay eggs
    • Main problem is nymph feeding (small, engorge quickly)
  57. What is the pathogenesis of lyme disease?
    • 48 hours for transmission
    • B. burgdorferi in tick midgut → hemocoel → salivary glands → infect mammalian host
    • Replicates and migrates through connective tissues and establishes a persistent infection
  58. What are the CS of lyme disease?
    • Most cases subclinical
    • In endemic areas, seropositivity may reach 85%
    • ~ 5-10% show clinical signs
    • Humans: EM, palsy, arthritis
    • Dogs: arthritis, fever, lymphadenopathy, protein-losing nephropathy 2-5 months after bite
  59. What is a common co-infection with lyme disease?
    Granulocytic anaplasmosis (A. phagocytophilum) which is also transmitted by I. scapularis
  60. How is lyme disease dx, and how good of a test is this?
    • Serology for Abs (e.g. SNAP test)
    • Looks for C6 protein from natural exposure (not vaccination) but doesn't tell you if it's an active infection
  61. How is lyme disease prevented?
    • whole bacterin with OspA and OspC
    • recombinant OspA
    • remove ticks and use topical repellants
  62. What are OspA and OspC?
    • OspA: expressed by B. burgdorferi in ticks to aid adherence
    • When dogs have anti-OspA abs, the tick's blood meal causes lysis of B. burgdorferi before entering the host
    • OspC: expressed when B. burgdorferi migrates to salivary glands, useful in dogs when B. burgdorferi is OspA-
  63. How is lyme disease tx, and what is the px?
    • Doxycycline for 4 weeks
    • Expect improvement in 24-48 hours
    • Consider NSAIDs
  64. What are the characteristics of Rickettsiae?
    • arthropod transmitted
    • obligate intracellular g- coccobacilli bacteria
  65. Which ticks can transmit RMSF?
    • D. andersoni: northwest USA
    • D. variabilis: east coast USA
  66. What is the transmission of RMSF?
    • Transovarial transmission allows laying infected eggs
    • Infected larvae trans-stadial transmission feed on rodents
    • Infected nymphs become infected adults
    • Adults feed on dogs and humans, must be attached for 5-20hrs
  67. What cells does Rickettsiae infect, and what does this cause?
    • Endothelial cells of small blood vessels
    • See vasculitis, necrosis and vascular permeability -> edema, hemorrhage, hypotension and shock
  68. What are the CS of RMSF?
    • 2-14 day incubation
    • fever, anorexia, depression, V, D
    • edema, necrosis of extremeties
    • mucopurulent ocular d/c
    • permanent CV, renal and neurological damage is possible
  69. What is a ddx for RMSF?
    Identical CS to Ehrlichia, but not >2 weeks (more acute)
  70. How do you dx RMSF, and what are the expected results?
    • CBC: anemia, thrombocytopenia
    • Chem: hypoalbuminemia, high liver enzymes
    • Serology: 4x rise in titer
    • Histo: direct FA staining
  71. What is the txt for RMSF?
    • Doxycycline for 2 weeks
    • Expect improvement in 24-48hrs
    • No IVF
  72. How can RMSF be prevented?
    • No vx, but natural infection is protective
    • Tick repellants and removal
  73. What are the types of Ehrlichia, and what ticks transmit them?
    • monocytic: E. canis (Rhipecephalus sanguineus), E. chaffeensis
    • granulocytic: E. ewingii (Amblyomma americanum), A. phagocytophilum (I. scapularis or I. pacificus)
    • thrombocytic: A. platys
  74. What is the transmission of E. canis?
    No transovarial transmission
  75. What are the CS of E. canis?
    • acute: first 2-4 weeks, multiplies in monocytes (spleen, liver, LN), infected cells adhere to lung, meninge and kidney endothelium, see thrombocytopenia, anemia, pitting edema, muscle twitching, CN deficits
    • subclinical: see 6-9 weeks, maybe thrombocytopenia
    • chronic: impaired marrow function -> pancytopenia, see pallor, coagulopathy, anterior uveitis, neuro signs
  76. How is E. canis infection dx, and what results do you expect?
    • CBC: pancytopenia, lymphocytosis, thrombocytopenia, maybe see morulae
    • Chem: elevated liver enzymes, azotemia
    • Serology: SNAP 4Dx (cross reacts with other Ehrlichia)
  77. How is E. canis infection tx, and what is the px?
    • Doxycycline 6-8 weeks
    • Px good if acute, poor if chronic (need to give Epo)
  78. What are the CS of granulocytic anaplasmosis?
    • Subclinical infection in many dogs
    • Fever, lethargy, lymphadenopathy, splenomegaly, scleral injection
    • Lameness
  79. How do you dx graulocytic anaplasmosis, and what results do you expect?
    • CBC: thrombocytopenia, mild anemia, lymphopenia, morulae in granulocytes
    • Chem: hypoalbuminemia, elevated ALP
    • Serology: SNAP 4Dx
  80. How do you tx granulocytic anaplasmosis?
  81. What causes salmon poisoning disease, and which animals are affected?
    • Neorickettsia helmonithoeca infection of Nanophyetus salmincola fluke infecting salmon
    • Disease of dogs and coyotes, not cats
  82. What is the transmission of salmon poisoning?
    • N. salmincola always infected by N. helmonithoeca
    • N. salmincola egg shed by dog, develops into miracidia, infects a snail (Auxodrome silicula)
    • Leaves snail as a cercaria which infects salmon, develops into metacercaria
    • Salmon eaten by dog, develops into adult fluke
    • Adult flukes in intestine release rickettsiae into epithelial cells -> lymphatics -> macrophage and plasma cells respond
    • Eggs in feces 5-8 days after fish ingested, and shed for 60-250 days
  83. What are the CS of salmon poisoning?
    • Fishing 5-8 days ago
    • Fever, anorexia, V, D, profound weight loss, lymphadenopathy, splenomegaly, DEATH in 7-10 days if untreated
  84. How is salmon poisoning dx, and what results do you expect?
    • Hx: fish exposure 50% cases
    • CBC: lymphopenia, thrombocytopenia
    • Chem: hypoalbuminemia, inc ALP
    • Flotation + sedimentation: trematode eggs (80%)
    • LN aspirate: macrophage inclusions
    • PCR: of feces or LN aspirates
  85. How is salmon poisoning tx?
    • tetracycline or doxycycline for 2 weeks
    • Prazi for fluke
    • IVF, blood products
  86. What causes parvo, and what are its characteristics?
    CPV-2, non-enveloped DNA virus
  87. Which canine virus can infect feline cells?
    CPV-2, causes feline enteritis
  88. What is the transmission of parvo?
    • Exposure to infected feces or vomit
    • In utero infection (dam asymptomatic
    • Often fomite transmission
    • Shed for weeks after the infection
  89. Which animals are more susceptible to parvo?
    • Young puppies (waning maternal abs, GI parasites, replicating GI cells)
    • Rotts, Dobies, Pits
    • Young kittens
  90. What is the pathophysiology of parvo infection?
    • oronasal exposure
    • oropharyngeal lymphoid tissue and viremia days 1-6
    • infects GI epi, lymphoid tissue, marrow, lungs, spleen, liver, kidney, heart
    • -> either intestinal crypt cell destruction -> neutrophil sequestration, impaired cell turnover, villous blunting, malabsorption, increased peramebility, +/- intussusception
    • Can lead directly or indirectly to...
    • -> marrow destruction -> neutropenia and leukopenia -> bacterial translocation -> sepsis, endotoxemia and DIC
  91. How is parvo treated?
    • Isolate!
    • Supportive with aggressive IVF, dextrose, plasma, TPN at admission
    • Abx
    • Anti-emetics
    • NPO until gradually introduce soft highly digestible food
    • Deworm and tx for Giardia when signs resolve
    • Palpate abd regularly for intussusception
  92. What are the sequelae of an in utero parvo infection?
    • Puppies have myocarditis, kittens have cerebellar hypoplasia
    • Reproductive failure in dam
    • Immune tolerance in neonates
  93. What are the CS of parvo?
    • Incubates 2 weeks
    • Lethargy, inappetance, bile stained V, bloody oderiferous D
    • Abd pain
    • Dehydration
    • Pyrexia
    • Leukopenia
    • Death in 1-2 days (from g- sepsis, shock, DIC)
    • Feline neuro signs: ataxia, intention tremors, incoordination, broad based stance seen at 2-3 weeks old, but mental status normal
  94. How is parvo dx?
    • CS, age, vx
    • CBC: leukopenia
    • Chem: liver enzymes, pre-renal azotemia, hypoglycemia
    • ELISA: fecal Ag, can detect some FPV but usually for CPV-2. Can be false+ 5-12 after MLV vx, and false- 5-7 days after CS
    • PCR: can distinguish from vx and active infection
  95. What is the px for parvo?
    • Fair if tx aggressively
    • Monitor with CBCs (leukopenia)
  96. How can canine parvo be prevented?
    • No killed vx in contaminated environments
    • Vx q 3 weeks from 4 - 16 weeks old, booster after 1 year, then every 3 years
    • Keep pupsindoors until 1 week after last vx
    • Natural infection -> lifelong immunity probably
    • Can monitor serology to know when to vx
  97. How can feline parvo be prevented?
    • MLV vx at 8 - 16 weeks old q 3 weeks
    • Use inactivated vx in queens, kittens <4 weeks, immunosuppressed cats
    • Can give therapeutic passive immunity in exposed kittens, will interfere with vx
  98. What are the characteristics of canine coronavirus?
    • Coronaviridae
    • Enveloped RNA virus
  99. What animals are susceptible to CCoV?
    Dogs < 6 weeks old
  100. How prevalent is CCoV infection?
    Subclinical infection widespread
  101. What are the CS of CCoV?
  102. How is CCoV dx?
    • fecal EM (insensitive)
    • RT-PCT
  103. How is CCoV prevented?
    Vx (unproven benefit, previous version were deleterious)
  104. What viruses can cause enteritis?
    • Rota
    • Astro
    • Calici
    • In puppies and kittens < 3months old
    • Will likely contribute to known enteritis infections
  105. What are the characteristics of FCoV, and what animals are susceptible?
    • 95% fatal
    • See in young cats, purebred catteries and shelters (3mo - 3years old)
    • Enveloped Coronavirus, RNA
    • Two strains: FIPV (causes FIP) and FECV (causes enteritis) are physical indistinguishable
    • FECV -> FIPV in some cats 6-18mo after infection
  106. How common is FCoV infection?
    • 30% cats in single cat households are seropositive
    • 80-90% cats in multicat households are seropositive
    • 0.02% (single) or 5% (multi) cats are actively infected
  107. How is FCoV transmitted?
    • fecal-oral
    • highly infectious - convert within 2 weeks of exposure
    • fomite transmission possible for 6 weeks
    • Infected cats shed intermittently, some cats become chronically infected
    • Infection can be worse in genetically pre-disposed cats and stressed / overcrowded cats
  108. When do maternal abs wane for FCoV?
    4-6 weeks old
  109. What is the pathogenesis of FCoV?
    • FECV replicates in mature enterocytes, esp lower GIT
    • FECV -> FIPV will replicate in macrophages
    • FIPV infects the macrophage -> lymphatics -> LNs -> trapped in small venules -> impaired or strong CMI response
    • Strong CMI = virus eliminated OR latent infection (rare) which leads to impaired CMI sequelae
    • Impaired CMI = Ag:Ab deposition, complement fixation -> attracts neutrophils -> pyogranulomatous vasculitis and FIP
    • Ab production is necessary for the disease to occur (aka ADDE) because Ab binds Fc receptors which enhances viral uptake by macrophages
    • Vx would ramp up this process
  110. What are the CS of FCoV?
    • FECV: mild fever, D, V
    • Not responsive to abx
    • Effusive FIP: dyspnea from pleural effusion, ascites
    • Non-effusive FIP: can enlarge any organ; liver (icterus), spleen, LNs, lung (C, dyspnea), kidneys, intestine (obstructive), eyes (anterior uveitis, retinal detachment, hemorrhage), brain (neuro signs in 25-35%)
    • CBC: lymphopenia
    • Chem: azotemia, elevated liver enzymes, coagulopathies, hyperproteinemia
    • Polyclonal gammopathy
    • Effusion fluid has exudate protein, is thick and may contain clots, but has low cellularity
  111. How can FCoV be dx?
    • NOT serology for FIP, just means exposure to any coronavirus including vx, and even paired samples won't help
    • However negative serology means not likely to have FIP
    • 7B test is also NOT and FIP test
    • RT-PCR of macrophages cannot tell between FECV and FIPV, so not good for FIP testing
    • Histopathology: necropsy or organ biopsy looks for disseminated pyogranulomatous and fibrinobecrotic reaction around small veins
    • If have dry FIP, looks for fluids
  112. What is the tx and px of FCoV?
    • Almost always fatal even with txt, within 5-7 weeks
    • Supportive care including IVF, feeding tube, thoracocentesis
    • Anti-inflammatory and immunosuppressive drugs (pred, chlorambucil)
    • Anti-viral drugs like interferon?
  113. How is FCoV prevented?
    • Happens mostly in seropositive multicat households
    • Control fecal contamination, overcrowding, fomites, concurrent diseases
    • Disinfect with bleach 1:32
    • Isolate queen and kittens until 4-6 weeks old
    • Use PCR and serology to ID chronic shedders and cull
    • In single cat households, will become seronegative in 6-12mo
    • Vx IN which replicates in mucosal surfaces -> systemic response but unknown efficacy. Can't vx seropsitive cats
  114. Where in the body can hemoplasmosis be found?
    epicellular hemotropic
  115. How can hemoplasmosis be dx?
    NO culture - never been cultured
  116. What causes hemoplasmosis?
    • Cats:
    • ‘Candidatus Mycoplasma haemominutum’, "small form", 0.3μm
    • Mycoplasma haemofelis, "large form ", 0.6μm, most pathogenic
    • ‘Candidatus Mycoplasma turicensis’, Swiss variant, never seen, low pathogenicity
    • Coinfections common
    • Dogs:
    • Mycoplasma haemocanis
  117. How do hemoplasma spp look different on a blood smear?
    • M. hemofelis is single cocci
    • M. hemocanis forms strings of cocci
  118. How is hemoplasmosis transmitted?
    Injection, blood sucking arthropods, TICKS (dogs), transplacental, biting
  119. Which animals are most susceptible to hemplasmosis?
    outdoor male cats who are fighting with FeLV/FIV+
  120. What is the pathogenesis of hemoplasmosis in cats?
    • Pre-bacteremic phase (1-3 weeks post infection)
    • Acute phase (cyclical fluctuations in organism numbers and decreased HCT, can see organisms on smears. Anemia from immune mediated splenic sequestration. Splenectomy very bad)
    • Recovery phase (2/3 of cats)
    • Chronic phase (no CS)
  121. What conditions make hemoplasmosis worse?
    • Splenectomy
    • FeLV / FIV+
    • Stress may re-activate
    • Immunosuppressive disease
  122. What are the CS of hemoplasmosis?
    • "Feline infectious anemia"
    • No clinical signs (especially M. haemominutum and turicensis)
    • Sometimes splenomegaly
    • Acute fever
    • Pallor (anemia) -> hemic murmur
    • Terminal hypothermia
  123. How is hemoplasmosis dx?
    • Organism visualization with Wright’s stain (seen in 50% cats in the acute phase, usually present in dogs)
    • R/O basophilic stippling, Cytauxzoon, H-J bodies
    • Nonregenerative then regenerative anemia (reticulocyte counts are invalid)
    • Coombs+
    • PCR - test of choice
  124. What are the ddx for hemoplasmosis?
    • Primary AIHA (super rare!)
    • FeLV
    • Toxins (onions, ingestion of local anesthetics)
  125. What is the txt for hemoplasmosis?
    • Supportive (blood transfusions)
    • Doxycycline
    • Consider prednisone for AIHA
  126. How is hemoplasmosis prevented?
    • House cats indoors (no more fighting)
    • Screen blood donor cats!
  127. What are the characteristics of Bartonella?
    • Small, curved, g- bacteria
    • Hemotrophic, agyrophilic
    • Fastidious
    • Chronic, largely subclinical infections in cats