SA Med Exam 3

• Antarctica
• Australia and NZ
• Taiwan
• Japan
• some Caribbean Islands
• England
• Ireland
• parts of Scandinavia
• Hawaii

• Rhabdoviridae, Lyssavirus
• enveloped -ssRNA

• 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!

2-24 weeks, but usually 1-2 months from time of bite

• 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

<2 weeks

• 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

• 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)

• 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

• Initial vaccine at 4 months of age, boostered 1 year later, then every 3 years after that
• Killed rabies vx in R rear leg

• Euthanize
• 6 month quarantine + vaccine at 5 months

Revaccinate, then confine for 45 days

case by case basis

confine animal for 10 days (they will develop CS that fast if were infective)

• Euthanize
• Potential quarantine at shelter

Euthanize

• wash wound under pressure with warm water and quat
• vaccine series (more extensive for unvaccinated humans)

• 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)

kennel cough

• enveloped RNA virus
• Paramyxovirus, Morbillivirus

• Racoons
• Most infections subclinical
• See at weaning in dogs and cats (vaccinated population)
• Shed in resp secretions, feces and urine for 1-3 months

• 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

CNS signs = poor prognosis, could develop at any time

• 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

• Treatment is purely supportive
• Fluid therapy
• Abx
• Antiemetics
• Nebulization and coupage
• Oxygen
• Neurologic signs are usually permanent, and may occur later

• 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

• Usually young puppies
• Preferentially targets endothelial cells and hepatocytes
• Caused by canine adenovirus 1 (non-enveloped DNA virus)
• Probably now extinct in the US

• 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

• 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)

• 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

Supportive care: IVF, anti-emetics, blood, dextrose, HE txt (lactulose, neomycin, restrict dietary protein)

• 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

12-16 weeks

• 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

aerosol, variable shedding for 2 weeks (viral) or >3 months (B. bronchispetica and Mycoplasma)

• Incubates for 3-10 days
• paroxysmal C, retching (V), tracheal sensitivity
• self-limiting

• Hx, CS, txt response
• Thrx rads
• TTW + C&S
• PCR

• +/- abx (e.g. doxycycline, enro, clavamox) for 4 weeks
• anti-tussive (e.g. hydrocodone) - but not if bronchopneumonia!
• supportive (e.g. O2, IVF

• 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

• Calici
• Herpes-1
• Chlamydia felis
• B. bronchiseptica
• Mycoplasma

FCV > FHV > Chlamydia

• direct close contact
• fomites
• carrier cat

• Incubation period 2-6 days
• Course 1-3 weeks
• Most severe signs in very young, elderly, or immunosuppressed cats

non-enveloped RNA, but >100 strains

• Conjunctivitis, sneezing, nasal discharge
• Facial ulceration, edema, coagulopathies, lethargy, fever
• Limping syndrome
• High mortality
• Self-limiting

• Severe oculonasal discharge
• CNS
• Reproductive (abortion, resorption, congenital defects)
• Ulcerative facial and nasal dermatitis

• 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

• Conjunctivitis, S, abortion?
• Younger cats (esp. 9 weeks to 6 months)
• Course 1-3 months

• Isolation
• FA
• Serology
• PCR

• Isolation
• PCR

• Culture (special for Mycoplasma, takes weeks)
• PCR

• IVF, TPN, O2
• Abx for C. felis (doxy of clavamox for ALL cats for 4 weeks)
• Topicals for FHV-keratitis
• Famciclovir

• FHV, FCV have MLV (IN, SC) or killed vx
• C. felis has MLV and killed vx
• Bord vx

dogs, cattle, humans, horses

• Ixodes scapularis: East coast, midwest
• Ixodes pacificus: West coast

• 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)

• 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

• 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

Granulocytic anaplasmosis (A. phagocytophilum) which is also transmitted by I. scapularis

• 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

• whole bacterin with OspA and OspC
• recombinant OspA
• remove ticks and use topical repellants

• 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-

• Doxycycline for 4 weeks
• Expect improvement in 24-48 hours
• Consider NSAIDs

• arthropod transmitted
• obligate intracellular g- coccobacilli bacteria

• D. andersoni: northwest USA
• D. variabilis: east coast USA

• 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

• Endothelial cells of small blood vessels
• See vasculitis, necrosis and vascular permeability -> edema, hemorrhage, hypotension and shock

• 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

Identical CS to Ehrlichia, but not >2 weeks (more acute)

• CBC: anemia, thrombocytopenia
• Chem: hypoalbuminemia, high liver enzymes
• Serology: 4x rise in titer
• Histo: direct FA staining

• Doxycycline for 2 weeks
• Expect improvement in 24-48hrs
• No IVF

• No vx, but natural infection is protective
• Tick repellants and removal

• monocytic: E. canis (Rhipecephalus sanguineus), E. chaffeensis
• granulocytic: E. ewingii (Amblyomma americanum), A. phagocytophilum (I. scapularis or I. pacificus)
• thrombocytic: A. platys

No transovarial transmission

• 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

• CBC: pancytopenia, lymphocytosis, thrombocytopenia, maybe see morulae
• Chem: elevated liver enzymes, azotemia
• Serology: SNAP 4Dx (cross reacts with other Ehrlichia)

• Doxycycline 6-8 weeks
• Px good if acute, poor if chronic (need to give Epo)

• Subclinical infection in many dogs
• Fever, lethargy, lymphadenopathy, splenomegaly, scleral injection
• Lameness

• CBC: thrombocytopenia, mild anemia, lymphopenia, morulae in granulocytes
• Chem: hypoalbuminemia, elevated ALP
• Serology: SNAP 4Dx

Doxycycline

• Neorickettsia helmonithoeca infection of Nanophyetus salmincola fluke infecting salmon
• Disease of dogs and coyotes, not cats

• 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

• Fishing 5-8 days ago
• Fever, anorexia, V, D, profound weight loss, lymphadenopathy, splenomegaly, DEATH in 7-10 days if untreated

• 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

• tetracycline or doxycycline for 2 weeks
• Prazi for fluke
• IVF, blood products

CPV-2, non-enveloped DNA virus

CPV-2, causes feline enteritis

• Exposure to infected feces or vomit
• In utero infection (dam asymptomatic
• Often fomite transmission
• Shed for weeks after the infection

• Young puppies (waning maternal abs, GI parasites, replicating GI cells)
• Rotts, Dobies, Pits
• Young kittens

• 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

• 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

• Puppies have myocarditis, kittens have cerebellar hypoplasia
• Reproductive failure in dam
• Immune tolerance in neonates

• 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

• 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

• Fair if tx aggressively
• Monitor with CBCs (leukopenia)

• 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

• 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

• Coronaviridae
• Enveloped RNA virus

Dogs < 6 weeks old

Subclinical infection widespread

enteritis

• fecal EM (insensitive)
• RT-PCT

Vx (unproven benefit, previous version were deleterious)

• Rota
• Astro
• Calici
• In puppies and kittens < 3months old
• Will likely contribute to known enteritis infections

• 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

• 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

• 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

4-6 weeks old

• 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

• 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

• 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

• 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?

• 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

epicellular hemotropic

NO culture - never been cultured

• 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

• M. hemofelis is single cocci
• M. hemocanis forms strings of cocci

Injection, blood sucking arthropods, TICKS (dogs), transplacental, biting

outdoor male cats who are fighting with FeLV/FIV+

• 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)

• Splenectomy
• FeLV / FIV+
• Stress may re-activate
• Immunosuppressive disease

• "Feline infectious anemia"
• No clinical signs (especially M. haemominutum and turicensis)
• Sometimes splenomegaly
• Acute fever
• Pallor (anemia) -> hemic murmur
• Terminal hypothermia

• 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

• Primary AIHA (super rare!)
• FeLV
• Toxins (onions, ingestion of local anesthetics)

• Supportive (blood transfusions)
• Doxycycline
• Consider prednisone for AIHA

• House cats indoors (no more fighting)
• Screen blood donor cats!

• Small, curved, g- bacteria
• Hemotrophic, agyrophilic
• Fastidious
• Chronic, largely subclinical infections in cats