Infectious Dz Flashcards
Exam 3
What are the 2 types of diagnostic tests?
antibody
organism
What are some advantages of organism testing?
- positive implies presence of organism
- can localize dz from sample
- sensitive in immunocompromised
- quantification may be possible
What are some disadvantages of organism testing?
- dec. sensitivity for some inf. (chronic, smoldering inf)
- false (+)s possible
- positive test =/= disease
- no sense of chronology
Culture (type, pros, cons)
- organism detection
- Pros: organism id + sensitivity testing
- Cons:
- -> false neg from low sample size
- -> some org. un-culturable
- -> transport and storage == death
- -> can be expensive
Immunoassays for antigen (type, pros, cons)
- organism detection
- Pros: n for organism detection, fast and easy (SNAP tests)
- Cons:
- -> false (-) w/ low [antigen]
- -> false (+) w/ cross reaction
- -> variable sens. and specificity
End Point PCR
- only gives + or -
- no level of quantification
Real Time PCR
- quantitative measurement of [DNA] present in sample
Cons of Real Time PCR
- false (-) w/ strain variation
- inhibition of certain enzymes
- potential for false (-) from degradation
- false (+) from contamination
- can detect dead/ inactive organisms
Antibody Detection (pros)
- sensitive as a single test in immunocompetent host w/ chronic dz
- paired serology (IgM/G) allows from chronology
Antibody Detection (cons)
- neg early on acute disease
- neg w/ URT infections
- neg w/ immunocompromised patients
- false (+) are problematic
- poor indicators of treatment success
When do to antibody vs organism?
Organism : acute disease, immunocompromised
Antibody: chronic persistent infection, organisms undetectable
Actinomyces (epidemiology/ etiology)
- does not exist freely in nature
- n oropharyngeal and gi inhabitant
- young adult to middle-aged large breed dogs/ usually immunocompetent
Actinomyces (pathogenesis)
- grass awns in oropharynx penetrate and migrate
- bite wound inoculation
- CNS actinomycosis: hematogenous spread from thorax (abscess)
Diagnosis of Actinomyces or Nocardia
- gram stain (thin, gram (+), filamentous bacteria)
- H&E not effective stain
- alert lab fro culture + mult samples
- Nocardia is variably acid-fast (+) while Actinomyces is acid fast (-)
Treatment of Actinomyces or Nocardia
- prolonged treatment w/ high dose abx to prevent relapse
- drain abscesses or pyothorax first
- Actinomyces: peneclillin is ideal
- Nocardia: much worse prognosis, but TMS
Nocardia (etiology, epidemiology)
- aerobe, ubiquitous soil saprophyte
- 1/3-4 are immunosuppressed
- much less common than actinomyces
Nocardia (pathogensis)
- inhalation –> pulm nocardiosis –> pleural or systemic spread
- hematogenous dissemination to other organs
- skin involvement: firm to fluctuant SQ swellings containing serosanguinous –> purulent fluid
3 major groups of mycobacterium
- Tuberculosis mycobacteria (m. tuberculosis and m. bovis)
- Opportunistic mycobacteria (slow and fast growing)
- Lepromatous mycobacteria
Tuberculous Mycobacteria
- m. tuberculosis and m. bovis
- highly pathogenic
- reverse zoonosis [m. tuberculosis is potentially zoonotic)
Opportunistic Mycobacteria
- saprophytic, survive > 2 years in env.
- slow-growing (m. avium complex)
- rapid-growing (RGM)
- not zoonotic
Pathogenesis of Opportunistic Mycobacteria (slow and RGM)
- multiply intracellularly at inoculation site and local LN
- Avium tend to be disseminated
- Defective cell-mediated immunity –> allows for persistence or dissemination –> granuloma formation
Rapidly-growing Mycobacterium
- inoculated into skin via trauma
- enhance pathogenicity in adipose
- most animals are immunocompetent
- cats are most susceptible (especially female)
Clinical signs of RGM
- cutaneous and subcutaneous granulomas (especially the inguinal area [mycobacterial panniculitis])
Diagnosis of RGM
- Histopath –> pyogranulomatous inflammation
- Isolation:
- -> tuberculous can take 4-6 weeks to grow
- -> RGM may take 3-5 days
Treatment of M. tuberculous
- not recommended but has been successful
- prolonged treatment time (>6months)
What are the Canine Core Vaccines?
- rabies
- distemper (D)
- adenovirus (A)
- parvovirus (P)
- lepto +/-
What are the feline Corse Vaccines?
- Rabies
- Feline Herpesvirus (FVR)
- Feline Calicivirus (C)
- Feline Panleukopenia (P)
Core Vaccine Protocol
- 6-8 wks, then every 3-4 wks until 16 weeks for FVRCP or DAP
- booster @ 6 months - 1 year then every 3 years except for: recombinant, lepto, lyme, bordatella
What is the Window of Susceptibility (for vaccination)?
- the period of time between which:
- -> the maternal antibodies are low enough to prevent disease
- -> minimum titer to block vaccine
christina’s favorite food
dim sum
Canine Distemper
- highly infectious
- enveloped RNA virus (readily inactivated)
- shep in resp secretions, feces, and urine for up to 3 months post infection
Canine Distemper Pathogenesis
Stage 1: Lymphoid Tissue
–> virus invades macrophages in URT –> lymphatic spread –> day 2-6 for systemic spread
–> fever, lymphopenia
Stage 2: epithelial and nervous tissue
–> day 8-9 –> epithelial and CNS invasion
Canine Distemper Clinical Signs
Early:
–> lethargy, inappetance, fever,
–> conjunctivitis, cough, serous ocular and nasal discharge
Progression:
–> obtundation, anorexia, comiting, diarrhea, –> moist cough, tachypnea
–> neuro signs
Canine Distemper Diagnosis
- Clinical signs
- CBC w/ viral inclusions
- thoracic rads
- CSF analysis
- conjunctival scrapings for inclusions
- RT-PCR
Infectious Canine Hepatitis (ICH)
- usually young puppies
- canine adenovirus-1 targets endothelial cells and hepatocytes
- virtually extinct in USA
ICH Clinical Signs
- most infections are sub-clinical Acute form: --> puppies age 6-10 wks --> fever, anorexia, lethargy, tonsiliitis, cough, tachypnea, hepatomegaly, abd. apin, edema, ascites, CNS signs (hepatic encephalopathy) --> corneal edema and anterior uveitis Peracute --> death within a few days
Hallmark lesion of ICH
- corneal edema and anterior uveitis
- type 3 hypersensitivity
ICH diagnosis
- clinical signs
- bloodwork abnormalities (liver signs)
- PCR or histopath (of liver)
ICH prevention
- vaccine for adenovirus-2 (protects for 1 & 2)
- do not use mucosal CAV-2 for CAV-1 prevention
Treatment of Canine Distemper Virus
- supportive care only
Parvovirus
- sever enteritis and leukopenia in dogs and cats
- highly contagious, often fatal if untreated
- feline panleuk is far less common than canine parvo
- non-enveloped virus requiring rapidly dividing cells to replicate
- shed for 4 wks post infection
- resists disinfection and can survive up to a year on fomites
Parvovirus pathogenesis
- oronasal exposure –> migration into local lymphoid tissues (viremia day 1-6) –> infection of gi, lymphoid, marrow tissues
- -> sepsis, endotoxemia, and DIC
- infections in utero or <8wks of age in cats causes cerebellar hypoplasia
Parvovirus Clinical Signs
- incubation period (3-14 days canine, 2-10 days feline)
- lethargy, fever –> vomiting and diarrhea
- leukopenia
- death in 1-2 days (peracute)
Parvovirus Diagnosis
- CBC –> leukopenia
- Fecal ELISA
- fecal PCR
- histopath –> gold-standard but on necropsy
Parvovirus Treatment
- isolation
- aggressive IV fluid therapy
- broad-spectrum IV antimicrobials
- IV dextrose
- plasma for hypoalbuminemia
- antiemetics
Parvovirus Prevention
- vaccination (attenuated live)
- vax to 16-18 wks of age
- titers correlate w/ protection
Leptospirosis epidemiology
- survives in stagnant or slow-moving warmer water, temp 0-25C
- transmission via direct contact w/ contaminated urine, bite wounds, or ingestion of infected tissue
- organisms penetrate intact mucous membranes or abraded skin
Leptospirosis Pathogenesis
- actue kindey injury
- +/- hepatic insufficiency
- +/- hemorrhagic disease
Leptospirosis Cliinical Signs
- fever, lethargy, inappetence
- PUPD or anuria/ oliguria
- abd. pain
- mild peripheral lymphadenopathy
- icterus
- +/- uveitis
- +/- tachypnea d/t pulm. hemorrhage
Leptospirosis Imaging findings
- n thoracic rads
- abd. ultrasound –> hyperechoic renal cortices, perirenal fluid, renomegaly
Leptospirosis Diagnosis
- antibody detection
- organisms detection –> kidney biopsy is less than ideal since there are low numbers of organisms
Leptospirosis Treatment
- ampicillin or penicililin for comiting dogs
- doxycyclin for 2wks post-vomiting
- aggressive IV fluids
- diuretics
- antiemtetics
- hemodialysis
Leptospirosis Prognosis
- 85% survival rate w/ aggressive therapy
Hyperthermia
- retained hypothalamic set-point
- undesirable heat retention or heat overproduction
- Cause: heat strokes, seizures, tetanus, adverse drug rxn, exercise
- not responsive to anti-pyretics
Fever
- exogenous pyrogens (LPS) stimulate release of endogenous pyrogens by macrophages –> IL1, 6, TNFa
2 Mechanisms of Fever
- Humoral mechanism: endogenous pyrogens activate arachidonic acid pathway in microglial cells; PGE2 raises set point in hypothalamus
- -> sympathetic generation/ retention of heat (vasoconstriction, shivering) - Neuronal hypothesis: C5a stimulates PGE2 production by liver; vagaly mediated neural response
What is a “drug fever”
- elevated body temp d/t drug-induced alterations in muscle activity or sensitivity of hypthalamic neurons
- actually a hyperthermia
What are 3 examples of “drug fever”s
- Malignant hyperthermia –> mutation in ryanodine receptor causes excessive influx of Ca and depletion of ATP
- Serotonin syndrome
- Opioid in cats: excitement, excessive sedation, staring, hyperthermia
Factors that modify a fever
- extremes of age
- renal failure (uremic acids are cryogenic)
- immunosuppression
- anti-inflammatory drugs
Fever Type
- Persistent: above n throughout day, but does not vary
- Remittent: above n throughout day, and does vary widely (eg. endocarditis)
- Intermittent or relapsing (cyclic neutropenia, borrelia)
Fever Magnitude
- Low grade (<104F)
- fungal inf.
- bartonellosis, lyme disease
- mycobacterial/ mycoplasma inf. - High grade (>104F)
- viral or bacterial inf.
- salmon poisoning
- rocky mountain spotted fever
- Plague and Tularemia
Fever of Unknown Origin (FUO)
- prolonged fever >3wks duration ass. w/ vague, non-specific signs of illness
- diagnosis uncertain after 1 wk of hospitalization involving thorough lab tests
- ~20% of fever cases are of unknown origin
FUO how to identify
- look for Infectious, Neoplastic, or Immune- mediated cause
- Localize the lesion (eyes, skin, rectal, musculoskeletal)
Exam and Tests for FUO
- CBC, Chem, UA –> rads, ultrasound
- repeat your physical exam
- Arthrocentesis (IMPA is a common cause of FUO), lymph nodes, blood culture, serology (tick borne, lepto, toxo, neospora, fungal)
Cause of FIP
- feline enteric coronavirus
Pathogenesis of FIP
- fecal-oral spread of avirulent form from another cat
- lives in GI tract
- mutates into virulent form (FIPV)
- multiplication in macrophages
T/F: pure bred cats have higher incidence of FIP than non-pure bred
Yes
PE findings with FIP
- fever
- tachypnea
- muffled heart sounds
- icterus
- organomegaly (liver, spleen, kdiney)
- ant uveitis
- ret. detachment, hemorrhage
- neuro signs
Lab findings with FIP
- NNN anemia
- neutrophilia, leukopenia, thrombocytopenia
- azotemia
- elevated liver enzymes
- high bilirubin
- high globulins
- low albumin
FIP Effusion
- high protein
- low cells
- straw colored and viscous
- modified transudate, most likely
FIP Diagnostic Testing
Serology (pos = exposure to any coronavirus)
RT-PCR (no specific mutation for FIP)
Biopsy and Cytology (ICC on effusion)(Biopsy/IHC –> fibrinous lymphadenitis)
FIP treatment
- supportive only
- prednisolone, +/- antivirals
FIP prognosis
- 1 day – 1 year (most 5-7 weeks)
FIP neg pronostic indicators
- wet/ effusive FIP
- high bilirubin
- lymphopenia
- failure to respond within 3 days of treatment
FIP prevention
- selective breeding programs
- inform breeder
- decrease stress
- don’t breed FIP + cats
FIP Vaccination
- temp-sensitive intranasal vax
- adm. at 16 weeks
- efficacy debated
FeLV (general)
- leading cause of feline mortality
FeLV (Etiology)
- enveloped RNA virus
- susceptible to desiccation heat, disinfections
FeLV (Epidemiology)
- transmission is in saliva (requires prolonged, close contact)
- viremic cats can live months to years (max 4 years)
- transmission via blood transfusion
FeLV (Age-Related Resistance)
- progressive dz incidence decrease as age increases
- uncommon to see it over 10 years
FeLV (prevalence)
- up to 30% of cats in cateries
- <3% of suburban and shelter cats (because of effective treatment and prevention protocols)
FeLV (prognostic factors)
- challenge dose
- immune status
- age
- viral strain
FeLV (Pathogenesis)
- oronasal exposure –> oropharyngeal lymphoid tissue –> few peripheral mononuclear cells (ELISA +) –> spleen, LNs, epithelial tissues, marrow (ELISA +, IFA +) –> poor immune response === FeLV disease
FeLV (regressive vs progressive)
Regressive:
- FeLV inserts itself into the genome, but is effectively silenced and will not replicate itself
Progressive:
- FeLV inserts itself into the genome and reproduces
- more common in younger animals
What kinds of diseases do you see with FeLV infection?
- Lymphoma : esp. mediastinal lymphoma causing a pleural effusion
- Leukemia : pancytopenia w/ lethargy, sepsis, hemorrhage
- Anemia : impaired red cell production w/ macrocytosis
FeLV (Diagnosis)
- Antigen-detection ELISA (screening) and IFA
- PCR (not recommended for screening) for both DNA (proviral) and RNA
T/F: a regressor FeLV cat will be PCR (+) and RT-PCR (-) and ELISA (-)
T
FeLV (Treatment)
- chemo for lymphoma
- transfusions for anemia
- abx for 2* lesions
- antivirals have not been effective
FeLV (Prevention)
- killed or recombinant vax
- 2 doses @ 9 wks then every year (recombinant) or every 2-3 years (killed)
- only vax FeLV (-) cats
FIV (general)
- worldwide distribution
- chronic infection –> immunodeficiency
FIV (Etiology)
- enveloped RNA virus
- infection is for life
FIV (Epidemiology)
- prevalence in sick cats 13-15%
- prevalence in healthy cats 2-3%
- 2-3x greater incidence in males
- mean age of 6-8 years
FIV (Transmission)
- saliva by biting
- transplacental transmission depends on: strain or degree of maternal viremia
- most kittens infected by saliva or milk
- indoor housing decreases transmission rates
FIV (Pathogenesis - target cells)
- T helper (CD4+) and then later attack of CD8 and B cells
- tissue macrophages
FIV (Pathogenesis results)
- gradual destruction of immune system
- promotion of neoplastic disease
- neurological disease
FIV (Clinical Findings)
Transient Primary Illness - transient lymphadenopathy, pyrexia, depression, anorexia, neutropenia, lymphopenia Subclinical Phase - hyperglobulinemia Terminal Phase - 2* infections = **stomatitis**, recurrent URTD, diarrhea, weight loss, chronic skin dz, opportunistic inf - ocular dz - eventual neuro signs - chronic wasting
FIV (diagnosis)
- Antibody Testing (ELISA, Western Blott)
- antigen levels are low in FIV
- ELISA has potential for false(+) - maternal antibodies, retest
- ELISA has potential for false(-) - cats w/ acute dz, end-stage dz
FIV (Treatment)
- antivirals (AZT –> improves stomatitis and CD4/8 ratios, protease inhibitors not useful, no effective treatment known)
- keep cats indoors
- identify and treat opportunistic infections
FIV (prevention)
- inactivated vaccine used to be available (interferes w/ snap idexx test)
5 Ground Rules of Immunosuppressive therapy
- make sure that it’s immune-mediated disease prior to treatment
- warn o that neoplasia/ infection may go undetected despite best efforts
- think before you clip
- minimize excessive immunosuppression - never use more than 2 drugs at once
- maintain contact w/ your patient
3 most common immune-mediated diseases
- IMHA
- ITP
- IMPA
Glucocorticoids (drug examples)
- prednisone/solone, dexamethasone
Glucocorticoids (adverse effects)
Think Cushing’s like symptoms
- PUPD, polyphagia
- panting
- muscle wasting
- skin thinning, hair loss
- hepatomegaly
- calcinosis cutis
T/F: it is ok to combine a glucocorticoid with an NSAID for increased effect.
False
Azathioprine (moa)
- competes with adenine, that prevents nucleic acid synthesis
Azathioprine (general facts)
- drug sparing effect for glucocorticoids
- almost always given with a glucocorticoid
- inexpensive drug, but monitoring costs money
Azathioprine (adverse effects)
Do not give to cats Dogs: - gi upset - impaired hair growth - bone marrow suppression - hepatotoxicity - pancreatitis - profound weakness and tetraparesis
Chlorambucil (species, disease uses, adverse effects)
- alkylating agent
- used most often in cats
- IBD, Lymphoma, immune diseases
- adverse effects uncommon
Cyclosporine A (moa)
- interacts w/ cyclophilins in lymphocytes, blocking formation of transcription factors needed for T cell activation and cytokine synthesis (mainly IL-2)
Cyclosporin A (uses)
- immune suppression
- atopic dermatitis
Cyclosporin (adverse effects)
- gi signs (most common)
- gingival hyperplasia
- hirstitism
- nephrotoxicity
- hepatotoxicity
- neoplasia
Ciclosporin (drugs)
- neoral and atopica are much better formulations than generic d/t bioavailability difference
Ciclosporin (metabolism)
- p450 metabolism
- binds p-glycoprotein (may predispose to ivermectin toxicity)
Mycophenolate mofetil
- inhibits purine synthesis
- glomerulonephritis
- will cause gi toxicity
IMHA
- type 2 hypersensitivity (antibody mediated) Prognostic factors: - intravascular hemolysis - absence of regeneration - auto-agglutination - thrombocytopenia - hyperbilirubinemia
IMPA
- Type 3 hypersensitivity reaction
- common in dogs, uncommon in cats
- may be 2* to infection, drugs, neoplasia
IMPA (treatment)
- azothioprine (number 1 choice), ciclosprin (good #2)
- -> no NSAIDs w/ pred
IMPA (clinical signs)
- stiffness, reluctant to rise, shifting leg lameness
- fever +/- joint signs
- peripheral lymphadenomegaly
- swollen, painful, warm joints
IMPA (diagnosis)
- cbc, chem, ua
- rads
- +/- joint radiographs (n in acute disease)
- arthrocentesis (minimum 3 joints)(ideal)
Rickettsia (general)
- arthropod transmitted
- obligate intracellular
- gram (-) bacteria
Rocky Mountain Spotted Fever (epidemiology)
- most cases march-october
Rocky Mountain Spotted Fever (pathogenesis)
- ticks must attach for 5-20 hours
- infects endothelial cells of small vessels –> vasculitis
- see a vasculitis, necrosis, increased vasc permeability
- edema, hemorrhage, hypotension, shock
Rocky Mountain Spotted Fever (clinical signs)
- ADR (fever, anorexia, depression)
- edema, hyperemia, necrosis of extremities
- mucopurulent ocular discharge
- joint pain/ swelling/ myocarditis
Rocky Mountain Spotted Fever (Diagnosis considerations)
- indistinguishable from acute ehrlychiosis but much shorter course (<2wks)
- very lethal disease
Rocky Mountain Spotted Fever (Diagnosis)
- Serology (IFA, ELISA)
- 4x increase in titers
- PCR
- Direct FA of biospy samples (75% positive by day 3-4)
Rocky Mountain Spotted Fever (Treatment)
- doxycycline for 2 weeks
Rocky Mountain Spotted Fever (Prevention)
- lifelong immunity following infection
- no vaccine
Canine Monocytic Ehrlichiosis (3 Pathogenic Phases)
Acute Phase (first 2-4 weeks):
–> multiplies in monocytes w/ splenomegaly and lymphadenopathy
–> infected cells adhere to lungs, kidney, meninges
–> thrombocytopenia, +/- leukopenia, anemia
Subclinical Phase (weeks 6-9)
–> no signs
Chronic Phase
–> impaired bone marrow fxn
Canine Monocytic Ehrlichiosis (Clinical Signs)
Acute: ADR, oculonasal discharge, edema of limbs and scrotum
Chronic: pallor, bleeding tendencies despite good platelet count, ant. uveitis, hemorrhage
Canine Monocytic Ehrlichiosis (Diagosis)
- pancytopenia, lymphocytosis, thrombocytopenia
- +/- coombs (+) anemia
- id of morula on blood smear (within monocytes)
- Serology: 4DX snap test
- IgG between 7-28 days post-inf
Canine Monocytic Ehrlichiosis (Treatment)
- Doxycycline for 6-8 weeks
- prognosis is good for acute ehrlichiosis
Canine Granulocytic Anaplasmosis (Pathogenesis)
- subclinical infeciton in many dogs
- fever, lethargy, lymphaneopathy, splenomegaly, scleral injection
Canine Granulocytic Anaplasmosis (Diagnosis)
- morulae w/in the granulocytes
- Serology: SNAP vs IFA
Canine Granulocytic Anaplasmosis (Treatment)
- doxycycline
Salmon Poisoning (etiology)
- neorickettsia helminthoeca
- transmitted via ingestion of a fish containing trematode/ fluke: nanophyetus salmincola
Salmon Poisoning (Pathogenesis)
- mature fluke in intestine release rickettsia into intestinal epithelium
- spreads systemically via lymph
- ulcerohemorrhage enteritis
- lymphoid tissue invasion by macs and plamsa cells
Salmon Poisoning (Clinical Signs)
- vomiting, hemorrhagic diarrhea
Salmon Poisoning (diagnosis)
- hx of fish exposure
- thrombocytopenia (in 90% of cases)
- id of eggs (>80% of cases)
- inclusions of macs in LN aspirates
Salmon Poisoning (treatment)
- tetracyclines for 2 weeks (doxycycline)
- praziquantil for fluke infestation
- IV fluids +/- blood products if needed
Borrelia burgdorferi (Pathogenesis)
- must be attached for 48 hours
- trans. via tick saliva
- replicates and migrates through connective tissue
Borrelia burgdorferi (Clinical Sings)
- arthritis, fever, lymphadenopathy, anorexia for 2-5 months after tick bite
- protein-losing nephropathy (IHC of renal biopsy)
Borrelia burgdorferi ( Diagnosis)
- non-specific signs
- joint taps (neutrophilic mono/polyarthritis)
- organism tests available but not sensitive
- Serology (+) result = exposure at some point
Borrelia burgdorferi (treatment)
- doxycycline for 4 weeks (1st choice)
Borrelia burgdorferi (prevention)
- tick inspection after outdoor activity
- topical ectoparasitides
- prophylactic abx not recommended
- vaccines (efficacious but controversial d/t high adverse effects and yearly dose rate)
Canine Bebesiosis (etiology)
- rbc parasite
- tick-borne disease
- can be trans. through blood transfusions
Large Babesia
- singly or paired in RBCs
- B. vogeli and B. canis (least pathogenic organisms)
- higher prevalence in kennels, adults, greyhounds
Large Babesia (clinical signs)
- hemolysis
- anemia, fever, hypotensive shock
- sometimes: icterus, splenomegaly, IMT
Babesia gibsoni
- small babesia
- found singly in RBCs
- mostly in pits/ staffies
Babesia gibsoni (clinical signs)
- fever, anorexia, weakness
- anemia, thrombocytopenia
- HCT may normalize 2-3 months post infection
Babesia conradae
- medium-size organism
- very similar to B. gibsoni
Canine Babesiosis (Diagnosis)
- CBC (low thomb, +/- regen anemia
- Detection of organisms of blood smear
- serology
- PCR - current test of choice
Canine Babesiosis (Treatment)
- blood transfusions
- fluids
- antibabesial drugs (imodocarb proprionate for large)(atovaquone and azithromycin for medium/small)
Canine Babesiosis (Prevention)
- tick control
- avoid splenectomy and immunosuppression in chronicity infected dogs
- screen blood donors serologically
Feline Cytauxzoonosis (etiology)
- usually fatal, tick borne dz of cats
- outdoor cats
- bobcat reservoir
- southern/ southereastern US
Feline Cytauxzoonosis (Pathogenesis)
- Shizogonous phase: infected mononuclear cells rupture and release organisms leading to DIC and shock
- Intraerythrocitic phase: 1-3 days after shizonts appear, hemolytic anemia w/ high fever, ring-shaped org in RBCs
Feline Cytauxzoonosis (Clinical Signs)
- usually rapidly fatal: dark urine, dehydration, icterus, pallow, prolonged CRT, hypothermia
- death w/in 5 days
Feline Cytauxzoonosis (Diagnosis)
- anemia, leukopenia, thrombocytopenia, hyperbilirubinemia
Feline Cytauxzoonosis (Treatment)
- high mortality despite treatment
- supportive care
- rare cats survive w/out treatment
Leishmaniosis (Etiology)
- important human dz
- mediterranian, central and south america
- sandfly vector
Leishmaniosis (Clinical Signs)
- hyperkeratosis and intradermal nodules
- splenomegaly, lymphadenopathy, polyarthritis, glomerulonephritis, uveitis, rhinitis
Leishmaniosis (Diagnosis)
- visualization of amastigotes in biopsies or aspirates
Leishmaniosis (Treatment)
- controversial
Hepatozoonosis (Epidemiology)
- H. americanum infects dogs in the southeastern US
Hepatozoonosis (Life cycle)
- dog eats tick
- cysts containing merozoites form in tissues
- pyogranulomatous inflammation
Hepatozoonosis (Clinical Signs)
- wasting disease/ myositits
- pain, gait abn
- glomerulonephritis
Hepatozoonosis (Diagnosis)
- marked luekocytosis
- hypoglycemia
- skeletal radiographs
- PCR of muscle biopsy is the gold standard
Hepatozoonosis ( treatment)
- longterm adminstration of decoquinate for remission, no cure
Neospora (Etiology)
- life cycle resembles that of toxoplasma w/ dog as definitive host
- transplacental transmission following ingestion of tissue cysts by carnivores or oocytes by herbivores
Neospora ( Clinical signs)
Herbivores: abortion
Carnivores: neuromuscular abnormalities, ascending paralysis and muscle atrophy and stiffness in dogs less than 6 months of age
Neospora (tranmission)
- ingestion of cysts will infect
- most are transplacental d/t reactivation of bradyzoite cysts during pregnancy
Toxoplasma (Etiology)
- toxoplasma gondii
- cats are definitive host
Toxoplasma (Epidemiology/ Cycles)
- sexual reproduction (enteroepithelial cycle) occurs only within the gi tract of the cat and sheds out oocysts
- asexual reproduction (extraintestinal cycle) occurs in all other species but does not result in shedding
Toxoplasma (Reactivation of bradyzoites)
- sever immune suppression from high steroids, HIV, chemotherapy, anti-organ-rejection
Toxoplasma (Transplacental Infection)
- naive humans and animals infected just prior to pregnancy
- placentitis and spread of tachyzoites to fetus
- pregnancy =/= reactivation
Toxoplasma (route of infection)
- transplacental
- bradyzoite cyst ingestion
- occyst-contaminated food, water, soil
Toxoplasma (Diagnosis)
- Cytology –> tachy rarely seen
- Radiology –> diffuse interstitial to alveolar patter/ pleural effusion; hepatomegaly, peritoneal effusion
- Fecal exam –> cats are rarely shedding
- Serology –> IgM >64 or 4x rise in titers
- Org. Detection –> histopath detection of tachyzoites aided by IHC (not bradyzoites)
Toxoplasma ( treatment)
- supportive therapy
- clindamycin
Toxoplasma (Risk of cat ownership)
- 30% of dogs and cats are seropositive
- Pet cats are of little risk
- seronegative cats at greatest risk to seronegative women
Toxoplasma ( Cat Clinical Signs)
- enteroepithelial cycle usually subclinical
- extraintestinal cycle:
- -> stillbirth, neonatal death
- -> anorexia, fever, CNS, dyspnea, coughing, comiting, diarrhea
- -> uveitis, chorioretinitis
Toxoplasma (Dogs clinical signs)
- similar to cats
- ocular disease less common
- chrnoic neuromuscular disaese
Toxoplasma ( Humans)
- immunocompetent –> flu-like symptoms
- AIDS and transplant patients:
- -> 95% of cases d/t bradyzoite cyst reactivation
- -> encephalitis, chorioretinitis, occasional pneumonia
Toxoplasma (Epidemiology - humans)
- 25-50% of humans seropositive
- cysts present in lamb, pork
- reduction of bradyzoite cyst levels (cook, salt, cure foods)(microwave doesn’t work)
