Fever & Immune

Question 1

Describe the difference between a fever and hyperthermia

Answer 1

Fever = raised thermoregulatory set point; hyperthermia = no alteration in the thermoregulatory set point but there is abnormalities with heat production or dissipation

Question 2

What controls the thermoregulatory set point?

Answer 2

Anterior hypothalamus

Question 3

Give examples of endogenous and exogenous pyrogens

Answer 3

Endogenous: inflammatory cytokines (IL1 and TNFalpha), exogenous: LPS, toxins

Question 4

What can cause hyperthermia?

Answer 4

Exercise, medications, seizures, environmental changes, stress, etc.

Question 5

____ is when the body is trying to cool; ______ is when the body is trying to create more heat

Answer 5

Hyperthermia; fever

Question 6

What can cause a fever?

Answer 6

neoplasia, infection, immune-mediated disease, inflammation (NIII)

Question 7

When do we consider a fever of unknown origin (FUO) in vet med?

Answer 7

Fever persists long enough that many common or self-limiting causes are ruled out (viruses, simple abscess, etc.). Initial diagnostics don’t reveal a cause of fever (history, PE, CBC/chem/urinalysis, imaging, failure to respond to antibiotic therapy)

Question 8

Clinical signs of fevers are specific or non-specific?

Answer 8

non-specific

Question 9

_____ and _____ can give important diagnostic clues to fevers!

Answer 9

History and physical exam

Question 10

Where do you even start to look when diagnosing a fever case

Answer 10

Look for a focus of disease, try to localize where the problem is to a system

Question 11

What are some first tier diagnostics (safe, inexpensive, simple, easy to interpret)

Answer 11

CBC with blood smear, biochem, UA, urine culture, FeLv/FIV in cats, imaging

Question 12

What are some second tier diagnostics?

Answer 12

Serial/repeated PE, blood culture, additional imaging (CT, U/S), joint taps (cytology + culture), specific infectious disease panels, FNA (mass + LN), CSF collection, biopsies

Question 13

What are some differentials for non-inflammatory joint disease causing pain?

Answer 13

Developmental joint disease, Degenerative joint disease, Trauma, Tumor

Question 14

What are some differentials for inflammatory joint disease causing pain?

Answer 14

Neutrophillic inflammation in joints, septic or sterile (within joint), joint emboli (septic, immune complexes < type 3 hypersensitivities can cause this)

Question 15

What’s the pathogenesis of how immune complexes could cause inflammation in a joint?

Answer 15

Immune complexes deposited in joint –> complement activation –> inflammation < usually sterile within joint

Question 16

When is sepsis and sterile inflammatory joint disease MORE LIKELY to occur?

Answer 16

Septic more likely to occur when: single swollen/painful joint, history of sx or trauma near/of joint, previous or current infection (hematogenous spread)

sterile more likely when multiple joints affected (smaller, distal joints), history of recent antibiotic use or vaccination.

Question 17

What’s the gold standard diagnostic test for septic OR sterile inflammatory joint disease?

Answer 17

JOINT TAPS AND CULTURE/CYTOLOGY THE FLUID

Question 18

When should we do a joint tap? X3

Answer 18

Solitary joint disease (inflammation, systemic illness), polyarthritis, fever of unknown origin (might not demonstrate joint pain or effusion but they like to hide here!)

Question 19

What should you always do with joint fluid once you obtain it?

Answer 19

culture

Question 20

Which of the two (polyarthritis or solitary joint disease) are you more likely to see in smaller vs bigger joints?

Answer 20

Polyarthritis think smaller joints, single joint disease think bigger joints

Question 21

What does normal joint fluid look like grossly and on cytology?

Answer 21

Grossly: clear, colourless, viscous (long stringy); cytologically: low cellularity (<2/hpf on 50x), mixture of mononuclear cells (large and small), <10% neutrophils

Question 22

What might synovial fluid look like grossly and on cytology if it’s abnormal?

Answer 22

Grossly: turbid/cloudy, discoloured (red: streaks = iatrogenic?, yellow = prior hemorrhage, high bilirubin?), thin and not sticky; cytology: high cellularity, >20% neutrophils (degenerate or non-degenerate), maybe bacteria

Question 23

On cytology what are the main differences between sterile vs septic inflammatory synovial fluid?

Answer 23

Sterile inflammatory: mostly non-degenerate neutrophils; septic inflammation: degenerate neutrophils with/without bacteria

Question 24

What kind of cells are mostly present in a degenerative or traumatic etiology synovial joint tap fluid?

Answer 24

Mostly mononuclear cells

Question 25

What kind of bone mainly is destroyed by erosive polyarthritis?

Answer 25

Subchondral bone mainly (very uncommon disease), but mostly affects carpal bones of small, middle aged dogs

Question 26

What’s more common, primary or secondary non-erosive joint disease?

Answer 26

Primary > secondary

Question 27

what’s the most common form of inflammatory joint disease?

Answer 27

Idiopathic (primary)

Question 28

What kind of joint disease (inflammatory, non-inflammatory, etc) is systemic lupus erythematosus? And what is it’s most common clinical sign

Answer 28

Inflammatory joint disease, non-erosive immune mediated polyarthritis. The most common clinical sign is polyarthropathy

Question 29

What’s the signalement/who is most often affected by idiopathic/primary IMPA

Answer 29

No inciting causes, middle-aged dogs > cats, no sex or reed predilections

Question 30

What are some causes of Reactive (secondary) IMPA

Answer 30

Underlying causes are distant from the joint: infectious (if it were in the joint we would call it septic), septic arthritis can arise from bacteremia, medications (antibiotics, vx), neoplasia, dietary elements (uncommon)

Question 31

What’s the pathogenesis of Type 3 hypersensitivities causing IMPA?

Answer 31

Chronic inflammation –> circulating immune complexes deposited in joint –> complement activation –> inflammation

Question 32

What kind of clinical signs specific to joints might you see with IMPA?

Answer 32

Lameness manifesting as a stiff gait, walking on egg shells look, joint pain or swelling (1 or >1), reluctance to move

Question 33

We know IMPA C/S are non specific, but if it gets polysystemic, what c/s will we see?

Answer 33

Dermatologic signs like pallor or bleeding, mucocutaneous ulcers

Question 34

What percentage will be lame or have palpable joint effusions with vague systemic signs?

Answer 34

50%

Question 35

Will you see a fever with IMPA?

Answer 35

Yes it’s a common sign and cause of FUO (but not always present)

Question 36

What might syou see on cytology from an IMPA arthrocentesis?

Answer 36

Non-degenerative neutrophilic inflammation in multiple joints, negative culture

Question 37

Before you can say “idiopathic” you have to rule out other diseases by doing….

Answer 37

thorough serial PE, CBC, chem, UA, infectious disease testing (tick borne diseases like Erlichia), urine or blood cultures, imaging

Question 38

Why do we do radiographs for IMPA? What are we looking for?

Answer 38

Osteomyelitis

Question 39

How many blood cultures do we run in a stable vs unstable patient?

Answer 39

Stable: 3 samples over 24 hour period; Unstable: 2-3 separate samples 30-60 minutes apart

Question 40

If we have an intermittent fever from IMPA, how should we collect blood cultures?

Answer 40

Separate sites, serially, increases sensitivity and specificity

Question 41

The SNAP 4Dx plus and Accuplex (Antech) measure what?

Answer 41

Antibodies to: anasplama, Borrelia burgodoferi (Lyme), Ehrlichia canis, ewingii. Antigens for heartworm

Question 42

Why might we get a false negative on the above tests?

Answer 42

It could be too early to test since it takes body up to a month to make antibodies

Question 43

If we have a case of joint pain and systemic fever, additional tests are unremarkable… what treatment do we do?

Answer 43

Treat with immunosuppressive dose of prednisone (1-2 mg/kg/day). If they’re previously on an NSAID, we need a washout period between getting NSAID and prednisone.

Question 44

What’s a good monitoring plan for an animal with IMPA?

Answer 44

Recommend a repeated joint tap in 1 month, prior to tapering prednisone (owner declines this often though due to costs).

If multisystemic immune, monitor other parameters that can be assessed.

Question 45

If a dog’s on prednisone, should you taper? If so what else do we do?

Answer 45

Taper dosage over time if the disease is controlled, can add in a second line like cyclosporine

Question 46

Bacterial endocarditis more often affects mitral or aortic?

Answer 46

Mitral > aortic ( if it’s on aortic = worst prognosis due to it putting pressure on closed valves)

Question 47

What are some common bacterial agents that cause endocarditis?

Answer 47

Staph, Strep, E. coli, Pasteuerella, Bartonella

Question 48

What’s the pathogenesis of bacterial endocarditis?

Answer 48

Bacteremia –> colonization of valves –> damage to valve + development of vegetative lesions

Question 49

What’s the typical signalement of dogs that are affected by bacterial endocarditis?

Answer 49

Large breed, males > females, have a predisposing factor (immunosuppressed, recent surgery, infection, wound, pyoderma, indwelling catheter, dental disease (sorta))

Question 50

T/F: bacterial endocarditis is associated with MMVD

Answer 50

FALSE

Question 51

How do we treat bacterial endocarditis?

Answer 51

Bactericidal broad-spectrums (ampicillin + aminoglycoside; ampicillin + clavulanate + enrofloxacin; doxycycline + enro or rifampin for bartonella), treat cardiac disease, thromboprophylaxis