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11. Acquired heart dz > Infectious myocarditis > Flashcards

Infectious myocarditis Flashcards

1
Q

Def and features of myocarditis

A
  • Inflammation of the myocardium
    o Focal/diffuse involvement
     Leucocytic infiltration
     Nonischemic myocyte degeneration/necrosis
    o Consequences depend on location, extent and duration
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2
Q

Dx myocarditis

A

endomyocardial biopsy is gold standard
o Elevated TnI suggest myocardial injury

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3
Q

most common etiology of myocarditis dogs

A

T cruzi
Parvovirus

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4
Q

Viral myocarditis

A

Parvovirus
West Nile virus
Distemper
K9 herpesvirus

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5
Q

Parvovirus: affected individuals

A
  • Neonatal parvovirus infection
    o Severe and fatal peracute myocarditis
     C/s from birth to 8wks
  • Cardiac form often w/o enteric involvement
     High mortality in litters btw 3-10wk/o
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6
Q

C/s parvovirus myocarditis

A

Vocalization, retching, dyspnea, sudden death

tachycardia, arrhythmia, gallop, apical systolic murmurs
 Cardiomegaly, pulmonary infiltrates

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7
Q

Survivors of parvovirus myocarditis

A

can develop fibrous scar tissue and develop arrhythmia/contractile dysfct

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8
Q

Pathophys parvo

A

cardiomyocytes mitotically active until 15 days after birth
o Viral tropism for active cells
 Major mechanism of cells death is apoptosis
 Cell cycle arrest: DNA damage
 Necrosis
o Infect the heart via leucocytes or in blood/lymph

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9
Q

Phases of pavoviral infection

A

o Acute phase: day 0-3 → viremic phase
 Systemic viremia → virus binding to myocyte coR → virus invasion into cardiomyocytes
 Virus replication → myocytolysis

o Subacute phase: day 4-14 → inflammatory phase
 Clearance of virus by natural killer cell, cytokins, perforins, neutralizing antibodies
 Mononuclear cell (cytotoxic T and B lymphocytes) enter myocardium → extensive cell damage
* Ongoing immune response perpetuates cell damage and death

o Final/chronic phase: >day 15 → healing phase
 Myofiber dropout and replacement fibrosis
 Viral persistence may lead to chronic inflammation → repetitive cycles of myocardial injury/repair → apoptosis, coronary microvascular spasms, autoimmune effects

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10
Q

Other than neonatal parvo myocarditis, what is another clinical presentation

A

o 2nd form of dz: juvenile dogs <1y/o
 Clinical presentation similar to DCM

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11
Q

Necropsy findings parvo myocarditis

A

o Pale myocardium with pale streaks
o Dilated/enlarged hearts
o +/- pericardial effusion

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12
Q

Histo findings parvo myocarditis

A

mild to severe multifocal lymphoplasmocytic myocarditis with degeneration and necrosis, fibrosis and intranuclear bodies
o Multifocal to locally extensive cardiomyocyte degeneration and necrosis
 Variable fiber size and staining affinity
 Fragmentation
 Loss of cross striation
o Mononuclear cells infiltration
 Lymphoplasmocytic
o Dense basophilic intranuclear inclusion
 Peripheralized the chromatin
o Interstitial fibrosis

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13
Q

Immunohistochemical analysis findings parvo myocarditis

A

canine parvovirus antigen found in nuclei +/- cytoplasm or myocytes

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14
Q

West nile virus myocarditis: features

A
  • Uncommon in dogs
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15
Q

West nile virus myocarditis: c/s

A

o Lethargy, inappetence, neurologic signs, fever, arrhythmias

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16
Q

West nile virus myocarditis: histo

A

o Sever lymphocytic neutrophilic myocarditis and vasculitis
o Focally extensive hemorrhage and myonecrosis

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17
Q

West nile virus myocarditis: dx

A

o Immunohistochemistry
o Reverse transcriptase polymerase chain rx testing
o Virus isolation
o Serology

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18
Q

Protozoal myocarditis agents

A

Chagas: trypanosoma cruzi
Neosporosis
Leishmaniosis

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19
Q

Chagas: prevalence

A

reported in young dogs in Southern US, Central/South America
o Zoonosis

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20
Q

Chagas hosts

A

raccoons, armadillos, opossums, dogs, cats, Guinea pigs

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21
Q

Chagas etiology

A

Trypanosoma cruzi: hemoflagellate protozoan parasite

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22
Q

Chagas life cycle/infection

A

o Transmitted by blood sucking insect of Triatoma subfamily
 Trypomastigote enters insect after feeding on infected host → transforms to epimastigote → multiply by binary fission → transforms back to trypomastigote in hindgut → excreted in feces deposit into fresh wound during feeding
 Infection in blood → remain free in circulation or trypomastigote infect macrophages → evade immune system and spread
 Hematogenous spread → infect cardiomyocytes → amastigotes → multiply by binary fission → convert back to trypomastigotes → rupture and release from cell back into circulation

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23
Q

Chagas: acute infection = c/s

A

weight loss, D+, lethargy, anorexia, lymphadenopathy, spleno/hepatomegaly, myocarditis, sudden death
 Parasitemia: as early as 3 days after infection, peak after 17 days, subpatent after 30 days
 C/s of myocarditis develop around day 14, resolve day 28
* Myocarditis develop 2nd to  damage and inflammation as trypomastigotes rupture from cardiomyocytes
* No echo changes, but arrhythmias may be present
 Dogs >6mo/o may not exhibit acute phase c/s

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24
Q

Chagas: latent phase

A

long 27-120 days
 Can remain asymptomatic for life
 Sudden death still possible

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25
Q

Chagas: chronic phase feature

A

progressive myocardial dz over next 8-36mo
 Arrhythmias, conduction disturbances:
* Atrial/ventricular arrhythmias: sinus tachycardia,
* 1 or 2AVB
* Axis shift, RBBB, T wave inversion
* ↓ R wave amplitude
 Chamber enlargement and CHF
* DCM occurs when fibrosis no longer permit compensatory hypertrophy
* Indistinguishable from DCM

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26
Q

Chagas dx

A

demonstrate parasitemia
o Blood smear: trypomastigote may be present in acute infection
o Serology/PCR
 Indirect fluorescent antibody assay
 Enzyme-linked immunosorbent assay
 Radioimmunoprecipitation assay
 *careful cross rx w Leishmania antibodies
o Culture
o Serum TnI progressively increase, peak at day 21 around 10-30mg/dL

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27
Q

Chagas echo findings

A

o ↓LV fct w ↓ FS/EF%
o ↓LVFW thickness
o ↑end systolic volume

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28
Q

Pathogenesis of myocarditis and DCM phenotype in Chagas

A

 Immune mediated mechanism
 Toxic parasitic products directed against cardiomyocytes
 Microvascular dz + platelet dysfct

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29
Q

Treatment chagas

A

c/s
o Destruction of intra form may result in severe exacerbation of host inflammatory response

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30
Q

Necropsy chagas

A

o Multiple pale areas in myocardium
 Especially RA/RV

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31
Q

Histology Chagas

A

active granulomatous myocarditis
o Infiltration of lymphocytes, plasma cells, macrophages
o Perivasculitis
o Clusters of T cruzi amastigotes (acute infection)
 Parasitic pseudocysts
o Fibrosis: chronically affected dogs (minimal if acute)
 Often extensive in RA/RV, around conduction system

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32
Q

Prevalence of toxoplasma myocarditis

A

commonly reported in cats

o Myocarditis rarely identified antemortem (1 reported case)
 Toxoplasma organisms identified in 63% of 59 in one study, and all 21 kittens in another study
 Not uncommon complication in Hu

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33
Q

Signs of toxoplasma infection

A

o Ocular, pulmonic, hepatic, neurological, GI, muscular abnormalites

34
Q

Etiology toxoplasmose

A

Toxoplasma gondii
o Can encyst in the myocardium
o Chronic infection

35
Q

Pathophys toxoplasmose

A

o Cyst rupture
 Myocardial necrosis
 Hypersensitivity reaction → myocarditis, pericarditis, CHF
* Polymorphonuclear leucocytic and lymphocytic infiltrates
o Infects multiple tissues
 Heart
 Peripheral muscles
 CNS

36
Q

Dx toxo myocarditis

A

o Serology → rising titers of serum antibodies (IgG, IgM)
o BW: neutrophilia, lymphocytosis, monocytosis
 Hypoalbuminemia in acute phase
 ↑CK
Echo changes

37
Q

Echo changes toxoplasmosis myocarditis

A

 Pericardial effusion
 ↑ myocardial echogenicity with granular appearance
* Generalized, symmetric thickening of ventricular walls
* Predominantly RVFW
 Distorted IAS
* ↑echogenicity
* Nodular appearance

38
Q

Echo changes evolution w/ toxoplasmosis

A

 After 3 weeks of tx: ↓ wall thickness, resolved pericardial effusion, ↓ nodularity of IAS
 After 8 weeks of tx: heart appeared normal except hyperechogenic line on IAS

39
Q

Etiology neosporosis

A

Neospora caninum
o Obligate intracell protozoan
o Worldwide distribution
o Similar life cycle to toxoplasma gondii

40
Q

Neosporosis in dogs

A

o Sporadic dz in dogs
 Adult dogs: meningomyeloencephalitis most common, myocarditis, sudden death, polymyositis, dermatitis, pneumonia reported
* Myocarditis reported in Mastiff, rare

41
Q

Neosporosis in cattles

A

o Important cause of abortion in cattles

42
Q

DX neosporosis

A

o Serology: antibodies
o Immunohistochemestry
o Electron microscopy

43
Q

Tx neosporosis

A

clindamycin, potentiated sulfonamide and/or pyrimethamide

44
Q

Necropsy findings neosporisis

A

1 dog (Mastiff): sudden death
o Raised, mottled red and white transmural infarct in apical RVFW and LV papillary muscle
 Sharply demarcated from adjacent myocardium
o Multifocal, irregular, small, firm, pale, raised subendocardial lesion in RAA and RVFW
o Pericardial effusion

45
Q

Histo findings neosporosis

A

acute necrotizing myocarditis with myocardial infarct and intra tachyzoites
o Infarct: edema +
 Thick interwoven bands of fibromuscular tissue
 Extensive loss of myocardial fibers
o Oval intracytoplasmic vacuoles containing dozens of lunate-shaped tachyzoites
o Perivascular to interstitial neutrophils, lymphocytes, plasma cells
o Mild interstitial non suppurative myocarditis focally extended to endocardial surface

46
Q

Leishmaniosis etiology

A

protozoal organism
o Endemic in Mediterranean basin

47
Q

Pathophys leshmaniosis myocarditis

A

direct action of parasite into myocardium → intense inflammatory response

48
Q

C/s leishmaniose myocarditis

A

arrhythmias → 1AVB

49
Q

Bacterial myocarditis can occur if

A

o Bacteremia, sepsis
o Endocarditis: suppurative myocarditis
 Extension of valvular lesion
 Coronary circulation

50
Q

Agents of bacterial myocarditis

A

o Staph/strep species, E coli: most common
o Gram – in cats
o Anaerobe/mycobacteria: less common
o Borrelia burgdorferi

51
Q

Most common manif of lyme disease w/ heart

A

 Lyme disease reported, proven cardiac sequelae rare (10% of patients in Hu)
 Most common manifestation: 3AVB (1 and 2AVB reported)

52
Q

Histo changes lyme dz myocarditis

A
  • Multifocal myocardial necrosis
  • Infiltration of lymphocytes, plasma cell, macrophages, neutrophils
53
Q

Dx lyme dz myocarditis

A

endomyocardial biopsies, antibody titers, necropsy

54
Q

Pathophys of bacterial myocarditis

A
  • Myocardial damage from bacterial toxins or immune mediated process
55
Q

C/s bacterial myocardtis

A

arrhythmia mostly

56
Q

Dx bacterial myocarditis

A

o Blood culture: if negative, may be secondary to Bartonella spp

57
Q

Endocarditis incidence

A

0.1-1% of cases
o Uncommon in cats
o Male > 2x females

58
Q

Endocarditis predisposition

A

o Valvular congenital defects predispose to development.
 SAS → majority of dogs will not develop endocarditis
 80% of dogs with endocarditis do not have any valvular lesions

59
Q

Etiology endocarditis

A

o Gram + more likely vs gram –
o Most common agents: staph, strept, gram – rods, enterococci, Bartonella
 Bartonella: most commonly involve AoV
* Absence of fever
* Negative culture
* Worse px, higher prevalence of CHF
 Streptococcus canis: most commonly involve MV
* Secondary polyarthritis
 Gram - → less likely to develop CHF

60
Q

What determine likelihood of infection

A

virulence factors of bacteria

61
Q

Which agent involves most commonly AoV

A

Bartonella

62
Q

Which agent involves most commonly MV

A

Strep canis

63
Q

Pathophys endocarditis

A

o MV and AoV most commonly affected
 MV: larger septal leaflet > mural leaflet
o TV and ventricular wall rarely involved

64
Q

Dx endocarditis

A

o BW: mild non regenerative anemia, neutrophilia w L shift and neutrophil toxicity, lymphopenia, monocytosis
 Azotemia, ↑liver enzymes, mild hyperbilirubinemia
 Electrolyte and acid base abnormalities: ↑anion gap, metabolic acidosis, lactic acidosis
 Hyperglycemia (early septic shock), hypoglycemia if liver failure
 Hypoalbuminemia: mild to severe, from
* ↓ hepatic production
* ↑ vascular permeability
* Inflammatory response (negative acute phase protein)
o UA: proteinuria, pyuria, cylindruria, microscopic hematuria, bacteriuria

65
Q

Mycotic/fungal myocarditis features

A
  • Extremely rare
    o Immunocompromised patients
    o Hematogenous spread
66
Q

Mycotic/fungal myocarditis agents

A

o Cryptococcosis
o Coccidioidomycosis
o Aspergillosis
o Saprophytic fongi
o Blastomycosis

67
Q

Mycotic/fungal myocarditis reports

A
  • Cardiac compression from extra cardiac granulomas reported in 2 dogs
    o Myocardial, epicardial, pericardial, valvular involvement
68
Q

Rickettsial myocarditis etiology

A

Ehrlichia canis, Rickettsia rickettsia, Bartonella elizabethae

69
Q

Sarcocystis etiology

A

Sarcocystic neurona
o Eosinophilic granulomatous reaction to degenerating cysts
 Heart and skeletal muscle
o Extremely rare

70
Q

Sarcocystis histology

A

o Necrotizing myocarditis in RV and LV
 Coalescing areas with lymphocytic infiltration
 Degenerated cysts w/I foci of myocarditis
 Cyst content = highly toxic
o Myocardial infarcts

71
Q

Angiostrongylosis etiology

A

Angiostrongylus vasorum
o Metastrongyloid parasite of the R heart and PAs in dogs

72
Q

Angiostrongylosis pathogenesis

A

multifocal granulomatous myocarditis centered around migrating larvae
o Adult worm: live in PA vessels and R heart
 Release eggs/larvae into pulmonary circulation

73
Q

Angiostrongylosis c/s

A

wide spectrum
o Mild respiratory signs
o Severe form: coagulative, respiratory, neurologic, cardiovascular, ocular signs
 Attenuated cardiac sounds, heart murmurs
 Myocarditis
 CHF
 Periarteritis
 Hematoma
o Pulmonary hypertension: <5% of cases, but 1/3 of dogs referred for echo

74
Q

Angiostrongylosis echo

A

o RAE, RVE
o Bulging IAS
o Dilated CaVC and hepatic veins
o Severe TR

75
Q

Angiostrongylosis CTX

A

RVE, truncated PAs, ↑VHS

76
Q

Angiostrongylosis histo

A

lesions involved 20% of myocardium
o Nematode larvae scattered into myocardium
o Surrounded by reactive macrophages, giant  of foreign body type, lymphocytes, eosinophils
o Focal degeneration of myocardiocytes
o Mild multifocal interstitial fibrosis

77
Q

Spirocercosis etiology

A

Spirocerca spp
o Endemic in some warm climates

78
Q

Spirocercosis pathophys

A

verminous arteritis
o Will invade lumen/wall of arteries
 Can migrate in tissues and cause vasculitis
 Genera Strongylus and Ascaris
o Aortic lesions can lead to Ao rupture/aneurysm
 Spirocerca lupi: adventitia of thoracic Ao during part of its life cycle
* Final habitat in esophagus
* Migration through Ao wall to esophagus may cause
o Mediastinitis, pleuritis, pyothorax

79
Q

Spirocercosis c/s

A

GI, respiratory, circulatory signs

80
Q

Transmissible myocarditis and diaphragmatitis features

A
  • Fever in cats usually biphasic
    o Day 9-16 and days 17-27 after infection
  • Normal testing: BW, UA, CTX, AUS, FIv/FeLV/FIP
81
Q

Transmissible myocarditis and diaphragmatitis necropsy

A

1-3mm pale foci w/I myocardium and diaphragm

82
Q

Transmissible myocarditis and diaphragmatitis histo

A

myonecrosis with inflammatory infiltrates
* No organism identified

11. Acquired heart dz (8 decks)

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