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CARDIO SPECIALTY EXAM MY OWN > Infectious cardiology > Flashcards

Infectious cardiology Flashcards

1
Q

The consequences of Infectious Endocarditis depend on several factors:

A
  • virulence of the infective agent
  • site of infection
  • degree of valvular destruction
  • influence of vegetation on valvular function
  • production of exo- or endotoxins
  • interaction with the immune system with the formation of immunocomplexes
  • development of thromboembolism and metastatic infections.
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2
Q

what bacterial features determine the degree of damage these can cause to a valve during infectious endocarditis

A
  • express special receptors: MSCRAMMS: microbial surface components recognising adhesive matrix molecules.
  • contain fibronectin-binding proteins and can trigger active internalization by host cells (e.g. S aureus)
  • trigger tissue factor production  platelet aggregation
  • have the ability to internalise within the endothelial cells (staph aurelius/Bartonella) or within red blood cells (Bartonella - without leading to haemolysis, which shields detection from the immune system).
  • Many bacteria are resistant to the bactericidal proteins released from white blood cells.
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3
Q

Gram-negative bacteremia cause _________ manifestation
Gram-positive _________ chronic condition.

A

peracute or acute clinical

bacteremia or subacute or

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4
Q

What secondary diseases may be seen in infectious endocarditis

A

Deposition of immunocomplexes in different organs may cause glomerulonephritis, myositis, or polyarthritis

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5
Q

where do infectious endocarditis lesions originate on the valve

A

Vegetations develop on the surface of the valve facing the blood flow – i.e. the ventricular surface of the aortic valve and the atrial surface of the mitral valve

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6
Q

what gross pathological changes maybe seen on endocarditis valves on necropsy

A

Affected leaflets appear grossly deformed and may be haemorrhagic, ulcerated or perforated. Initially may be small and finely granular in appearance, but may become large and polypoid, demonstrating marked variability and distortion, oedema and hyperaemia of adjacent valve tissue.
Vegetations typically have a broad based attachment and can appear relatively smooth however the free margins are often rough as sections break off an embolise to leave a roughened edge. Lesions may extend between leaflets or between valves or from valve leaflet to atrial endocardium, interventricular/interatrial septum, chordae tendinae or aortic intima. Chordal rupture and perforating myocardial ulcers may occur. There maybe fibrosis and mineralization of some lesions.
Necrotic debris may be intermixed with the stroma.

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7
Q

what stains assist in identifying bacteria in infectious endocarditis

A

BROWN AND BRENN STAINING

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8
Q

what changes do you see in subacute infectious endocarditis on histo?

A

Subacute: Mainly histiocytes and lymphocytes and occasional plasma cells. Few pmns. More mature and organized vegetative lesions.

  • smaller outer layers contain fibrin and leukocytes
  • inner layers contain capillary proliferation, granulation tissue, fibroblasts and collagen
  • deep later consist of histiocytes and fibrous tissue
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9
Q

what changes may you see in chronic endocarditis on histo

A

Contain varying degrees of organization- granulations tissue, scar and segments of calcium deposition

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10
Q

What stain maybe used to highlight fibrosis on histopath?

A

Masson trichrome stain

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11
Q

What stain may be used to highlight calcification of the valve?

A

von Kassa stain

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12
Q

what are Polymorphonuclear leukocytes?

A

PMNs) are a type of white blood cell (WBC) that include neutrophils, eosinophils, basophils, and mast cells. PMNs are a subtype of leukocytes released by bone marrow as a first line of defense against infection or inflammation in the body.

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13
Q

what are common predisposing conditions to infectious endocarditis?

A

discospondylitis, pneumonia, prostatitis, UTI, pyoderma, periodontal disease, long term indwelling catheters

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14
Q

infectious endocarditis, by extension, can have what side effects?

A

involvement of the valve annulus, sinus of valsalva, pericardium and myocardium and may result in abscess formation, communicating fistulae, conduction system destruction or pericarditis. Infarcts are common, especially to the kidney, spleen and left ventricle. These are frequently septic. Sepsis may cause focal or diffuse myocarditis and myonecrosis, perivascular infiltrates or occasionally micro abscesses and small infarct.

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15
Q

What sequela to bacterial endocarditis are seen?

A
  • CONGESTIVE HEART FAILURE:
  • ARRHYTHMIA
  • IMMUNE-MEDIATED DISEASE
  • SEPTIC EMBOLISM
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16
Q

how does CHF occur secondary to infectious endocarditis?

A

valve degeneration more commonly. Rarely due to stenosis

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17
Q

How may arrythmias occur secondary to infectious endocarditis?

A

Arrhythmias develop as a consequence of bacterial invasion into the myocardium, from myocardial hypoxia, from embolism of portions of vegetations into the coronary circulation, and as a result of immune-mediated vasculitis

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18
Q

Why may immune mediated disease develop secondary to endocarditis?

A

Patient response is the development of high titres of abs against the infections -> continuous formation of IgM, IgG and C3 (complement)

Rheumatoid factor may impair the ability of the complement to solubilize immune complexes ->immune complex depositionand further complement activation and tissue destruction -> glomerulophritis / polyarthritis (observed in 36% and 75% of dogs respectively in one study).
Levels of circulating immune complexes reduce rapidly after introducing ab therapy in people with IE. Septic arthritis is also possible but is less common than immune-mediated arthritis.

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19
Q

How often are glomerulonephritis and polyathritis seen in patients with infectious endocarditis?

A

glomerulophritis / polyarthritis was observed in 36% and 75% of dogs respectively in one study

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20
Q

How often do septic emboli occur in infectious endocarditis?

A

occurs in 70-80% of dogs with IE examined at histopathology

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21
Q

what are common sequela of septic emboli?

A

Infarction of the kidneys and spleen are the most common sites, followed by infarction of the myocardium, brain and peripheral arteries, Vascular encephalopathy is uncommon in dogs

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22
Q

what is the most common neurological sequella of septic emboli in dogs ?

A

Most commonly due to emboli getting lodged in the MIDDLE CEREBRAL ARTERY in people in people and dogs

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23
Q

what are the most common causes of death in patients with infectious endocarditis?

A

Death due to the combined effects of renal infarction, infection, and glomerulonephritis occurs in a substantial percentage of affected dogs. On occasion, death results from myocardial infarction caused by embolic occlusion of a coronary artery

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24
Q

How useful are blood cultures in the diagnosis of infectious endocarditis ?
Why?

A

Positive blood cultures are invaluable for establishing a diagnosis and selecting appropriate antibacterial treatment. - 60% to 70% of obtained blood cultures have been reported to be negative in dogs with IE, presumably associated with a high proportion of dogs receiving ab treatment prior to sampling. Some bacteria may be occult due to encapsulation within the lesion. Others are slow growing

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25
Q

How long should infectious endocarditis blood samples be cultured for?

A

slow growing – samples should not be considered to be truly negative until after 10 days of culture, although rapid growth is more common it 90% of cultures growing positive within 72h.

26
Q

what are the most common causative agents of infectious endocarditis?

A

Staphylococcus – aureus, intermedius, coagulase-positive, coagulase negative
Streptococcus – canis, bovis, beta-hemolytic
Bartonella vinsonii (and related proteobacteria: B henselae, clarridgeiae, washoensis)
E.coli

Pseudomonas
Corynebacterium
Erysiplthrix rhusiopathiaw
Pasteurella spp
Proteus

Bartonella spp may account for 28% of cases of IE in dogs, rising to nearly 50% of cases in which a blood culture is negative.

27
Q

concurrent seroreactivity to what pathogens is common in patients with IE infected with bartonella?

A

Ehrlichia canis, Anaplasma phagocytophilum, and Rickettsia rickettsii is common in dogs with IE cause by Bartonella spp

28
Q

except blood cultures, what are common laboratory findings in endocarditis patiets?

A

Regenerative anaemia – 50-60% cases – normocytic, normochromic
Leukocytosis in 80% cases: Neutrophillia and left shift

Elevated BUN and cretatinine, elevtate ALKP caused by circulating endotoxins-, ↓ hepatic function may result in hypoalbuminaemia.

29
Q

based on the modified dukes criteria, what are definitive and possible mrkers for endocarditis?

A

Definite endocarditis:
* Histopathology of the valve
* Two Major criteria
* One major and 2 minor criteria

Possible
* One major and one minor
* Three minor criteria

30
Q

what are major dukes criteria and minor?

A

MAJOR
Echocardiographic Valve lesions
New regurgitation
Blood cultures
>2 + cultures
>3 + cultures if a common skin contaminant

MINOR
Immune mediated disease: polyarthritis/glomerulonephritis
TE disease
Fever
>15kg breed
SAS
Bartonella:
PCR
Serology: 1:1024

31
Q

what is 16s primer PCR?

A

PCR testing of blood is to test for 16s primers: identify bacteremia in dog. Studies that have used the 16s ribosomal primer based sequencing on whole blood from human patients with IE polymerase chain reaction (PCR) has shown significantly greater sensitivity and specificity than conventional microbiological methods.

32
Q

what is the major finding in Meurs et al 2001: Comparison of Polymerase Chain Reaction with Bacterial 16s Primers to Blood Culture to Identify Bacteremia in Dogs with Suspected Bacterial Endocarditis

A

Blood culture identified noncontaminant bacteria in 6/18 dogs (33%). PCR identified noncontaminant bacteria in 7/18 dogs (39%). Statistically, the proportion of times each test identified bacteria was not different. An organism was identified by one or both of the tests in 61% of dogs, but there were only 2 dogs in which both tests identified bacteremia. An organism was not identified in 7 dogs involving 3 aortic and 4 mitral valves.

From the normal group, blood culture identified a noncontaminant bacteria (S. aureus) in 1/15 dogs. PCR did not identify bacteria in this dog or any others.

33
Q

why may bartonella PCR for infectous endocarditis have false negative resutls ?

A

This is likely due to a relapsing pattern of bacteremia and the localization of Bartonella organisms within endothelial cells or vegetative lesions without large numbers of circulating bacteria.

34
Q

why may bartonella blood cultures show false negative results?

A

This is likely due to a relapsing pattern of bacteremia and the localization of Bartonella organisms within endothelial cells or vegetative lesions without large numbers of circulating bacteria.

35
Q

what are the most common subspecies of bartonella that cause infectous endocarditis?

A

Vindonii subsp berkhoffi and henselae

36
Q

How does bartonella evate the immune system?

A

Evades the immune system by colonization of RBCs and endothelial cells and impairs immune function by
* ↓ numbers of CD8+ lymphocytes and their cell adhesion molecule expression,
* inhibiting monocyte phagocytosis
* impairing B cell ag presentation within lymph nodes.

37
Q

what valve is most commonly affected by Bartonella?

A

primarily affect the aortic valve- MV less common

38
Q

what unique lesions do bartonella cause in infectious endocarditis when analyzed on histopath

A

unique lesions: fibrosis, mineralization, endothelial proliferation and neovascularization.

39
Q

what are the major findings of MacDonald et al 2004: A Prospective Study of Canine Infective Endocarditis in NorthernCalifornia (1999–2001): Emergence of Bartonella as a Prevalent Etiologic Agent

A

IE was diagnosed antemortem based on clinical signs and echocardiography in 18 dogs. The etiologic agent was Bartonella sp. 28% (n=5) and was diagnosed by high seroreactivity to Bartonella confirmed postmortem by positive PCR.
Conventional bacteria were causative agents in 39% dogs. An etiologic agent was not identified in 33%,

Bartonella vinsonii berkhoffii (n = 3), B clarridgeiae (n = 1), and a B clarridgeiae-like organism (n = 1) were identified. Blood culture was positive only for the IE case due to B clarridgeiae. All dogs with IE due to Bartonella were also seroreactive to Anaplasma phagocytophilum. All dogs with IE due to Bartonella had lesions only on the aortic valve. Of the cases of IE not due to Bartonella, 31% involved the aortic valve, 61% the mitral valve, and 8% both valves. Dogs with mitral valve lived longer than all dogs with aortic valve IE and dogs with IE of the aortic valve due to Bartonella.

40
Q

what are the major findings in Perez et al 2011: Molecular and Serological Diagnosis of Bartonella Infection in 61 Dogs from the United States.

A

Between 2003 and 2009, 924 samples from 663 dogs were submitted for diagnostic testing with BAPGM culture medium. 61/663 dogs were culture positive or had Bartonella DNA detected by PCR, including:
B.henselae(30/61), B. vinsonii subsp. berkhoffii (17/61), Bartonella koehlerae (7/61), Bartonella volans-like (2/61), and Bartonella bovis (2/61).

Coinfection with more than 1 Bartonella sp. was documented in 9/61 dogs. BAPGM culture was required for PCR detection in 32/61 cases.

41
Q

What is the prognosis for infectious endocarditis?

A

Aortic endocarditis: Grave – MST 3 days vs 476d for mitral endocarditis

In another case series 1/3 aortic endocarditis cases died within the 1st week and 90% within the first 5m.

42
Q

How common is infectious endocarditis in cats?

A

very rare – incidence of 0.006-0.0018% cats presented for examination.

In a large path study including 4933 necropsied cats, 13 cases were identified

43
Q

what valves are most commonly affected by endocarditis in cats?

A

mitral and aortic

44
Q

what are the most common pathogens which cause aortic endocarditis in cats?

A

Gram positives (staph aureus and strep spp) are most common.
Case reports have reported;
Staphylococcus aureus, Escherichia coli, Streptococcus sp., Bartonella, and Pasteurella haemolytica from a tiger.

45
Q

What are predisposing factors to valvular infectious endocarditis are known?

A

None know - too little data

46
Q

What are common clinical presenting signs and in cats?
What common valve changes are seen?

A

In contrast to acute bacterial endocarditis in dogs, cats may experience clinically undetected extended disease -> valvular dystrophic calcification. Valve lesions most commonly -> regurgitation rather than stenosis.

In many of the isolated feline cases, the primary presenting complaints were signs related fulminant congestive heart failure, such as tachypnea, dyspnea, weakness, and anorexia.

47
Q

what are the main findings of - Malik et al 99: Vegetative endocarditis in six cats

A

The first four cats were presented principally for signs of congestive heart failure referable to volume overload of the left side of the heart secondary to aortic and,or, mitral insufficiency, and had been systemically well until immediately prior to presentation.

In none of these four patients was fever, an inflammatory leukogram, or other clinical signs of systemic bacterial infection prominent from the history or physical findings.

Case 5 and 6 presented with more acute signs and both cats had a recent history of cat fight abcesses.

Case 5 presented with signs of severe systemic disease, with accelerated red blood cell destruction, prehepatic jaundice, marked neutrophilia with left shift and a bacteraemia. These changes were likely a consequence of sepsis, and it is conceivable that a streptococcal haemolysin, low grade disseminated intravascular coagulation and, or, turbulence within the left ventricle associated with the extensive vegetative lesions contributed to the severe on-going erythrocyte destruction observed in this cat.
Case 6 was presented for signs of multisystem disease, but in contrast to the first five patients, physical findings suggestive of bacterial endocarditis were absent.

Prognosis in this series was poor- only 2 cats survived for a reasonable length of time one cats for 11 months, the other for 5 months.

48
Q

what is a common resevoir host for Bartoneall species?

A

Domestic cats are a major natural reservoir host for B henselae, Bartonella clarridgeiae and B koehlerae. Cats are considered healthy carriers of these bacteria.

49
Q

what are the main findings of Porter at al 2008: Vegetative Endocarditis in Equids (1994 –2006)

A

2 forms can be distinguished:
* acute form: pyrexia, depression, reluctance to move due to thoracic discomfort or lameness and rapid development of congestive heart failure sequelae.
* Subacute/chronic: intermittent pyrexia, weght loss, shifting lamenss. Poor performance, lethargy/depression, a heart murmur  weeks –months.
CHF is usually a terminal event. There may be concurrent arrhythmia including ventricular ectopy and premature ventricular contractions.
Once established the endocarditis lesions septic thromboemboli leading to metastatic infection and secondary organ disfunction +/- immune complex deposition.

treatment logically consists of a high dose of bactericidal antibiotic, ideally based on the results of the blood culture for a minimum period of 4–6 weeks.

Resolution of clinical signs, improvement of echocardiographic findings, and reduction in leukocytosis and hyperfibrinogenemia should be used to evaluate the response and determine the duration of therapy.

Prognosis is poor in all cases of infective endocarditis. Valvular insufficiency caused by vegetative endocarditis can remain despite reduction of the size and sterilization of the lesion. In addition, infarctions, metastatic infections, and financial limitations can also complicate treatment and affect prognosis

50
Q

what biochemical changes maybe seen in horsed with infectious endocsarditis?

A

Hyperfibrinogenemia, leukocytosis, hypoalbuminaeami, hyperglobulinaemia, neutrophilia, aneamia and increased ALKP were seen frequently.

51
Q

How do patients present with leishmania?

A

Canine leishmaniasis may be subclinical or may manifest as a systemic disease with weight loss, muscular atrophy, anemia, hepatosplenomegaly, and cutaneous, renal, or ocular lesions

52
Q

What are the main findings from Rosa et al Cardiac Lesions in 30 Dogs Naturally Infected With Leishmania infantum chagas

A

The hearts of 30 dogs naturally infected with Leishmania infantum chagasi were evaluated histologically and immunohistochemi- cally. Myocardial lesions were detected in all dogs, including lymphoplasmacytic myocarditis (27/30), myonecrosis (24/30), increased interstitial collagen (22/30), lepromatous-type granulomatous myocarditis (7/30), fibrinoid vascular change (3/30), and vasculitis (1/30). The parasite amastigotes were detected in the hearts of 20 of 30 dogs. The number of parasitized cells correlated with the intensity of the inflammation and with the number of granulomas. The results indicate that cardiac lesions are prevalent in dogs with naturally occurring leishmaniasis even in the absence of clinical signs of cardiac disease.

53
Q

What features of toxoplasma do you see on heart histology

A

tachyzoites

54
Q

what diseases can be diagnosed on histology by the presence of amastigotes in the cytoplasm of macrophages?
how do you differentiate them

A

Chagas disease and Leishmania

The difference in amastigots is that the kinetoblast is parallel to nucleous in leishmania and perpendicular in chagas

55
Q
A
56
Q

What histological findings do you find with leishmania infections

A
  • contraction band necrosis (myocytes look shredded)
  • the presence of amastigotes with horizontal kinetoblasts
  • Mononuclear cell infiltration
  • fibrin deposition
  • granulomatous change
57
Q

What do you need to form endocarditis?

A
  • bacteremia with bacteria that can bind to the valve
  • valvular lesions
  • presence of a sterile thrombus on the valve
58
Q

What is the most common cause of endocarditis in cattle and how does bacteremia occur

A

Streptococcus bovis - this can attach to the valve.
This occurs due to translocation from rumenitis or iatrogenic from non clean injection site

59
Q

What are the major criteria for the modified dukes criteria

A

Echocardiographic Valve lesions
New regurgitation
Blood cultures
>2 + cultures (from a typical bug)
>3 + cultures if a common skin contaminant or there is an atypical buy

60
Q

What are the minor criteria for the modified dukes criteria

A

Immune mediated disease: polyarthritis/glomerulonephritis
TE disease
Fever
>15kg breed
SAS
Bartonella:PCR or Serology: 1:1024
Surgery within the last 6 weeks

61
Q
A

CARDIO SPECIALTY EXAM MY OWN (14 decks)

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