Cardiovascular System Infections

Kirsten Culver, PhD

Science Lead
School of Nursing, McMaster University
Bacteremia
 Presence of bacteria in the bloodstream; may or may not be clinically
significant
Transient Bacteremia
 Self-resolving in clients with NO underlying illness, immune deficiency or
turbulent cardiac blood flow
Primary Bacteremia (e.g., nosocomial, IV drug use)
 Direct inoculation of the blood stream
Secondary Bacteremia (e.g., opportunistic)
 Microorganisms causing infection at another site (e.g., pneumonia) invade the
blood stream and disseminate via the circulation to other body areas
(hematogenous spread)
Sepsis
Sepsis
 Life-threatening organ dysfunction due to a dysregulated host response to
infection
 In lay terms, sepsis is a life-threatening condition arising when the body's
response to an infection injures its own tissues and organs
Characterized by…
 Infection (suspected or confirmed) AND
 Acute, life-threatening organ dysfunction as defined by a Sepsis-related Organ
Failure Assessment (SOFA) tool
 SOFA measures respiratory, hepatic, cardiovascular, renal, central nervous
system, and platelet dysfunction
Septic Shock
Septic shock
 Subset of sepsis in which underlying circulatory and cellular/metabolic
abnormalities are profound enough to substantially increase mortality
Clinical criteria for septic shock
1. Sepsis, AND
2. Hypotension requiring vasopressors to maintain mean arterial pressure (MAP)
= 65 mm Hg despite fluid resuscitation, AND
3. Lactate ≥ to 2 mmol/L

With these criteria, hospital mortality is in excess of 40%

Structure of the Heart

Endocardium - Thin continuous lining inside chambers of the heart; extends to cover
valves
Myocardium – Muscle tissue of the heart
Pericardium – Thin double-layered sac that encloses the heart
Rheumatic Fever
 Complication of streptococcal pharyngitis (strep throat) infections
 Streptococcus pyogenes aka Group A streptococcus (GAS)
 Despite near elimination of rheumatic heart disease in high-resource settings,
40 million people worldwide have rheumatic heart disease and 300 000 die
from rheumatic heart disease each year
 Most are socioeconomically disadvantaged, living in low-income and
middle-income countries (LMICs) or in marginalized populations within
high-income countries
 Indigenous children and young peoples (Canada, Australia, New Zealand)
live with an inequitable burden of acute rheumatic fever and rheumatic heart
disease
Rheumatic Fever
 Autoimmune reaction, lasting approximately 3 months
 Form of molecular mimicry; microorganisms with epitopes similar to host self-
antigens triggers autoimmune-mediated tissue damage
 Carditis
 Inflammation of heart valves (valvulitis), no infection
 Acute valvulitis: valvular regurgitation, chronic valvulitis: valve stenosis
 Typically affects left-sided valves, with greater affinity for the mitral valve
 Heart failure symptoms develop with progressive heart valve damage
 Polyarthritis: Large joints, lasting approximately 2 – 4 weeks
 Erythema marginatum: Rarely observed in adults
 Chorea: Rarely observed in adults, observed in children
Rheumatic Fever
 Acute rheumatic fever (ARF)
 Symptomatic management, no specific treatment or cure
 Anti-inflammatory drugs to relieve inflammation and bed rest
 Pharmacological therapies used for HF (in symptomatic patients)
 Treatment for GAS regardless of the presence/absence of pharyngitis at the
time of diagnosis; to eradicate any residual GAS carriage
 Valvuloplasty and valve replacement may be required for those with residual
heart disease
 Percutaneous mitral balloon commissurotomy for mitral valve stenosis is the
treatment of choice in those with a suitable valve
Rheumatic Fever
 Prevention of future (subsequent) cases of ARF is key
 Prophylaxis with targeted antibiotics (American Medical Association)
 No residual heart disease: Benzathine penicillin G (BPG) IM, every 4 weeks
until age 21 years, or 10 years after last ARF
 Residual heart disease: BPG (IM), every 4 weeks until age 40 years, or 10
years after last ARF, lifetime prophylaxis may be needed
 Residual heart disease refers to persistent valvular disease (documented by
clinical or echocardiographic evidence) – sometimes referred to as rheumatic
valve
Rheumatic Heart Disease
 Clients with a rheumatic heart valve are at an increased risk of complications
associated with bacteremia
 This increased risk is associated with the turbulent blood flow at the site of the
damaged valve and the resulting damage to the endocardium
 Minor fibrin and platelet deposition can occur on the low-pressure side of the
damaged valve and can lead to non-bacterial thrombotic endocarditis (NBTE)
 Those with certain congenital heart defects and damaged/prosthetic valves
can be similarly predisposed
 Transient cases of bacteremia become problematic; microbe now has a place to
adhere (due to roughening of endocardium), increasing the risk of infective
endocarditis
A Care Scenario
 35-year-old client
 History of IV drug use
 HIV status unknown
 Presents with high fevers, SOB, and fatigue
 While in the ED, displays symptoms consistent with ischemic stroke
 Muscle weakness, loss sensation on left side, difficulty speaking and confusion
 3/3 blood cultures reveal Staphylococcus aureus
 Septic pulmonary emboli observed on chest x-ray
 Transesophageal echocardiogram (TEE) reveals a large vegetation on tricuspid
valve
Echocardiography - Vegetation

VEGETATIONS

tricuspid valve
Vegetation

CDC/Dr. Edwin P. Ewing, Jr., 1972

Endocarditis
Infection and inflammation of the endocardium; commonly affects heart valves
Subacute endocarditis
 Symptoms develop slowly (weeks to months); mild fever, malaise/fatigue, weakness,
myalgias, cough, headache, back and/or chest pain, weight loss
 New or changing heart murmur, peripheral manifestations
 Associated with commensal (low virulence) microorganisms (e.g., viridans group
streptococci from oropharynx) and mostly seen in cases of pre-existing valve damage
Acute endocarditis
 Symptoms develop quickly (within days); high fever (38.9 – 40 ºC), chills,
tachycardia
 New or changing heart murmur, peripheral manifestations
Endocarditis – Peripheral Manifestations
 Splinter hemorrhages; linear lesions in the long axis of the distal third of
the nail
 Red in appearance, then brown/black in a few days; non-specific
finding
 Janeway lesions; painless macular lesions, commonly on palmar surfaces
of hands and feet (septic emboli)
 Osler’s nodes; small painful nodular lesions, commonly on pads of fingers
and toes, mainly seen in cases of subacute endocarditis
 Roth spots; pale-centered retinal hemorrhages; fibrin and platelet
aggregation in white center
Endocarditis – Peripheral Manifestations

Roth’s spots

Janeway lesions

Osler’s nodes
Splinter hemorrhages
Endocarditis – Risk Factors
 Bacteremia
 Cardiac conditions
 Abnormal valves (e.g., rheumatic valve, prosthetic valve,
mitral valve prolapse, congenitally abnormal valve)
Damage to
 Prior infective endocarditis endocardiu
 Implanted cardiac devices (pacemakers, defibrillator leads) m
 IV drug use, indwelling line for venous access
Endocarditis – Risk Factors
Endocarditis – Complications
Persistent bacteremia & risk of seeding distant sites
 Risk of secondary infections and sepsis
Direct cardiovascular tissue damage
 Damage to heart valve, heart failure
Fragmentation of the vegetation
 Pulmonary embolism, MI, stroke, seizure, vascular insufficiency and necrosis
Stimulation of antibodies
 Combine with bacterial antigens and form circulating immune complexes that
deposit in kidneys (glomerulonephritis) or skin (Osler’s nodes) impairing
perfusion of tissues
Endocarditis – Clinical Criteria
Duke Criteria for Endocarditis
Definitive IE: 2 major or, 1major and 3 minor or, 5 minor criteria must be satisfied
Possible IE: 1 major and 1 minor or, 3 minor criteria
Major criteria
 Blood cultures that demonstrate continuous bacteremia
A. Presence of typical microorganism consistent with IE in 2 separate blood cultures
(e.g., Viridans group streptococci, Staphylococcus aureus, enterococci)
B. Persistently persistently positive blood cultures for these pathogens, defined as:
1. At least 2 positive blood cultures drawn more than 12 hours apart, or
2. All 3 or a majority of ≥4 separate blood cultures (with first and last sample
drawn at least 1 hour apart)
Endocarditis – Clinical Criteria
Duke Criteria for Endocarditis
Definitive IE: 2 major or, 1major and 3 minor or, 5 minor criteria must be satisfied
Possible IE: 1 major and 1 minor or, 3 minor criteria
Major criteria
 Evidence of endocardial involvement
 Echocardiogram positive for IE (e.g., vegetation or abscess or partial
dehiscence of prosthetic valve or new onset valvular regurgitation)
 Transesophageal echocardiogram (TEE) provides better detection and
characterization of local abnormalities – especially in cases of cardiovascular
implantable electronic devices and prosthetic valves, otherwise TTE
sufficient
Endocarditis – Clinical Criteria
Duke Criteria for Endocarditis
Minor criteria
 Predisposing heart condition or IV drug use
 Fever > 38 °C
 Vascular phenomena e.g., arterial emboli, intracranial hemorrhage, Janeway
lesions
 Immunologic phenomena e.g., Osler’s nodes, Roth’s spots, glomerulonephritis
 Positive blood cultures not meeting major criteria
Endocarditis
Treatment
 Targeted parenteral antimicrobial therapy (long duration e.g., 4 – 6 weeks depending
on susceptibility, and nature of valve (native vs prosthetic valve)
 Some clients may switch to oral therapy if clinically stable (e.g., after 2 weeks)
 50% of clients will require valve surgery; cases of heart failure, uncontrolled infection
or to prevent embolism
 Risk of repeat endocarditis
Prevention
 Patients at high risk of IE who undergo procedures that are associated with transient
bacteremia should receive antibiotic prophylaxis
(Wilson, W. et al. (2007) Prevention of Infective Endocarditis. Circulation.
http://circ.ahajournals.org/content/116/15/1736.full)
A Care Scenario
 35-year-old male
 History of IV drug use
 HIV status unknown
 Presents with high fevers, SOB, and fatigue
 While in the ED, displays symptoms consistent with ischemic stroke
 Muscle weakness, loss sensation on left side, difficulty speaking and
confusion
 3/3 blood cultures reveal Staphylococcus aureus
 Septic pulmonary emboli observed on chest x-ray
 Trans-esophageal echocardiogram reveals a large vegetation on tricuspid valve
Myocarditis
 Most often associated with a viral infection of the myocardium and infiltration of
cardiac muscle by T-lymphocytes
 Enteroviruses (coxsackievirus B), adenovirus, HHV, influenza virus, SARS-CoV-2,
HIV
 Non-infectious causes should be considered (e.g., medications, vaccines)
 More commonly associated with pediatric cases
 Variable symptoms
 History of recent (within 1-2 weeks) flulike syndrome of fevers & malaise,
pharyngitis, tonsillitis, or upper respiratory tract infection
 Symptoms of mild heart failure (fatigue, weakness, shortness of breath, edema,
palpitations), arrhythmia
 Pain reported in those with concomitant pericarditis
Myocarditis
 Different clinical phenotypes based on age
 Acute symptoms in pediatric patients - cardiogenic shock & acute heart
failure, sudden death
 In adults, symptoms progress slowly; progressive HF & dilated
cardiomyopathy
 CAR (coxsackie-adenoviral receptor) acts as the portal of entry
 Expressed in myocytes - higher concentration in children (younger hearts)
than adults (older hearts)
 Explains increased risk of coxsackieviral infections in newborns and young
children & risk of more clinically acute disease
Myocarditis
Treatment
 Similar to that of heart failure (ACE inhibitors, beta blockers)
 Avoid NSAIDs – this drug class increases the risk of mortality from heart failure
 NSAIDs induce fluid retention (due to vasoconstriction of blood vessels in the
kidney and the resulting retention of sodium and potassium)
 Immunosuppressive therapy (steroids)
Complications
 Early resolution of of symptoms (< 2 weeks); complete recovery
 Prolonged symptoms (> 2 weeks to months)
 Dilated cardiomyopathy, heart attack & stroke
 Worsening heart failure, death (or cardiac transplantation)
Pericarditis
Inflammation of the pericardium
 May co-exist with myocarditis
 Infectious causes of pericarditis
 Viruses (like those that cause myocarditis) are the most causative pathogen,
appears 2 - 3 weeks post “flu-like” illness
 Non-infectious causes should be considered (medications, vaccines)
Symptoms
 Sharp, stabbing chest pain caused by rubbing of two layers of the pericardium
 Pain worsens when laying down, with deep breaths, swallowing and
coughing
 Pain improves with sitting upright or forward
Pericarditis
Diagnostic findings
 Abnormal heart sounds “pericardial rub”
 Abnormal ECG
 Echocardiogram – appearance of fluid surrounding heart
Treatment
 Analgesics & anti-inflammatory drugs (NSAIDS or steroids); assess for concomitant
myocarditis
 Antibiotics for bacterial causes (more severe illness)
 Pericardial tamponade (tachycardia, SOB, increased RR & prominent neck veins) -
pericardiocentesis; drainage of pericardial fluid
 Constrictive pericarditis – pericardiectomy; surgical removal of pericardium
Lyme Disease
 Most common vector-borne infectious
disease in the temperate northern
hemisphere; affecting hundreds of
thousands of people annually in North
America
 Found predominantly in 3 regions: the
northeastern states from Virginia to
eastern Canada including Ontario,
Quebec, and the eastern maritime
provinces; the upper Midwest,
particularly Wisconsin and Minnesota;
and northern California
Lyme Disease
 Borrelia burgdorferi
 Spirochete-shaped bacteria with periplasmic flagella, motile
 Transmitted to humans by infected deer ticks; also referred to as the blacklegged tick
 Ixodes scapularis and Ixodes pacificus
 No evidence of person-to-person transmission
 Transmission and Infection (reportable to Public Health)
 Tick bite (portal of entry); spirochetes spread locally in the dermis at a rate of 4 µm/sec
 Tick saliva induces local inflammation at the site of the bite; ring of inflammation follows
the migrating bacteria (accounting for distinctive rash present in 80% of cases)
 Bacteria move from the site of infection into blood and lymph, causing systemic symptoms
 Local and disseminated phases of infection; symptoms mimic those of other diseases
Deer Ticks – Complex Life Cycle
Deer Ticks – Complex Life Cycle
 Complex life cycle; deer ticks live for 2 years
 3 developmental stages; Larva, Nymph, Adult; all stages can feed on humans, but typically
feed on different hosts
 Larvae become infected with first blood meal; bacteria replicate in their digestive system
during Winter
 The following spring, ticks molt into nymphs and feed a second time, infecting new hosts with
Borrelia
 Nymphs drop of host and develop into adults; feed a final time (infecting their host), then
mate, lay eggs and die
 Infected ticks must remain attached to host for 36-48 hours to transmit sufficient spirochetes to
establish Borrelia infection
 Adults are larger than nymphs so humans often see and remove adults before they can transmit
the bacteria; nymphs most often responsible for human infection
Deer Ticks
 Nymphs are ~ the size of a poppy seed; adult deer ticks ~ the size of a sesame seed

Larva, Nymph, Adult Male, Adult

Nymphs at Female
various stages of
engorgement
Lyme Disease – Transmission
 Ticks can’t fly or jump; they wait for a host on grasses and shrubs “questing”
 Hold upper pair of legs outstretched, waiting to climb onto a passing host;
then bites
 Blacklegged tick attaches to host (human or animal) and sucks blood slowly for
several days
 Acquires and transmits Borrelia during the blood meal
 Removing a tick quickly (within 24 hours of bite) can greatly reduce risk of
Lyme Disease
 Takes time for Borrelia to move from the tick to the host through the saliva
 The longer the tick is attached, the greater the risk of acquiring Lyme Disease
Lyme Disease – Prevention
Tick removal
 Do not crush, squeeze or damage the tick; this could facilitate infection
 Do not use a lit match or cigarette, nail polish or nail polish remover, petroleum
jelly, liquid soap or kerosene to remove the tick
 If the tick is still alive, put the tick in a secure container and contact your local
public health unit
 Submit a photo of the tick to
etick.ca for identification
Lyme Disease – Prevention
How to avoid tick bites
 Many individuals bitten by a tick have no idea; increased risk of exposure for
individuals who live, work, play in, or visit a wooded area, or an area with tall grasses
and bushes (including city gardens and parks) especially in Spring/Summer
1. Cover up
 Wear light-coloured clothing (easier to see ticks), closed-toed shoes, long-sleeved
shirts, long pants, tucked into your socks
2. Use insect repellent
 Use a repellent with DEET or icaridin; use on both clothes and exposed skin
3. Do a “tick check” and put clothes in the dryer for at least 10 minutes
 High heat kills ticks that might be on clothing; this should be done before washing
them
Lyme Disease – Prevention
Tick checks
 After being outdoors in higher-risk areas,
check for ticks!
 Don’t forget the back of the body
 Use a mirror, or ask someone to check for you
 Good idea to have a shower to wash off any
ticks
 Check pets for ticks (groin)

 After being outdoors, check your pet’s skin and

remove any ticks you find (removal is the same
process for humans and pets)
Localized Lyme Disease – Symptoms
Most common sign (~70%); expanding skin rash
typically at the site of infection (tick bite) that
appears within 3 – 30 days (average 7 days)
 Erythema migrans; slowly grows (expands)
over several days and can reach up to 30 cm
across, lasting several weeks
 May feel warm, but not itchy or painful
 Can be circular or oval-shaped, look like a
target or “bull's eye”
 Can also go unnoticed especially on an
area that is difficult to see
 Some individuals never develop a rash,
despite experiencing other symptoms
Localized Lyme Disease – Symptoms
 Other early signs and symptoms include (rash may or may not be present)
 Fever, chills, headache, stiff neck, fatigue, decreased appetite, muscle and joint
aches, swollen lymph nodes
 Typically appear 3 – 30 days (average 7 days) post-infection
 If left untreated, infection can spread to the joints, heart and nervous system
(disseminated infection)
Localized Lyme Disease – Diagnosis
 Challenging as symptoms vary
from person to person
 Diagnosis based on:
 Symptoms
 Travel history
 Exposure to blacklegged ticks
 Blood test (serology) may be
required
Localized Lyme Disease – Treatment
 Most individuals treated
with antibiotics in the early
localized phase of Lyme
Disease recover rapidly and
completely
 Early diagnosis and proper
antibiotic treatment of
Lyme Disease can help
prevent disseminated
infection

https://www.hqontario.ca/Portals/0/documents/evidence/qs-clinical-guidance-lyme-disease-en.pdf
Disseminated Lyme Disease – Symptoms
In the absence of prompt identification and treatment, the infection can disseminate; leading to
musculoskeletal, neurologic or cardiac manifestations within 1 to 4 months after the initial
infection
 Skin rashes distal to the portal of entry and original rash
 Arthritis; pain, redness, and swelling in one or more large joints (often the knee)
 Intermittent pain, weakness, or numbness in arms and/or legs (peripheral neuropathy), facial
palsy
 Shooting pain, numbness, or tingling of hands or feet
 Headaches, neck stiffness, poor memory and reduced ability to concentrate
 Meningitis, encephalitis
 Conjunctivitis and/or damage to deep tissue in the eyes
 Lyme Carditis; palpitations, arrythmias, myocarditis, pericarditis
 Episodes of dizziness or shortness of breath
Disseminated Lyme Disease
Diagnosis
 Signs and Symptoms
 Serologic testing for the presence of antibodies
 Borrelia burgdorferi antigens differ from region to region; travel history is
important
 IgG or combined IgG/IgM testing should be performed
 Due to antibody persistence, single positive serologic test results cannot distinguish
between active and past infection
Treatment
 Antibiotic regimen determined by system(s) affected e.g., neurologic Lyme Disease,
Lyme carditis, Lyme arthritis; referral to infectious disease (or another) specialist
 Supportive therapy (e.g., anti-inflammatory drugs)
Lyme Disease – Prophylaxis (post-exposure)

The risk of developing Lyme disease from an infected tick is 1-3% in Ontario. In
many instances, it is reasonable to take a “wait and see” approach (for 30 days) and
treat patients only if they develop symptoms
Post-exposure prophylaxis can be considered if these four criteria are met:
1. The tick was attached > 24 hours
2. The tick was removed within the past 72 hours
3. The tick bite occurred in an area with a prevalence of ticks infected with
Borrelia burgdorferi > 20%
4. Doxycycline is not contraindicated
Adults: 1 dose of doxycycline 200 mg PO
Children ≥ 8 years: 1 dose of doxycycline 4 mg/kg PO (maximum dose of 200 mg)
Late-Persistent Lyme Disease Syndrome
(PTLDS)
 Some individuals (10 - 20%) with Lyme Disease will experience symptoms of pain, fatigue,
insomnia, difficulty thinking, etc. that lasts 6 months post-treatment
 Why some patients experience PTLDS is not clear
 Thought to be associated with tissue damage that occurred before the infection was eliminated
 Borrelia burgdorferi may trigger an autoimmune response causing symptoms that persist well
after the infection is eradicated; autoimmune responses occur following other bacterial
infections
 Campylobacter jejuni (Guillain-Barré syndrome), Chlamydia trachomatis (reactive arthritis),
and streptococcal pharyngitis (rheumatic heart disease)
 This is not a chronic infection
 Osteoarthritis, rheumatoid arthritis, multiple sclerosis, demyelinating disease, ALS,
neuropathies, dementia, depression, have all been misdiagnosed as “Chronic Lyme”
 No credible research to demonstrate that Lyme disease is a chronic infection