Cardiovascular Microbiology Flashcards
Myocarditis can present as a wide array of symptoms with variable presentation. What are some clinical features of myocarditis?
FEVER, precordial discomfort (chest pain), dyspnea, fatigue
Others include unexplained sinus tachycardia, S3 or S4 or summation gallop, abnormal ECG, abnormal echo, new cardiomegaly on CXR, arrhythmia, partial or complete heart block, new-onset BBB, new-onset or worsening heart failure, acute pericarditis, cardiogenic shock, sudden cardiac death, respiratory distress/tachypnea, hepatomegaly
Physical exam findings of myocarditis
Soft S3/S4 (impaired ventricular function), new murmur (secondary to valvular insufficiency), pericardial friction rub (if there is extension into pericardium)
Think systolic CHF — decreased contractility, orthopnea, dyspnea on exertion, crackles, PND
Workup considerations for suspected myocarditis
EKG — assess for arrhythmia (sinus tachycardia most common), transient ST-T wave abnormalities (findings can be nonspecific)
CXR — pt is presenting with CP and/or sx of CHF — must consider all etiologies especially: pulmonary disease, heart failure, dissection. Assess for cardiomegaly
Echocardiogram — assessment of ventricular function and structure; eval of EF, LV size, wall motion abnormalities
PCR — detection of viral genome
Labs — CBC (for leukocytosis), cardiac enzymes (likely elevated secondary to myocyte damage), BNP (heart failure), CPK (muscle damage), ESR and CRP = acute phase reactants
Endomyocardial biopsy can aid in definitive dx
3 major complications of myocarditis
Dilated cardiomyopathy
Myopericarditis (myocarditis extended into pericardium)
Sudden cardiac death (20%)
Tx for myocarditis; how is prognosis determined?
Heart failure therapy, therapy for arrhythmias
Beta blocker, ACEI, diuretics
Avoid NSAIDs, EtOH, and exercise (restricted)
Prognosis is dependent upon clinicopathologic types of myocarditis
Infectious etiologies for myocarditis
Typically Coxsackie B, Trypanosoma cruzi, or Trichinella spiralis
Other considerations: HIV, Chalmydophyla psittaci, Rickettsial sp., Corynebacterium diphtheriae, Neisseria meningitidis, Borrelia burgorferi, Candida
Morphology, transmission, and peak incidence times for coxsackie B virus
+ssRNA virus, small, naked, icosahedral
Transmission = fecal oral
Peak incidence = summer, fall
Clinical manifestations of coxsackie B infection
URI, pleurodynia (“devil’s grip” - severe intercostal pain and fever), myocarditis (most common infectious etiology), aseptic meningitis
Endemic locations and transmission of trypanosoma cruzi (hemoflagellate)
Location: southern US, Mexico, South America
Transmission = reduviid bug, animal carriers
Phases of Chagas dz
Acute: chagoma, romana sign, fever, malaise, LAD, myocarditis, severe meningoencephalitis (usually in younger pts)
Intermediate: asymptomatic
Chronic: dilated cardiomyopathy, arrhythmia, megacolon, achalasia
Diagnostics for chagas dz
Peripheral smear for trypomastigotes, xenodiagnosis
Invasive nematode transmitted via ingestion of cysts from raw pork (boars or horses too)
Trichinella spiralis
Humans are dead-end hosts for trichinella spiralis - describe its lifecycle
Larvae develop in gut —> mate —> larvae disseminate hematogenously —> penetrate muscle tissue
Affect skeletal m, heart, and brain
It is an invasive cycle that can be lethal with heavy infection
Symptoms and diagnostics associated with trichinella spiralis infxn
Abdominal pain, diarrhea, fever (while in small intestine); after muscle invasion get myalgias and other sx based on location
Consider the dx if — periorbital edema, mositis, eosinophilia
Dx: Serologic (ELISA, etc.) or latex agglutination, CPK levels, muscle bx
Infectious agents implicated in pericarditis
Viruses, bacteria, TB (caseating pericarditis), fungi, parasites
Presentation and clinical features for infectious pericarditis
Chest pain — often sharp, positional, and pleuritic in nature, relieved by leaning forwards
Fever
Palpitations
Physical exam findings in infectious pericarditis
Friction rub upon cardiac auscultation, rapid or irregular pulse
What would you see on EKG for infectious pericarditis?
Diffuse ST elevations with reciprocal depressions in leads aVR and V1
PR depression
What would you find on CXR with infectious pericarditis?
Minimal abnormalities in the majority
Exception: pericardial effusion > 250 mL will cause symmetrically enlarged cardiac sillhouette = “water bottle” sign [diaphragm will appear flat to compensate for weight of effusion]
If you suspect infectious pericarditis, what test should you do to assess for pericardial effusion and/or tamponade, as it is more sensitive than a CXR?
Transthoracic echocardiogram
Labs to do when infectious pericarditis suspected
Serial cardiac enzymes CBC with diff ESR CRP Blood cultures if temp >38 C
Major complication of infectious pericarditis
Cardiac tamponade (tx with pericardiocentesis) — counsel about activity restrictions
Tx for infectious pericarditis
High dose ASA TID and colchicine
[ibuprofen, indomethacin options too] — or tx underlying cause!
_______ are CONTRAINDICATED in pericarditis
Anticoagulants
Ziehl Neelson and Auramine-rhodamine stains are used to identify which organism that can potentially cause infectious pericarditis?
Mycobacterium tuberculosis
[Ziehl Neelson is acid-fast stain that shows red rods; Auramine-rhodamine shows apple green color]
Morphology of M.tuberculosis + virulence factors
Acid fast bacillus (weakly G+), obligate aerobes, facultative intracellular (macrophages)
[AFB secondary to mycolic acid cell wall composition — highly resistant to desiccation including NaOH]
Virulence: facultative intracellular, sulfatides, cord factor, surface protein can cause a delayed hypersensitivity and cell mediated immunity reaction (utilized for PPD test), Wax D
The major manifestation of mycobacterium tuberculosis is pulmonary TB, how does it cause a caseating pericarditis?
Through direct lymphatic or hematogenous dissemination of the bacteria
Risk factors for infective endocarditis
Age > 60, M>F
Poor dentition, IV drug abuse, structural heart dz, congenital heart dz, valvular heart dz, prosthetic valve replacement, RHD
IE manifestations can be variable and generally depend on virulence of organism involved. What are some general clinical manifestations seen with IE?
Constituational sx = onset of sx nonspecific in nature then progress toward fever, chills, weight loss, new/worsening murmur, fatigue, arthralgia, and myalgia
Differentiate some clinical manifestations in acute IE vs. subacute IE
Major difference = timeline — acute will have much more rapid onset (<7d)
Acute: rapid progression of sx and cardiac damage; high fever, chills, weakness, SOB, pleuritic CP
Subacute: indolent course; low grade fever, weight loss over time, fatigue, arthralgia/myalgia
Complications of IE
CHF, abscess formation, hematogenous spread, embolism, systemic immune reaction, death
Cardiac manifestations in IE (including difference betwen acute vs. subacute)
Heart murmurs - new or worsening
Acute IE: R side of heart > L side (tricuspid > aortic; especially with S.aureus involvement)
Subacute IE: L side of heart > R side of heart
Diagnostic workup for infective IE
Blood culture x3, CBC with diff, CMP
EKG, ESR, CRP, UA (assess for hematuria)
Transesophageal echo, CXR
What set of criteria are used for the dx of endocarditis, and how many are needed to qualify for definitive dx?
Modified DUKE criteria for diagnosis of endocarditis (consists of major and minor)
Definite dx requires one of the following:
- Meets 2 major criteria
- Meets 1 major and 3 minor
- Meets 5 minor
For infectious endocarditis that presents with cardiogenic shock, primary tx is _____ ASAP. If the pt is toxic, empiric abx should be started immediately, typically including _______ and _______. Culture and sensitivities will then determine how to tailor tx. However, this may not be necessary if the infection is ________
Surgery; vancomycin; gentamycin; subacute
Abx prophylaxis for pts at high risk for IE prior to dental or respiratory procedures
Able to take PO: amoxicillin
Need IV: ampicillin or cefazolin or ceftriaxone
Allergic to PCN: desensitize or cephalexin or clindamycin or azithromycin
Common vs. rare infectious etiologies for IE
Common = S.aureus, S.epidermidis, S.viridans, Enterococcus (Group D Strep)
Rare = HACEK, Coxiella burnetti, brucella sp., S.agalactiae
Morphology of S.aureus
G+ cocci in clusters
Coagulase and catalase +
Facultative anaerobe
[normal flora on skin — can breach and colonize respiratory tract]
Virulence factors of S.aureus
Host cell evasion: Protein A, coagulase, catalase, hemolysins, leukocydins
Invasion of tissue and bloodstream (hyaluronidase, staphylokinase, lipase)
Toxin
Toxin mediated manifestations of S.aureus
Food poisoning, scalded skin syndrome, TSS
Local manifestations of S.aureus
Skin — impetigo, cellulitis, furuncles, carbuncles
Respiratory — pneumonia (cavitary)
Systemic manifestations of S.aureus
Acute endocarditis (tricuspid valve), meningitis, osteomyelitis (#1 cause in adults and kids), septic arthritis
For MSSA [methicillin-susceptible S.aureus], _______ is a great starting point of tx
Nafcillin
Morphology of S.viridans
Gram+ cocci in chains, alpha-hemolytic, catalase negative, facultative anaerobe, optochin resistant
Normal oral flora, nasopharynx, and GI tract
Virulence factors and manifestations of S.viridans infection
Extracellular dextran binds heart valves
Manifestations = dental caries, subacute endocarditis
Tx for S.viridans
PCN
Morphology of S.epidermidis
Gram+ cocci in clusters Coagulase negative Catalase + Novobicin sensitive Facultative anaerobe
[normal flora on skin]
Virulence of S.epidermidis
Adhesion polysaccharide capsule — adherence to prosthetic devices, indwelling catheters
Biofilm formation
Manifestations of S.epidermidis
Subacute endocarditis, infection and bacteremia in neutropenic pts (susceptible)
Tx of S.epidermidis
Extremely abx resistant — use Vancomycin
Organism that is part of normal flora in human bowel that has extracellular dextran to bind heart valves; gram+ cocci that is catalase negative, facultative anaerobe, variable hemolyic nature (alpha or gamma)
Enterococcus faecalis
Manifestations of E.faecalis infxn
Subacute bacterial endocarditis, UTI, biliary tract infxns
Media requirements for E.faecalis
Can grow on 40% bile AND 6.5% NaCl, blood agar
T/F: vancomycin resistant forms of enterococcus faecalis are not of concern at this time
False — vancomycin resistant forms are on the rise!
What organism associated with subacute bacterial endocarditis is associated with colon cancer and IBD?
Streptococcus bovis (group D strep)
Morphology of S.bovis
Gram+ cocci in chains, catalase negative, facultative anaerobe, variable hemolytic nature [normal flora in human bowel; has virulence factor of extracellular dextran to help bind heart valves]
Manifestations and media specifics for S.bovis
Biliary tract infxns, UTIs, subacute bacterial endocarditis
Media: 40% bile, blood agar
The HACEK organisms are a gram _____ group of bacilli, fastidious, suspected cause of “culture negative” endocarditis. Media option of _______ agar should be considered. They are part of the normal ____ flora
Negative; chocolate; oral
What are the HACEK organisms?
Haemophilus sp (H.parainfluenzae most common) Aggregatibacter sp Cardiobacterium sp Eikenella corrodens Kingella sp
T/F: haemophilus sp should be grown on blood agar
False — Haemophilus have the ability to be grown on chocolate agar (contains Factors V and X, aka NAD+ and Hemin); Haemophilus CANNOT be grown on blood agar
One exception — will show stellate growth on blood agar if placed on same place as S.aureus because S.aureus has hemolysins to lyse RBCs
Gram- pleomorphic obligate intracellular, aerobic, zoonotic, aerosol transmitted organism
Coxiella burnetti
Major illness caused by coxiella burnetti
Q fever — flu-like sickness carried by goats, sheep, cows, and other animals
Animals spread the germ when they give birth; farmers and vets at higher risk
Wind can carry barnyard dust mixed with Q fever germs for miles
A 48 y/o female presents to your office with the CC of fatigue, fever, and abdominal pain. Sx have been occurring over the past 3 weeks. She never feels completely rested and is beginning to take frequent naps. Her abdominal pain is diffuse, 3/10, occasional nausea with no vomiting, no radiation. At home temps have been 38.4◦C and have not been abated with Tylenol. She denies recent travel, sick contacts, insect bites, or rashes. She also denies orthopnea or edema. PMH of PNA 3 weeks ago w/ PICC line for abx infusion. PE is significant for retinal hemorrhages, petechiae on buccal mucosa, III/VI holosystolic murmur at 5th ICS MCL on L, no thrills. CTAB with crackles at b/l lung bases, linear hemorrhages present in b/l nail beds.
Based on pts presentation and PE you are suspecting which of the following?
a. pericarditis
b. acute IE
c. subacute IE
d. myocarditis
e. malingering
c. subacute IE
A 48 y/o female presents to your office with the CC of fatigue, fever, and abdominal pain. Sx have been occurring over the past 3 weeks. She never feels completely rested and is beginning to take frequent naps. Her abdominal pain is diffuse, 3/10, occasional nausea with no vomiting, no radiation. At home temps have been 38.4◦C and have not been abated with Tylenol. She denies recent travel, sick contacts, insect bites, or rashes. She also denies orthopnea or edema. PMH of PNA 3 weeks ago w/ PICC line for abx infusion. PE is significant for retinal hemorrhages, petechiae on buccal mucosa, III/VI holosystolic murmur at 5th ICS MCL on L, no thrills. CTAB with crackles at b/l lung bases, linear hemorrhages present in b/l nail beds.
Based on your clinical suspicions, your workup includes blood cultures x3 + which of the following?
a. cardiac bx
b. trans esophageal US
c. trans thoracic US
d. abdominal CT
e. bronchoscopy
b. trans esophageal US
A 48 y/o female presents to your office with the CC of fatigue, fever, and abdominal pain. Sx have been occurring over the past 3 weeks. She never feels completely rested and is beginning to take frequent naps. Her abdominal pain is diffuse, 3/10, occasional nausea with no vomiting, no radiation. At home temps have been 38.4◦C and have not been abated with Tylenol. She denies recent travel, sick contacts, insect bites, or rashes. She also denies orthopnea or edema. PMH of PNA 3 weeks ago w/ PICC line for abx infusion. PE is significant for retinal hemorrhages, petechiae on buccal mucosa, III/VI holosystolic murmur at 5th ICS MCL on L, no thrills. CTAB with crackles at b/l lung bases, linear hemorrhages present in b/l nail beds.
Blood cultures reveal G+ cocci in clusters that are catalase positive, coagulase negative. Based on this information and patient presentation, the most likely etiologic organism is?
a. S.aureus
b. S.viridans
c. E.faecalis
d. S.bovis
e. S.epidermidis
e. S.epidermidis
A 48 y/o female presents to your office with the CC of fatigue, fever, and abdominal pain. Sx have been occurring over the past 3 weeks. She never feels completely rested and is beginning to take frequent naps. Her abdominal pain is diffuse, 3/10, occasional nausea with no vomiting, no radiation. At home temps have been 38.4◦C and have not been abated with Tylenol. She denies recent travel, sick contacts, insect bites, or rashes. She also denies orthopnea or edema. PMH of PNA 3 weeks ago w/ PICC line for abx infusion. PE is significant for retinal hemorrhages, petechiae on buccal mucosa, III/VI holosystolic murmur at 5th ICS MCL on L, no thrills. CTAB with crackles at b/l lung bases, linear hemorrhages present in b/l nail beds.
You suspect that the patient acquired their infection secondary to the PICC line. Cultures confirm that S.epidermidis is the infectious etiology. What virulence factor contributed in this patient’s pathology?
a. Protein A
b. EC dextran that binds cardiac valves
c. Adhesion polysaccharide capsule
d. Elaboration of coagulase
e. Protein M
c. Adhesion polysaccharide capsule
A 58 y/o male with a PMH of HCV presents with dyspnea and pleuritic chest pain that has progressed over the past 2 days. He states that he was in his previous state of health until this point. The chest pain is pronounced when inhaling and feels like a burning sensation, 7/10, with associated hemoptysis. Pt also states he has developed a non-pruritic rash on his B/L LE. He states that he has also developed fevers, chills, and myalgias. He denies sick contacts, recent travel, exposures to pulmonary irritants, or insect bites. Hx reveals 30 pack year hx, in recovery for drug use. PE reveals hypotension, tachycardia, febrile at 40 C, and 89% on RA, coughing frequently, pale and toxic appearing, diaphoretic, pinpoint pupils, IV/VI blowing holosystolic murmur at LLSB 4th ICS with palpable thrill, CR 4 sec; diffuse coarse crackles in all lung fields, intercostal retractions, poor thoracic expansion and use of accessory mm for breathing, as well as splenomegaly. He also has 3/5 muscle strength in b/l UE and LE as well as diffuse palpable purport on b/l LE, non-blanchable.
Based on pt presentation and PE, what is your #1 DDx?
a. Active TB
b. SCLC
c. Acute IE
d. Pericarditis
e. Subacute IE
c. acute IE
A 58 y/o male with a PMH of HCV presents with dyspnea and pleuritic chest pain that has progressed over the past 2 days. He states that he was in his previous state of health until this point. The chest pain is pronounced when inhaling and feels like a burning sensation, 7/10, with associated hemoptysis. Pt also states he has developed a non-pruritic rash on his B/L LE. He states that he has also developed fevers, chills, and myalgias. He denies sick contacts, recent travel, exposures to pulmonary irritants, or insect bites. Hx reveals 30 pack year hx, in recovery for drug use. PE reveals hypotension, tachycardia, febrile at 40 C, and 89% on RA, coughing frequently, pale and toxic appearing, diaphoretic, pinpoint pupils, IV/VI blowing holosystolic murmur at LLSB 4th ICS with palpable thrill, CR 4 sec; diffuse coarse crackles in all lung fields, intercostal retractions, poor thoracic expansion and use of accessory mm for breathing, as well as splenomegaly. He also has 3/5 muscle strength in b/l UE and LE as well as diffuse palpable purport on b/l LE, non-blanchable.
Blood cultures are taken and grown G(+) cocci in clusters that are catalase and coagulase positive. What virulence factor likely contributes to symptom severity?
a. EC dextran
b. protein A
c. biofilm formation
d. polysaccharide capsule
e. opa proteins
b. protein a
A 58 y/o male with a PMH of HCV presents with dyspnea and pleuritic chest pain that has progressed over the past 2 days. He states that he was in his previous state of health until this point. The chest pain is pronounced when inhaling and feels like a burning sensation, 7/10, with associated hemoptysis. Pt also states he has developed a non-pruritic rash on his B/L LE. He states that he has also developed fevers, chills, and myalgias. He denies sick contacts, recent travel, exposures to pulmonary irritants, or insect bites. Hx reveals 30 pack year hx, in recovery for drug use. PE reveals hypotension, tachycardia, febrile at 40 C, and 89% on RA, coughing frequently, pale and toxic appearing, diaphoretic, pinpoint pupils, IV/VI blowing holosystolic murmur at LLSB 4th ICS with palpable thrill, CR 4 sec; diffuse coarse crackles in all lung fields, intercostal retractions, poor thoracic expansion and use of accessory mm for breathing, as well as splenomegaly. He also has 3/5 muscle strength in b/l UE and LE as well as diffuse palpable purport on b/l LE, non-blanchable.
Blood cultures x 3 are immediately sent to the lab. Of the following, which is the best empiric treatment for this patient?
a. penicillin and ergocalciferol
b. vancomycin +/- gentamycin
c. nafcillin and ceftriaxone
d. TMP-SMX and ceftriaxone
e. amoxicillin and vancomycin
b. vancomycin +/- gentamycin
A 64 y/o male presents to the ED with CP, fever, fatigue, cough, and arthralgias. He admits to experiencing night sweats. His PMH is significant for rheumatic heart disease and a dental procedure a few weeks before admission. He currently does not show any vasculitis or immunologic phenomena of endocarditis on PE, although endocarditis is suspected. What is the likely etiology?
a. HACEK organisms
b. S.viridans
c. E.faecalis
d. S.aureus
e. S.bovis
b. S.viridans
A 67 y/o male with a PMHx of poorly controlled T1DM is being managed in the ICU after a diagnosis of DKA stemming from an infection. He is currently on Day 2 of IV Vancomycin. 4 days into his hospital stay, he develops a fever. Labs reveal a G(+) cocci that grows in chains. The organism demonstrates growth on 40%bile media and 6.5% NaCl. What is the likely infectious etiology?
a. S.bovis
b. S.epidermidis
c. S.viridans
d. E.faecalis
e. H.influenzae
d. E.faecalis
A 68 y/o female with a PMHx of MVP with mitral valve replacement presents with fevers of 2 weeks duration. In addition to positive blood cultures, which of the following would confirm a diagnosis of infective endocarditis?
a. CXR showing pulmonary edema and anemia
b. retinal hemorrhages, temp >38 C
c. elevated ESR, thrombocytopenia
d. petechial rash, leukocytosis
b. retinal hemorrhages, temp >38
23 y/o male presents with retrosternal chest pain that radiates to the neck and left shoulder. He reports a low grade fever for 3 weeks duration, cough, and difficulty swallowing. He also reports night sweats. He recently emigrated from Peru where he spent the last year in prison for having one kilo of “high quality blow” in his personal possession. He is leaning forwards in the chair during history taking. His PPD skin test is 10mm. His CD4 count is 350, CBC shows leukocytosis at 12,000. EKG shows ST elevations. The most likely cause of his illness?
a. evolving acute MI
b. pneumocystis pneumonia secondar to HIV/AIDS
c. M.tuberculosis pericarditis
d. hyperkalemia
e. Q fever secondary to coxiella burnetti
c. M.tuberculosis pericarditis
treatment for M.tuberculosis pericarditis?
A. Vancomycin + ceftriaxone
B. Isoniazid + rifampin + ethambutol+ pyrazinamide C. High dose corticosteroids + colchicine
D. High dose aspirin + colchicine
E. High dose Indomethacin
B. Isoniazid + rifampin + ethambutol + pyrazinamide
A 28 y/o male with a recent URI presents with substernal chest pain that radiates to B/L shoulders. The pain is central in nature with associated diaphoresis and fever. Cardiac auscultation reveals the following:
The most likely etiology of his chest pain is?
a. single stranded 8 segmented RNA virus
b. dsDNA enveloped virus
c. retrovirus
d. -ssRNA virus
e. +ssRNA naked virus
e. +ssRNA naked virus
The patient in the previous question was subsequently diagnosed with viral pericarditis. Prior to presentation, the patient likely had a recent history of?
a. herpangia
b. URI
c. reduviid bite
d. hand, foot, mouth dz
e. dysphagia
b. URI
Our patient was diagnosed with acute pericarditis secondary to Coxsackie virus. Patient began a regimen of high dose ASA and colchicine. Aside from EKG stabilization, which laboratory can we monitor to ensure treatment effectiveness?
a. CBC
b. INR
c. CMP
d. CRP
e. Hemoccult
d. CRP
A 60 y/o female with no significant PMH presents with pleuritic chest pain of 72 hours duration. She is leaning forward and sitting upright. Her temperature is 40°C and she is hemodynamically stable. Of the following, which laboratory result could you expect for this patient’s presentation?
a. elevation of cardiac enzymes
b. leukopenia
c. hematuria
d. elevated BUN/Cr
e. WNL ESR
a. elevation of cardiac enzymes
A 24 y/o professional football player that was recently discharged from the hospital with viral pericarditis presents to the office for followup. He states he is compliant with his ASA and colchicine treatment and wonders when he can get back on the field. The best response for this athlete is?
a. you are cleared for practice
b. expect a 3 mo break
c. suspended indefinitely
d. when an ST normalization is present on EKG
e. when there are T wave inversions on EKG
b. expect a 3 mo break
