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Flashcards in Microbiology DSA Deck (40)
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Essentials of diagnosis of Acute Inflammatory Pericarditis

o Anterior pleuritic chest pain worse supine than upright
o Pericardial rub
o Fever common
o Erythocyte sedimentation rate elevated
o ECG: diffuse ST-segment elevation with associated PR depression


Viral causes of pericarditis

o Coxsackieviruses
o Echoviruses
o Influenza
o Epstein Barr
o Varicella
o Hepatitis
o Mumps


Viral pericarditis dx

o dx made clinically, leukocytosis often present
o Rising viral titers – rarely done
o Cardiac enzymes slightly elevated – epicardial myocarditis component
o Echocardiogram normal, or trivial amount of extra fluid during acute inflammatory process


Tuberculous Pericarditis

direct lymphatic or hematogenous spread
o Clinical pulmonary involvement absent or minor, pleural effusions common
o S/S: subacute, fever, night sweats, fatigue for days to months
o Acid-fast bacilli found elsewhere
o Low yield of organisms by pericardiocentesis, pericardial biopsy higher yield but may also be negative, pericardiectomy may be required
o Tx: antituberculous drug therapy, constrictive pericarditis can occur


Bacterial pericarditis

direct extension from pulmonary infections
o Pneumococci
o Borrelia burgdorferi – myopericarditis, occasional heart block
o Patients appear toxic, often critically ill
o Suspected on clinical grounds, pericardiocentesis confirmatory


Uremic pericarditis

complication of CKD
o Untreated uremia and stable dialysis patients
o w/ or w/o symptoms – fever absent
o If not on dialysis – incidence correlates to level of BUN and Cr
o “Shaggy” pericardium and effusion is hemorrhagic and exudative
o Tx dialysis


Myxedema pericarditis


cholesterol crystals within fluids


Neoplastic pericarditis

most frequent causes of pericardium tamponade
• Hodgkin Disease
• Lymphomas
• Painless, presenting symptoms related to hemodynamic compromise or primary disease
• Pericardial effusion may be very large, consistent with chronic nature
• Cytologic examination of effusion or pericardial biopsy
• Difficult to establish clinically if medialstinal radiation within previous year
• Pericardial effusions develop over long period of time, may become quite large (2L+)
• Poor prognosis, drain effusion percutaneously initially, pericardial window
• Chemotherapeutic agents or tetracycline reduce recurrence rate


Radiation pericarditis

4000 cGy delivered to 30%+ of heart
• Initiate fibrinous and fibrotic process in pericardium
• Presents as subacute pericarditis or constriction
• Within first year, may delayed for many years before constriction evident
• Symptomatic therapy, recurrent effusions and constriction require surgery


Drug toxicity causing pericarditis

• Minoxidil
• Penicillins
• Clozapine


Dressler Syndrome

postcardiotomy pericarditis, post MI
o Days to weeks after MI or open heart surgery
o Recurrence of pain with pleural-pericardial features
o Rub audible
o Repolarization changes on ECG may be confused with ischemia
o Pain, fever, malaise, leukocytosis
o Autoimmune disorder symptoms – joint pain, fever
o Tamponade rare after MI, but not postoperatively
o High sedimentation rate helps confirm dx
o Large pericardial effusions and accompanying pleural effusions frequent


Pericarditis post MI

occur 2-5 days after infarct due to inflammatory reaction to transmural myocardial necrosis


S/S of pericarditis

• Substernal pain, may radiate to neck, shoulders, back, or epigastrium
• Dyspnea
• Febrile
• Characteristic pericardial friction rub with or without evidence of fluid accumulation or constriction


ECG findings in pericarditis

• ST and T wave changes
• Begins with diffuse ST elevation
• Followed by return to baseline
• Then to T wave inversion

• Atrial injury manifested by PR depression in limb leads


CXR findings in pericarditis

frequently normal, may show cardiac enlargement if pericardial fluid present
• Pulmonary disease signs
• Mass lesions and enlarged LNs suggest neoplastic process


Echocardiography in pericarditis

mild pericardial effusion in 60%


MRI and CT in pericarditis

visualize tumor
• Screening to ensure no extracardiac diseases contiguous to pericardium


CRP and late gadolinium in pericarditis

elevated CRP
late gadolinium enhancement of pericardium


Treatment of pericarditis

o Restrict activity until symptom resolution

o Athletes: restriction until resolution of symptoms and normalization of all lab tests – generally 3 mo

o Aspirin 750-1000 mg Q8h for 1-2 weeks with taper by decreasing dose 250-500 mg every 1-2 weeks or ibuprofen 600 mg Q8h for 1-2 weeks with taper by decreasing dose by 200-400 mg every 1-2 weeks.
• GI protection with colchicine 0.5-0.6 mg once (under 70 kg) or twice (over 70kg) daily for 3 months
• Taper: Reduce dose every other day for patients 70 kg or under, or once a day for over 70 kg in last week.

• Use Aspirin and Colchine in postMI (Dressler syndrome)
• NSAIDs have adverse effect on MI healing

• Use Colchine for at least 6 mo in all refractory cases and in recurrent pericarditis

o CRP used to assess effectiveness of treatment – once normal, tapering initiated



25-50 mg Q8h in recurrent pericarditis in place of ibuprofen


Systemic corticosteroids

severe symptoms, refractory cases, with immune-mediated etiologies
• Higher risk of recurrence, prolonged illness
• Recommend colchicine with corticosteroids for at least 3 mo to help prevent recurrences
• Prednisone 0.25-0.5 mg/kg/d orally with taper over 4-6 week period


Treatment if colchicine therapy fails or cannot be tolerated

immunosuppression required
• Cyclophosphamide, azathioprine, IV human Ig, interleukin-1 receptor agonsits (anakinra), methotrexate

o If colchicine and significant immunosuppression fails – surgical pericardial stripping considered in recurrent cases even without clinical evidence for constrictive pericarditis



early complication, less than 5% of patients

treated with partial pericardiectomy (pericardial window)


Characteristics of Picornaviridae family

i. Spread fecal-oral route, respiratory secretions, infect intestinal epithelial and lymphoid cells (tonsils, Peyer’s patches)
ii. Positive single stranded RNA viruses, smallest RNA viruses
iii. Naked icosahedral symmetry
iv. Replication in cytoplasm


Symptoms of Picornaviridae family

i. Asymptomatic or mild febrile infections
ii. Respiratory symptoms “colds”
iii. Rashes
iv. Aseptic meningitis


Coxsackie B pathology

a. Heart, brain, liver, pancreas, skeletal muscle damage

b. Pleurodynia:
i. Fever, headache, severe lower thoracic pain on breathing (pleuritic pain)

c. Myocarditis/Pericarditis
i. Infection and inflammation of the heart muscle and pericardial membrane
ii. Self-limited CP or more serious arrhythmias, cardiomyopathy, heart failure


M. tuberculosis morphology

i. 40% lipid
ii. composed of mycolic acids
iii. Thin rods
iv. Non-motile


M. tuberculosis metabolism

i. Aerobic
ii. Catalase-positive
iii. Slow growth rate


M. tuberculosis virulence

i. Mycosides:
1. Cord factor – only found in virulent strains – release TNF (cachectin) causing wt loss
2. Sulfatides – inhibit phagosome-lysosome fusion
3. Wax D – acts as adjuvant

ii. Iron siderophore – mycobactin

iii. Faculative intracellular growth – can survive and multiply in macrophages

iv. Non-motile, no capsule, no attachment pili


Clinical presentation of M. tuberculosis

i. Primary tuberculosis – asymptomatic or overt disease involving lungs or other organs
ii. Reactivation or secondary tuberculosis –
1. Pulmonary, pleural or pericardial, LN infection, kidney, skeletal, joints, CNS, miliary TB