CRR Pathogens

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  1. What immunoglobulin is critical for dealing with respiratory pathogens?
  2. What are the three main purposes of toxins?
    • Inhibit immune cells
    • Kill host epithelial cells
    • Promote inflammation
  3. How do organisms generally avoid immune clearance?
    Through production of an anti-phagocytic capsule
  4. Extensive inflammation breaks down critical tight junction barriers at the epithelium, preventing effective gas exchange. Inflammation can be triggered in a variety of way. What is one of the most common?
    Lysis of bacteria, which leads to release of inflammatory debris
  5. Which type of infection should be treated with antibiotics, viral or bacterial?
  6. What are the two most common causes of Acute Rhinosinusitis?
    • Streptococcus pneumonia
    • Haemophilus influenza
  7. Are infections of the nasal passages most commonly caused by viruses or bacteria?
  8. Are infections of the pharynx most common caused by viruses or bacteria?
  9. What are two bacterial causes of concern in pharyngitis?
    • Streptococcus pyrogenes
    • Corynebacterium diptheriae
  10. Identify the pathogen:
    Gram + cocci
    Causes a fever, painful throat, and is sudden in onset
    Tonsillopharyngeal erythema, lymphadentitis, petechiae on palate
    Rheumatic Fever
    Adherence: M protein, Lipoteichoic acid, fibronectin binding protein
    Virulence Factors: Hyaluronic Acid Capsule, Hemolysin, Proteases
    Streptococcus pyrogenes
  11. What adherence factor in Streptococcus pyrogenes is implicated in Rheumatic Fever?
    M protein
  12. Identify the pathogen:
    Gram-positive, aerobic, toxin-producing rod shaped bacterium
    Causes sore throat, low-grade fever, membrane on tonsils or pharynx, neck swelling
    Low prevalence in US, but continues to be a prob world-wide
    Vaccine (DTaP)
    Corynebacterium diphtheriae
  13. What are the virulence factors associated with Corynebacterium diphtheriae?
    Diphtheria toxin (A-B toxin) blocks protein synthesis, vaccine target
  14. Corynebacterium diphtheriae causes illness when the organism colonizes the mucosal region of the oropharynx and releases diphtheria toxin. How does this kill cells?
    By ADP-ribosylation of elongation factor 2 to block protein synthesis. Immune cells respond to the cells killed by the toxin and form a pseudomembrane that blocks the airway.
  15. How is infection of Corynebacterium diphtheriae treated?
    • Erythromycin
    • Antitoxin
  16. Disease caused by Corynebacterium diphtheriae progresses when diphtheria toxin is released into the bloodstream. What does this cause?
    Myocarditis and Cranial Nerve Damage
  17. What is the major cause of Epiglottitis?
    Haemophilus influenza
  18. What are the two most common causes of bronchitis?
    • Mycoplasma pneumonia
    • Chlamydophila pneumonia
  19. What is the most common infection of the trachea?
    Bordetella pertussis
  20. Identify the pathogen:
    Gram-negative, encapsulated, pleomorphic, fastidious rod, requires heme (Factor X) and NAD (Factor V) for growth
    Mulitple serotypes, type B is most common
    Epiglottitis and pneumonia
    Virulence Factors: polysaccharide capsule, outer membrane protein OMP, Lipooligosaccharide LOS (endotoxin-like), IgA protease
    Prevention: vaccine
    Haemophilus influenza
  21. Haemophilus influenza is normal flora for the human nasopharynx, but appears to colonize humans exclusively. It is highly inflammatory and can trigger a strong, damaging inflammatory response. Growth and detection can be difficult due to the fastidious nature of the organism. A classic hallmark of H. influenza is its requirement for growth media supplemented with _______ and ________?
    Heme and NAD
  22. Haemophilus influenza causes epiglottitis and pneumonia. What are two other diseases, unrelated to the respiratory tract, that this pathogen causes?
    Otitis media and Meningitis
  23. Identify the pathogen:
    Gram-negative, encapsulated, aerobic, fastidious, coccobacillus
    HIGHLY contagious, humans are the only known host
    Colonizes trachea and produces multiple toxins
    Four stages with different manifestations
    Outbreaks every 3-5 years, primarily in children less than 1 year in age
    Virulence Factors: Fimbriae, toxins (pertussis toxin, tracheal toxin, adenylate cyclase toxin)
    Bordetella pertussis
  24. What are the four stages of Bordetella pertussis?
    • Incubation: 7-10 days
    • Catarrhal: 7-14 days, symptoms of common cold
    • Paroxysmal: 3-8 weeks, severe sustained cough
    • Convalescent: 3-12 months
  25. Why is Bordetella pertussis tricky to diagnose and treat?
    • Initial stages of disease can be confused with common cold, but this is when antibiotics would be most effective.
    • The paroxysmal stage can progress in the absense of the organism, thus antibiotic treatment at this point may not be effective.
    • Disease even after the organism is gone is due to the potent toxins released by the organism and the severe tissue damage and inflammation
  26. During the most severe stage of the disease in Bordetella pertussis, the paroxysmal stage, patients can experience coughs so severe that what can result?
    • Severe hemorrhages around the eyes
    • Brain damage
  27. What are the two virulence factors associated with Bordetella pertussis?
    • Adherence pili (fimbriae hemagglutinin)
    • Antiphagocytic capsule
  28. What 3 toxins are associated with Bordetella pertussis?
    • Pertussis toxin -- ADP-ribosyltransferase, which blocks an inhibitor of an adenyl cyclase causing an increase in levels of cAMP. Inhibits phagocytic activity
    • Tracheal Cytotoxin
    • Adenylate Cyclase Toxin -- impairs leukocyte chemotaxis, inhibits phagocytosis
  29. What disease should be considered in children and adults with coughs lasting greater than 6 days?
  30. What is the Gold Standard Test for diagnosing Bordetella pertussis?
    • Culture from nasopharyngeal aspirates on Regan-Lowe medium or Bordet-Gengou
    • Must be performed in the Catarrhal
    • Recommended within the first 3 weeks
  31. What does the CDC recommend for diagnosis of Bordetella pertussis?
    • Culture and PCR during first four weeks of symptoms
    • PCR and serology for coughs 3-4 weeks
    • Serology for cough > 4 weeks
  32. What are the treatment options for Bordetella pertussis?
    • Erythromycin
    • Azithromycin
    • Clarithromycin
    • Most effective during first week; recommended within first 4 weeks
  33. Which form of vaccine is used for children as the initial vaccine and booster for pertussis? What is used in older children and adults as boosters?
    • DTaP -- diphtheria, tetanus, acellular pertussis
    • Tdap
  34. What are the two most common types of pneumonia seen in children aged 0-1 month?
    • Escherichia coli
    • Group B Strep (Streptococcus agalactiae)
  35. What are the two most common types of pneumonia seen in children aged 1-6 months?
    • Chlamydia trachomatis
    • Respiratory Syncytial Virus (RSV)
  36. What are the two most common types of pneumonia seen in children aged 6 months to 5 years?
    • Respiratory Syncytial Virus (RSV)
    • Influenza Virus Type A
  37. What are the two most common types of pneumonia seen in people aged 16-30 years?
    • M. pneumonia
    • Streptococcus pneumonia
  38. What are the two most common types of pneumonia seen in older adults?
    • S. pneumonia
    • H. influenza
  39. Identify the pathogen:
    Gram-positive, catalase-negative, Optochin sensitive, alpha-hemolytic, encapsulated diplococci
    Pneumonia with rapid onset and blood sputum
    Most prevalent cause of death due to acute infection in US, 6th leading cause of disease in the US
    Polysaccharide capsule is a major part of virulence and the target of current vaccines
    Streptococcus pneumonia
  40. Streptococus pneumonia is a serious healthcare problem in hospitalized elderly patients. What are the 3 characteristics that are used to differentiate this from other gram-positive cocci?
    • Optochin sensitivity
    • Catalase-negative
    • Alpha-hemolysis
  41. Identify the pathogen:
    Abrupt onset of fever and chills
    Productive blood sputum
    Can follow recent viral infections
    Primarily targets children
    6th leading cause of disease in US
    Cause of about 6 million cases of otitis media
    Most prevalent cause of death due to acute infection in the US
    Streptococcus pneumonia
  42. Streptococcus pneumonia has an antiphagocytic capsule. What does it prevent?
    C3b opsonization
  43. What protease is associated with Streptococcus pneumonia? What toxin is responsible for disrupting the alveolar-capillary boundary?
    • IgA protease
    • PLY pore-forming toxin
  44. What 3 cell components are associated with Streptococcus pneumonia?
    • PspA, anti-complement
    • CbpA, cell adhesion
    • LytA, autolysin
  45. What pathogen is the following pathogenesis associated with?
    Following colonization at site of disease:
    -- Capsule prevents phagocytosis
    -- PspA blocks complement
    -- IgA protease destroys IgA
    -- CpbA adheres to cells
    -- Ply disrupts barriers
    -- Autolysin lysis the organism (release debri causes massive inflammatory response)
    Streptococcus Pneumonia
  46. What two vaccines are available for streptococcus pneumonia?
    • Prevnar, 7-11 valent pneumococcal conjugate vaccine: given to children <2 and kids 2-5 with increased risk
    • Pneumovax, 23 Valent Vaccine: individuals >50, children >2 with predisposing conditions
  47. What are the treatment options for streptococcus pneumonia?
    • Cefotaxime
    • Ceftiaxone
    • Clindamycin
    • (about 1/3 of isolates in US are now resistant to penicillin)
  48. Identify the pathogen:
    Gram-negative, fastidious, aerobic, facultative intracellular pathogen
    Legionnaire's disease and atypical walking pneumonia
    High mortality rate, few reported cases in the US
    Virulence Factors: phospholipase, macrophage infectivity protein, and endotoxin
    Pathogenesis-growth to very high numbers in macrophages and stimulation of inflammatory responses
    Detection: direct observation of the organism in sputum, antibody reactivity, urine test for circulating antigen
    Legionella pneumophila
  49. What disease is unusual in combining pneumonia with several other systemic complications including altered liver and renal function along with heightened serum creatinine phosphokinase?
    Legionnaire's Disease
  50. How is Legionnella pneumophila transmitted?
    Aerosolization or aspiration of contaminated water
  51. Identify the pathogen:
    Gram-negative, aerobic rod with large polysaccharide capsule
    Normal flora of upper respiratory tract, enteric and genitourinary tracts
    Pneumonia observed in alcoholics following aspiration of this pathogen into lungs
    Signs and symptoms include sudden onset, high fever, hemoptysis (currant jelly sputum)
    <1% of cases require hospitalization
    Klebsiella pneumoniae
  52. How is Klebsiella pneumonia generally detected? How can it be prevented? What is the treatment for this pathogen?
    • PCR-based tests
    • Proper sanitation for nosocomial infections
    • Third generation cephalosporins and fluoroquinolones
  53. Identify the pathogen:
    Smallest bacterial genome
    No peptidoglycan cell wall
    Membrane contains cholesterol like eukaryotes
    Normal inhabitants of respiratory tracts
    Similar in size to some viruses
    Primary cause of walking or "atypical" pneumonia
    Usually mild
    Upper respiratory tract infection with fever, cough, malaise, and headache
    May lead to tracheobronchitis with fever and nonproductive cough
    Rare extrapulmonary syndromes, including cardiologic, neurologic, and dermatologic findings
    Impacts infants and immunocompromised patients
    Occurs most frequently among people who are in close quarters
    Mycoplasma pneumonia
  54. The virulence factor associated with Mycoplasma pneumonia is an adhesion protein that inhibits ciliary action. It produces hydrogen peroxide and cytolytic enzymes, and triggers a strong proinflammatory response. What is this adhesion protein called?
  55. _______ __________ with respiratory illness is commonly associated with Mycoplasma pneumonia infection.
    Cold agglutination
  56. How is infection with Mycoplasma pneumonia treated?
    • Erythromycin
    • Azithromycin
    • Clarithromycin
    • (has no peptidoglycan cell wall, so beta-lactam and similar antibiotics will not affect this organism)
  57. Identify the pathogen:
    Aerobic, acid-fast rods, with high membrane lipid content
    Grow very slowly
    Resistant to intracellular killing by phagocytes
  58. What are the two respiratory pathogens included in Mycobacteria?
    • Mycobacterium avium
    • Mycobacterium tuberculosis
  59. Identify the pathogen:
    Acid-fast, aerobic, slow growing, facultative intracellular bacilli, with a unique cell wall -- contains mycolic acid and arabinogalactan in addition to peptidoglycan.
    This cell wall allows this pathogen to survive inside macrophages, and makes it impervious to many different antibiotics.
    85% of cases are pulmonary, with a slow onset and chronic course.
    It originates in the lungs and moves to other regions of the body
    This is the most common infectious cause of mortality worldwide
    One-third of world's population is infected
    Mycobacterium tuberculosis
  60. What are the two unique features of the cell of wall of Mycobacterium tuberculosis?
    Contains mycolic acid and arabinogalactan in addition to peptidoglycan
  61. Mycobacterium tuberculosis does not produce toxins, so the virulence of this organism is largely determined by its survival in the presence of immune responses and intracellular environment. What is the major virulence factor of M. tuberculosis? What are the other two?
    • Cord Factor (trehalose dimycolate, cell wall component): inhibits neutrophil chemotaxis; potent immunological adjuvant; helps prevent lysosomal killing of the organism following engulfment by macrophages
    • Sulfatides: inhibits phagosome-lysosome fusion in macrophages, allows intracellular survival
    • Tuberculin: stimulates cell-mediated immunity promoting granuloma formation
  62. Identify the pathogen:
    Collection of activated macrophages surrounding an area of necrosis (caseous necrosis)
    CD4+ T-cells, produce cytokines
    Mycobacterial antigens persistently activate T-cells in the granuloma
    Chronic inflammation and type IV hypersensitivity
    Tuberculosis Granuloma
  63. What is the most definitive test for detection of Tuberculosis Granuloma?
    Growth on Lowenstein-Jensen Agar (2-4 weeks)
  64. Which type of viral respiratory infection, upper or lower, is associated with a higher morbidity and mortality?
    Lower Respiratory Infections
  65. What are the two most common causes of the common cold in infants and children? In adults?
    • Rhino/Adeno
    • Rhino/Corona
  66. What are the two most common causes of pharyngitis in infants <1 yr? In children and adults?
    • Adeno/HSV
    • Adeno/Coxsackie
  67. What are the two most common causes of laryngitis?
    Parainfluenza and Influenza
  68. What are the two most common causes of LTB/croup in infants and children? In adults?
    • Parainfluenza/Influenza
    • Influenza/Adeno
  69. What are the two most common causes of Bronchiolitis in infants less than 1 year? (rare in children and adults)
  70. What are the two most common causes of pneumonia in infants less than 1 year? In children? In adults?
    • RSV/Influenza
    • Influenza/Parainfluenza
    • Influenza/Adeno
  71. What type of virus is the influenza virus?
    • Orthomyxovirus
    • (-) RNA virus
  72. Which influenza serotype causes the most severe disease (causes pandemics)? It undergoes antigenic shift.
    Type A
  73. Differences within the type A class of influenza virus are determined by what two things?
    Hemagglutinin (HA) and Neuroaminidase (NA)
  74. In the influenza virus structure, what external protein is the object by which the virus attaches to cells? Antibodies to this neutralize the virus. It attaches to cell sialoglycoproteins and sialoglycolipids. It is the primary target of vaccines. Contains a peptide sequence with fusion activity.
  75. In the influenza virus structure, what is the enzyme that cleaves sialic acid, enhances release, and prevents clustering of the virus or binding by mucous (contains SA)?
  76. In the influenza virus, there are two matrix proteins inside of the envelope. _____ is important in virus assembly. _____ is an ion channel protein involved in controlling internal pH
    • M1
    • M2
  77. There are two non-structural proteins in the influenza virus. First is _______, which is produced in cells only, and interferes with cellular antiviral response. Second is ______ -- present in small amounts and functions in transport of viral nucleoproteins, and regulation of viral RNA synthesis.
    • NS1
    • NS2
  78. What does the influenza virus require for replication?
    A viral polymerase carried in the virion
  79. Identify the virus from the clinical presentation:
    Typical infection begins with fever, headache, myalgia and malaise, cough and sore throat. Usually improves over 2-5 days, may last for a week or more. May have weakness, fatigability.
    Can also result in Reye's Syndrome (liver failure) with increased risk with ASA use -- so aspirin should not be used in childen with this
    Influenza Virus
  80. Antigenic shift is limited to influenza virus serotype _____ only.
  81. What involves point mutations in HA; NA can alter the virus enough that a person's AB from a previous infection may not completely protect them, but results in milder disease. These changes can be in the A or B serotypes.
    Antigenic Drift
  82. Does Antigenic Shift involve point mutations in HA, NA, or both?
  83. Does antigenic shift involve changes in the HA, NA or both?
  84. Which can cause full-scale pandemics, antigenic drift or antigenic shift?
    Antigenic Shift
  85. What is the main type of influenza vaccine?
    Trivalent Inactivated Vaccine (TIV)
  86. What two drugs were previously used to treat active influenza A, but are not used anymore due to resistance? What two drugs work somewhat for both serotypes A and B and are sometimes used?
    • Rimantidine & Amantadine
    • Oseltamavir & Zanamavir (Neuraminidase Inhibitors)
  87. What type of agents are indicated as prophylaxis in high risk patients who cannot take the influenza vaccine?
    Neuraminidase Inhibitors (Oseltamavir & Zanamavir)
  88. In what patients is Zanamavir (a neuraminidase inhibitor to treat influenza) contraindicated for?
    COPD and asthma, because can cause decrease in FEV1
  89. Parainfluenza virus 1-4, respiratory syncytial virus, measles, and mumps viruses are all what type of viruses?
  90. Respiratory Syncytial Virus (RSV) is an exception to the structure within the paramyxovirus group. What is the main difference?
    The hemagglutinin/neuroaminidase is replaced by a G surface glycoprotein
  91. Southeast US; symptoms include malaise, weight loss, night sweats, chest pain, hoarseness, fever; bilateral rales; rhonchi; raised verrucous, crusted lesions; multiple nodular lesions; thick-walled, refractile broad-based budding yeast cell; white fluffy fungus; necrosis and cavitation; dimorphic; inhalation; 4-6 week innoculation period; indolent pulmonary inf; opportunistic; can disseminate; KOH preps, culture, serology
    Blastomyces dermatitidis
  92. Smoker; Central/SA; asymptomatic; CXR = cavitary lesion; S. American blastomycosis; forest workers -- males more bc more male lumberjacks; has receptors for estrogen; dimorphic; inhalation; yeast; chonic granulomatous disease; primary inf is pulmonary, reactivates yrs later, disseminates to buccal, nasal, GI mucosa; mariner's wheel; KOH prep/sputum stain.
    Paracoccidiodes brasiliensis
  93. Type I diabetes; ketoacidosis; periorbital swelling; mucopurulent postnasal discharge; black ulceration of nasal mucosa; 3rd CN palsy; no improvement w antibiotics; rapidly growing fungus with wide, irregular nonseptate hyphae branching at wide angles; rhizopus spp. and mucor spp., uncontrolled diabetics and leukemics; monomorphic; loves blood vessels; rhinocerebral zygomycosis; destruction of lung parenchyma; grows very rapidly; black fungus in mouth; CT of paranasal sinuses, detect microscopy, biopsy; Ampho B and debridement; high MORTALITY
  94. Leukemic on cytotoxic therapy; chest pain, fever, chills, hemoptosis, resp. distress; bilateral rales; ANC; fungus with septate, acutely branching hyphae; vascular thrombi due to hyphal invasion of blood vessels; catalase +; chronic granulomatous disease and neutropenia; necrotizing pneumonia and aspergilloma (fungus ball); direct microscopy, biopsy; monomorphic; dichotomously branching hyphae
    Aspergillus fumigatos
  95. Trouble breathing, fever, chills, wheezing, productive cough with black sputum; eosinophilia; low O2 sat; IgE antibodies against Aspergillus; CXR shows infiltrates in upper lobes with branching, finger-like shadows.
    Allergic Bronchopulmonary Aspergillosus (ABPA)
  96. Actinomyces (anaerobic); Nocardia (aerobic); gram-+, non-AF; slow-growing filamentous, branched rods; commensals; produce granules.
  97. Dental procedure; painless mass on mandible draining pus and yellowish granules; branching, gram + rods; actinomyces israelli; must have pre-disposing factor: dental procedure or oromaxillofacial trauma; submandibular jaws; suppuration with draining abscess; grains or "sulfur granules" in tissues; rx = penicillin, + oral penicillin or amoxicillin
    Cervicofacial actinomycosis
  98. Chronic asthma; high dose steroids; productive cough, weight loss, night sweats; abscesses in lungs and brain; gram + filaments that are weakly acid fast; bilateral nodular opacities; GMS stain; opportunistic; ubiquitous saprophytes; local traumatic innoculation or inhalation; CMI-deficient at risk; cutaneous cellulitis/ mycetoma; pneumonia; disseminated -- deep abscesses and necrosis CNS; urease; rx = antibiotics TMP-SMX
    Nocardia asteroides
  99. What is the most common etiology for Pericarditis?
    Viral -- enteroviruses (fecal-oral to bloodstream): coxsackie A/B, echovirus
  100. How are enteroviruses spread?
    Fecal-oral to bloodstream
  101. What is purulent spread? What are two examples that are spread this way?
    • Bloodstream or lungs
    • Staph/Strep
  102. What is are two chronic pathogens implicated in pericarditis?
  103. How do cardiotropic viruses spread to the heart?
    Via the bloodstream
  104. Do enteroviruses cause massive diarrhea?
  105. Fatigue; progressive dyspnea 6 weeks after episode of massive diarrhea; bilateral pleural effusion; extensive pericardial effusion; acute inflammation confined to visceral and parietal pericardial layers; Latin America; small mammal reservoirs; transmission -- bite of the "kissing bug" or "assassin bug"; Triatoma, Rhodnius, or Panstrongylus; most people can clear this easily, but becomes chronic for some -- myocarditis is presenting symptom; incubation period of 4 days to 2 wks; localized infection -- initial lesion is a nodule with facial edema (chagoma or chancre); systemic infection via lymphatics or bloodstream; fever, lymphadenopathy, hepatosplenomegaly, myocarditis, megacolon, megaesophagus, denervation and loss of tone in GI tract; Ramana's sign; Trypomastigote stage in thick or thin blood smears; amastigote in BM aspirates/ muscle biopsies; PCR/serology; rx = benzidazole or nifurtimox
    • Trypanosoma cruzi myocarditis
    • (chagas' disease or American trypanosomiasis)
  106. What are the two types of infective endocarditis?
    • Acute
    • Subacute
  107. What agents are responsible for the acute form of endocarditis?
    • S. aureus
    • Group A/B strep
    • Gram-negative rods
  108. What agents are responsible for the subacute form of endocarditis (native-valve)?
    • Oral streptococci
    • Enterococci
    • S. aureus
    • HACEK
  109. What agents are responsible for the subacute form of endocarditis (prosthetic valve)?
    • S. epidermidis
    • S. aureus
    • Oral streptococci
  110. How do we differentiate between S. epidermidis and S. aureus?
    S. epidermidis is coagulase negative
  111. How do we differentiate between staph and strep?
    Staph is catalase positive; strep is catalase negative
  112. Streptococci are initially classified based on hemolysis. which two are beta-hemolytic? How do we differentiate between these two?
    • Strep A and B
    • A: pyogenes -- bacitracin sensitive
    • B: agalactiae -- bacitracin resistant
  113. Streptococci are initially classified based on hemolysis. Which agent is gama-hemolytic?
  114. Streptococci are initially classified based on hemolysis. Which two are alpha-hemolytic? How are these differentiated?
    • Strep pneumonia: optochin sensitive, bile soluble, capsule
    • Strep viridans: mutans, sanguis, optochin resistant, no bile soluble, no capsule
  115. What type of strep are alpha-hemolytic, normal flora in oral cavity, and are responsible for dental carries?
    Oral or virdans streptococci
  116. What organisms are classified as viridans streptococci?
    • S. mitis
    • S. milleri
    • S. salivarius
    • S. sanguinis
    • S. mutans
  117. What type of strep is classified as alpha/gamma hemolytic, normal flora of large intestine, causes UTI, sepsis, and nosocomial infections. Can hydrolize esculin/grow in 6.5% NaCl and 40% bile salts
    Enterococci or Group D strep
  118. What organisms are classified as Enterococci or group D strep?
    • E. faecalis
    • E. faecium
    • E. durans
  119. Which type of endocarditis, acute or subacute, has an abrupt onset of high-grade fevers, chills, and rapid heart rate? There is rapid destruction of the infected valve. Look for a history of antecedent procedures or illicit drugs; can be rapidly fatal.
  120. Which type of endocarditis, acute or subacute, has symptoms that may be subtle and non-specific, including a low-grade fever, anorexia, weight loss, flu-like symtpoms, and anemia. Rarely causes metastatic infections. Symptoms may persist for weeks.
  121. Identify the syndrome:
    New/worsened regurgitant murmur
    Cardiac complications
    Arterial emboli
    Neurological manifestations
    Pulmonary symptoms
    Subconjunctival hemorrhage
    Janeway lesions
    Osler's nodes
Card Set
CRR Pathogens
CRR Pathogens
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