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DRx Infectious Disease > Infectious Disease ALL > Flashcards

Infectious Disease ALL Flashcards

1
Q

What are the top 6 infectious diseases that causes 90% of deaths worldwide due to infection?

A

Respiratory infection (pneumonia), diarrhea, malaria, HIV/AIDS, tuberculosis, meningitis

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2
Q

Reasons for decrease in infectious disease death

A

Improved hygiene, vaccinations, antibiotics

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3
Q

Name new challenges for infectious disease

A

Emerging and re-emerging infectious disease
Increased elderly population, increased immunocompromised individuals
Hospital/invasive procedures and devices
Food outside of home
Antibiotic resistance, virulent strains, new strains resistant to vaccines

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4
Q

Exogenous sources of microorganisms

A

Other people, animals, contaminated food or water, fomites

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5
Q

Endogenous sources of microorganisms

A

One’s own normal flora

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6
Q

Modes of transmission from exogenous sources

A

Direct transmission from another person
Indirect transmission from non-human sources
Vertical transmission (mother to fetus)
Healthcare associated infections

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7
Q

Endogenous Infection Causes

A

Release of bacteria from normal compartments
Invasion of inappropriate sites by opportunistic pathogens
Overgrowth of opportunistic pathogens
Introduction of opportunistic pathogens to deeper tissue

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8
Q

Koch’s Postulates

A

To prove a particular microorganism is cause, must:

  • Be found in body in all causes of disease
  • Be isolated from a case of disease and grown in a series of pure cultures in vitro
  • Reproduce the disease when a pure culture is inoculated into a susceptible animal
  • Be recovered from the inoculated animal
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9
Q

Relative sizes of microorganisms (large to small)

A

Some protozoa > RBC > some protozoa > yeast > bacteria > mycoplasma > viruses

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10
Q

Common systemic clinical signs of infection

A

Fever, chills, myalgia, fatigue, loss of appetite

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11
Q

Common localized signs of infection

A

pain, swelling, redness, warmth (abscess, cellulitis), symptoms in specific organ systems

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12
Q

CBC in infection

A

Leukocytosis: WBC > 11,000 or leukopenia: WBC < 4,000 in severe infection

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13
Q

2 main approaches to diagnostic microbiology

A

Bacteriologic (staining/culture)

Immunologic (serologic): detection of antibodies in blood

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14
Q

Presumptive identification

A

Staining/observing organism by microscopy

Obtaining pure culture of organism by inoculating onto a bacteriologic medium

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15
Q

Definitive identification

A

Sugar fermentation, molecular tests, antibody based tests

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16
Q

General approach to identify bacteria

A 
Obtain specimen
Stain using appropriate protocol
Culture on to appropriate media
Definitively ID using appropriate tests
Perform antibody susceptibility tests
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17
Q

What does a IgM in acute serum indicate?

A

Ongoing infection

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18
Q

What does a 4-fold or more increase in titer between acute and convalescent sample indicate?

A

Current infection

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19
Q

Blood culture

A

Performed when sepsis, endocarditis, meningitis, pneumonia suspected

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20
Q

Throat culture

A

Performed when patient presents with pharyngitis or upper respiratory tract infection

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21
Q

Sputum culture

A

Performed when tuberculosis or pneumonia suspected

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22
Q

Spinal fluid culture

A

Performed when meningitis suspected

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23
Q

Stool culture

A

Performed when gastroenteritis suspected

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24
Q

Urine culture

A

Performed when UTI suspected

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25
Q

Genital tract culture

A

Performed when STD suspected

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26
Q

Wound and abscess culture

A

Many organisms

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27
Q

Properties of staphylococcus

A 
Gram-positive cocci
Capsule, slim layer, techioic acid
Catalase positive
Skin and mucous membranes
Most facultative anaerobes
S. aureus is coag-positive, others coag-negative
Most produce beta-lactamase
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28
Q

Where does S. aureus colonize?

A

Skin, mucosal membranes, anterior nares

Resident or transient

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29
Q

What is the hallmark of a S. aureus infection?

A

Abscess

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30
Q

Virulence factors in cell wall of S. aureus

A

Protein A
Techioic acid
Polysaccharide capsule

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31
Q

Exotoxins of S. aureus

A

Enterotoxin –> food poisoning
Toxic shock syndrome toxin (TSST) –> toxic shock syndrome
Exfoliative toxins (ETA and ETB) –> scalded skin syndrome

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32
Q

Enzymes produced by S. aureus

A

Coagulase

Fibrinolysin

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33
Q

Suppurative diseases caused by S. aureus

A

Impetigo, furuncles, carbuncles, cellulitis, folliculitis, conjunctivitis, blepharitis, keratitis, mastitis
Endocarditis
Osteomyelitis, arthritis
Post surgical wound infections
Pneumonia in post-operative patients or following viral respiratory infections
Abscess

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34
Q

Lab diagnosis of S. aureus

A

Gram positive cocci in clusters
Golden yellow, beta hemolytic
Catalase positive, coagulase positive
Ferments mannitol

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35
Q

Treatment of S. aureus

A

30-50% resistant to penicillin

Nafcillin, oxacillin, vancomycin (MRSA)

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36
Q

Risk factors for S. epidermididis

A

IV catheters, PROSTHETIC IMPLANTS, vascular grafts

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37
Q

Clinical findings of S. epidermididis

A 
Joint infection
Prosthetic implant infection (biofilm)
IV catheters
Endocarditis
Neonatal sepsis
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38
Q

Lab diagosis of S. epidermididis

A

Catalase positive
White, non-hemolytic
Coagulase NEGATIVE
Sensitive to novobiocin

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39
Q

Treatment of S. epidermididis

A

Vancomycin, removal of infected devices

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40
Q

Where is S. saprophyticus found?

A

Genitourinary tract

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41
Q

What is the main clinical finding of S. saprophyticus?

A

UTI, second leading cause in sexually active females

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42
Q

Lab findings for S. saprophyticus

A

Gram postive cocci
White, non-hemolytic
Catalase positive, coagulase negative
Resistant to novobiocin

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43
Q

How is S. saprophyticus treated?

A

Trimethoprim-sulfamethoxazole

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44
Q

Name some common properties of streptococcus

A

Gram-positive cocci in pairs or chains
Catalase NEGATIVE
Most facultative anaerobes

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45
Q

Where does S. pyogenes (Group A strep) inhabit?

A

Throat, transient on skin

Transmitted by respiratory droplets

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46
Q

Structural virulence factors of S. pyogenes?

A

M protein***
Techioic acid
Hyaluronic CAPSULE

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47
Q

Virulence enzymes of S. pyogenes?

A

Hyaluronidase
Streptokinase A and B
DNases
C5a peptidase

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48
Q

Toxins and hemolysis of S. pyogenes?

A 
Erythrogenic toxins --> streptococcal toxic shock syndrome
Streptolysin O (oxygen labile)
Streptolysin S (oxygen stabile)
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49
Q

Suppurative diseases caused by S. pyogenes

A 
Pharyngitis
Scarlet Fever
Skin infection
Necrotizing fasciitis
Streptococcal toxic shock syndrome
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50
Q

Non-suppurative diseases causes by S. pyogenes

A

Acute glomerulonephritis

Acute rheumatic fever

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51
Q

Lab diagnosis of S. pyogenes

A

Rapid immunologic tests (throat swab)
Translucent beta-hemolytic
Bacitracin sensitive

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52
Q

Treatment of S. pyogenes

A

Penicillin

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53
Q

Where does S. agalactiae colonize? Who does it affect?

A

Lower GI tract and genital tract of some women

Affects babies, can be transmitted during birth

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54
Q

What is the main virulence factor in S. agalactiae?

A

Capsule

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55
Q

What does S. agalactiae cause?

A

Leading cause of neonatal sepsis and meningitis, pneumonia

Can cause pneumonia, endocarditis, arthritis and osteomyelitis in adults

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56
Q

Lab diagnosis of S. agalactiae

A

Translucent, beta hemolytic
Bacitracin resistant!
Hydrolyzes sodium hippurate and positive CAMP test

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57
Q

How is S. agalactiae treated?

A

Penicillin

Pregnant women should be screened!

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58
Q

Where is S. pneumoniae found?

A

Oro and nasopharynx

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59
Q

What types of S. pneumoniae are virulent?

A

Encapsulated

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60
Q

Virulence factors of S. pneumoniae

A

IgA protease
Pneumolysin
Techioic acid/peptidoglycan
phosphocoline

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61
Q

What is the main clinical finding for S. pneumoniae?

A

Community acquired pneumonia

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62
Q

Other clinical findings in S. pneumonia

A 
Meningitis
Otitis media
Sinusitis
Conjunctivitis
Keratitis
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63
Q

Lab diagnosis of S. pneumoniae

A

Gram positive diplococci
Alpha-hemolytic
Bile solube, optochin sensitive
Urinary antigen tests

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64
Q

Vaccine for S. pneumoniae

A 
23 valent (adults over 65 and children)
13 valent (children under 2)
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65
Q

What does viridans streptococci cause?

A

Endocarditis
Dental caries
Brain abscesses

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66
Q

Lab diagnosis for Viridans streptococi

A

Alpha-hemolytic

Bile insoluble and optochin resistant

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67
Q

Where is enterococcus normally found?

A

Colon, urethra, female gentical tract

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68
Q

What does Enterococcus faecalis most commonly cause?

A

UTI, endocarditis, wound infection

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69
Q

Lab diagnosis of enterococcus?

A

Gram positive cocci

Grows in NaCL

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70
Q

Treatment for enterococcus

A

MANY antibiotic resistant, including to vancomycin

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71
Q

Common structures of Neisseria

A 
Gram-negative diplococci
Aerobic, grow best at 35-37
Oxidase and catalase positive
Cell surface molecules -- pili, antigenic variation, LOS and release blebs, lacks repeating O-antigen
Porin variations
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72
Q

Properties of N. meningitidis

A

Utilizes maltose and glucose
CAPSULE
Classified by serotypes determined by antigenic variations of polysaccharide capsule
No opacity proteins

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73
Q

N. gonorrhoeae

A

Utilizes only glucose
No capsule
Several strains, including clinical isolates and lab strains
Opacity proteins on outer membrane

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74
Q

How is N. gonorrhoeae trasmitted

A

Sexual contact

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75
Q

N. gonorrhoeae virulence

A

Pili, OPa proteins, porins, LOS, IgA protease, B-lactamase
LOS stimulate release of TNF-alpha and influx of cytokins
Antibodies not protective

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76
Q

Clinical findings of N. gonorrhoeae

A

Infect mucosal sites = genital tract, rectum, conjunctiva, oropharynx
Men = acute urethritis, purulent discharge
Women = normally asymptomatic, leads to PID
Infection of conjunctiva of newborns
Rarely disseminates

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77
Q

Lab diagnosis N. gonorrhoeae

A

Gram strain of urethral specimens for men only

Chocolate agar used

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78
Q

Treatment for N. gonorrhoeae

A

Ceftriaxone (+ aziothromycin to cotreat chlamydia)

No vaccine

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79
Q

How is N. meningitidis transmitted?

A

Respiratory droplets (kissing, inhaling, sharing cup); close contact

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80
Q

Pathogenesis of N. meningitidis

A

Colonization of nasopharynx required for systemic infection
Internalized into phagocytic vesicles and replicates intracellularly
LOS endotoxin
Antibodies only type specific
CAPSULE, IgA protease

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81
Q

Clinical findings of N. meningitidis

A

Leading cause of bacterial meningitis
Sudden fever, nausea, vomiting, headache, loss of ability to concentrate, myalgias
Thrombosis of small vessels, petechial skin lesions, DIC, septic shock

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82
Q

Lab diagnosis of N. meningitidis

A

Detect organism in sterile fluid (CSF)
Gram stain, culture needed
Fragile, fastidious

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83
Q

Treatment and Prevention

A

Penicillin, cephalosporin until definitive results received
PROMPT treatment
Prophlyaxis for those with close contact
Vaccines available (conjugated to diphtheria toxoid)

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84
Q

Properties of Treponema Pallidum

A

Spirochaete
Neither gram positive or negative
Flagella between inner and outer membrane that runs lengthwise

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85
Q

How is Treponema pallidum transmitted?

A

Sexual contact of moist lesion of primary/secondary lesion
Transplacental
Blood contact (need large inocolum)

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86
Q

Clinical manifestations of primary syphilis

A

Emerges 10-90 days, symptoms resolve in 2-8 weeks
Chancre = painless, induced, solitary lesion at site of inoculation
Hard, mobile regional lymphadenopathy bilaterally

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87
Q

Clinical manifestations of secondary syphilis

A

Emerges 6 weeks to several months, may resolve in 2-10 weeks
Lymphatic/hematogenous dissemination
RASH (includes palm/soles), lymphadenopathy, condylomata lata, patchy alopecia, hepatitis, meningitis

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88
Q

Clinical manifestations of tertiary syphilis

A

Late benign syphilis: gumma (skin/bones)
Cardiovascular syphilis: aortitis, vaso vasorum
Neurosyphilis: presents as meningitis; paresis, tabes dorsalis, Argyll Robertson pupil (does not constrict to light)

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89
Q

Clinical Syphilis clinical findings

A

Rhinitis, skin eruptions, hepatosplenomegaly, pseudoparlysis, lymphadenopathy, anemia
Dental abnormalities, deafness, eye damage

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90
Q

Diagnosis of Treponema pallidum

A

Non-treponemal (VDRL, RPR) = reported as titer, must be followed, reliable indicator of untreated infection
Treponemal tests = Detect antibodies, confirmatory test, not a titer (positive vs. negative); once positive ALWAYS positive

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91
Q

Treatment of Treponema pallidum

A

Penicillin

Pregnant women with penicillin allergy should be desensitized and then treated with penicillin

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92
Q

Jarisch-Herxheimer Reaction

A

Acute febrile reaction due to dying spirochetes releasing LOS

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93
Q

What is significant for response to treatment of Treponema pallidum?

A

Fourfold decrease in titer (2 dilutions)

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94
Q

Properties of Chancroid

A

Gram-negative
Facultative anaerobic coccobacillus
Agglutination properties and clumping (school of fish)

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95
Q

Transmission and clinical manifestations of Chancroid

A 
Transmitted via sexual contact
3-10 day incubation period
Soft chance = ragged, non-indurated, sharply demarcated ulcer with necrotic, friable base
PAINFUL in men
Some get painful inguinal lymphadenitis
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96
Q

Diagnosis of Chancroid

A

History and physical exam

Gram stain suggestive

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97
Q

Treatment of Chancroid

A

Azithromycin

Ceftriaxone, ciprofloxacin, erythromycin

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98
Q

Important Properties of Chlamydia and Chlamydophila

A

Gram-negative like but cannot gram stain
Intracellular (obligate)
Cell wall, no peptidoglycan
Biphasic life cycle = elementary body (infectious) into reticulate bodies (replicative)

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99
Q

Chlamydia trachomatis epidemiology and transmission

A 
Infects ONLY humans
Sexual contact
Passage through birth canal
Eye infections
Most common bacterial STI
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100
Q

What toxins and virulence factors does Chlamydia trachomatis have?

A

NONE

Infection results in cytokine release

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101
Q

Clinical findings of Chlamydia trachomatis

A 
Trachoma
Men = 50% symptomatic, urethritis, epididymitis, proctitis
Women = asymptomatic, PID, cervicitis
Conjunctivitis
Reiter's Syndrome
Lymphogranuloma venereum
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102
Q

Lab diagnosis of Chlamydia trachomatis

A

No gram stain

NAATs

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103
Q

Treatment of Chlamydia trachomatis

A

Azithromycin

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104
Q

Transmission of Chlamydophila pneumoniae

A

Aerosol transmission person to person, no animal reservoir

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105
Q

Where does Chlamydophila pneumoniae infect

A

Epithelial cells of mucous membranes of lungs

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106
Q

Clinical findings of Chlamydophila pneumoniae

A

Atypical pneumonia
Upper/lower respiratory tract infection
Bronchitis, sinusitis, pharyngitis

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107
Q

Diagnosis of Chlamydophila pneumoniae

A

PCR nucleic-acid based tests

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108
Q

Treatment of chlamydophila pneumoniae

A

Tetracyclines or macrolides
Hard to control transmission
No vaccine

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109
Q

Transmission of Chlamydophila psittaci

A

Transmitted to humans by close contact with birds via aerosolized dust

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110
Q

Pathogenesis of Chlamydophila psittaci

A

Infects epithelial cells and phagocytes in respiratory tract and can spread through body
Edema, thickening of alveolar wall, mucous plugs

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111
Q

Clinical findings of Chlamydophila psittaci

A

Varies
Parrot fever
Headache, high fever, chills, malaise, myalgia
Non-productive cough, rales, consolidation

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112
Q

Treatment of Chlamydophila psittaci

A

Tetracyclines

Limiting contact, barrier prevention

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113
Q

Properites of Legionella pneumophila

A 
Gram-negative
Pleomorphic rod
Does not stain well, grown on charcoal, yeast extract with iron and cysteine
Facultative intracellular parasite
Obligate aerobe
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114
Q

How does Legionella pneumophila replicate?

A

Binds alveolar macrophage in lung via pili and outer membrane proteins that facilitate endocytosis; fusion of phagosome inhibited; produces enzymes to kill macrophage

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115
Q

How is Legionella pneumophila transmitted

A

Inhalation of aerosolized organisms from water source, hospital acquired
Not usually person to person

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116
Q

Clinical findings of Legionella pneumophila

A

Community and hospital acquired pneumonia
Legionnaire’s Disease (severe pneumonia form)
Pontiac Fever (mild-influenza type illness)

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117
Q

Lab diagnosis of Legionella pneumophila

A

Isolation of culture from respiratory specimen

Charcoal with yeast, iron and cysteine

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118
Q

How is Legionnaire’’s and Pontiac Fever treated?

A

Levofloxacin, azithromycin

Supportive care

No vaccine

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119
Q

Properties of Mycoplasma pneumoniae

A 
Gram stain poorly
No cell wall
Sterols in cell membrane
Strict aerobic
Resistant to antibiotics that target cell wall synthesis
Replicate extracellularly
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120
Q

Epidemiology and transmission in Mycoplasma pneumoniae

A

Strict human pathogen
Colonizes throat, trachea, nose, lower airways
Transmitted by respiratory droplets during coughing to close contacts
High attack rate
Can carry asymptomatically

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121
Q

Pathogenesis of Mycoplasma pneumoniae

A

Attach to specific ciliated glycoprotein on surface of both respiratory epithelial cells and erythrocytes
Ciliastasis and destruction
Mucociliary clearance irritated

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122
Q

Clinical findings of mycoplasma pneumoniae

A

Incubation 2-3 weeks
Tracheobronchitis = low grade fever, malaise, headache, non-productive cough, pharyngitis
Walking or atypical pneumonia

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123
Q

Lag diagnosis of mycoplasma pneumoniae

A

No gram stain

Serology or PCR but not usually done

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124
Q

Treatment of Mycoplasma pneumoniae

A

Usually empiric for atypical pneumonia

No vaccine

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125
Q

Important properties of Bordatella pertussis

A

Small, gram-negative rod
Strictly aerobic
Slow growing (requires NAD), special media with charcoal, starch, horse blood

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126
Q

Epidemiology and transmission of Bordatella pertussis

A 
Highly contagious
Strict human pathogen
Colonized in nasopharynx
Adults source for infants
Transmitted by aerosolized respiratory droplets
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127
Q

Virulence factors for Bordatella pertussis

A 
Pertactin (PERT) and filamentous HA (FHA)
Fimbriae (FIM)
Pertussis toxin (PT)
Trachael cytotoxin
LPS
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128
Q

Clinical stages of Bordatella pertussis

A

Catarrhal stage (1-2 weeks post exposure)
Paroxysmal stage
Convalescent stage

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129
Q

Lab diagnosis of Bordatella pertussis

A

Clinical symptoms alone
Very sensitive to drying
Culture difficult
PCR with culture is best

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130
Q

Prevention of Bordatella pertussis

A

Acellular pertussis vaccine: PT, FHA and either pertactin and/or fimbriae
Pediatrics got shots and booster, adults get boosters every 10 years

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131
Q

Important properties of Corynebacterium diphtheriae

A

Gram positive, pleomorphic rods arranged in clumps/short chains
Metachromatic (red) granules with rod
Aerobic, non-motile, catalase-positive

132
Q

Transmission of Corynebacterium diphtheriae

A

Humans only known reservoir

Person to person contact with respiratory secretions or cutaneous lesions

133
Q

Clinical Findings of Corynebacterium diphtheriae

A

Only strains lysogenized by bacteriophage causing tox gene encoding exotoxin can produce the toxin

Respiratory diphtheria – get pseudomembrane, neck swelling
Cutaneous diphtheria – contact with skin and get papule that develops into a chronic, non-healing ulcer

134
Q

Lab diagnosis of Corynebacterium diphtheriae

A

Clinical presentation
Gram stain not definitive
Culture: Loeffler’s medium, tellurite agar plate, test for toxin

135
Q

Treatment and prevention of Corynebacterium diphtheriae

A

Empirical
Diphtheria toxin only if given early
Antibiotics to kill bacteria
Prevent by vaccine

136
Q

Properties of Haemophilus influenzae

A

Small, gram-negative rods, pleomorphic
Facultative anaerobes require Factor X and V
Encapsulated and non-encapsulated (non-typeable)

137
Q

Where is non-typeable H. influenzae located?

A

Colonize upper respiratory tract and spread disease locally = otitis media, sinusitis, bronchitis, pneumonia

138
Q

Transmission of encapsulated H. influenzae

A

Transmitted by direct contact with respiratory droplets
Hib is human pathogen only and invasive
Children at risk and those immunocompromised

139
Q

Lab diagnosis of H. influenzae

A

Gram stain sensitive and specific

Culture with chocolate agar, hemin, NAD; antigen detection Hib

140
Q

Treatment and Prevention of H. influenzae

A

Bete-lactams
Immunization (capsular polysaccharide conjugated to diphtheria toxoid carrier)
Prophylaxis with rifampin

141
Q

Listeria monocytogenes Properties

A

Gram positive coccobacilli/short rods in pairs or short chains
End over end tumbling
Facultative anaerobe
Facultative intracellular pathogen
Can grow at cold temperatures (fridge gand freezer)

142
Q

Epidemiology and transmission of Listeria monocytogenes

A

Ubiquitous in environment
Transient colonization
Contaminated food
Infected mother to fetus transplacentally or perinatally

143
Q

Pathogenesis of Listeria monocytogenes

A

Attach to receptors on enterocytes and M cells in Peyer’s Patches
Listeriolysin O is a pore-forming toxin

144
Q

Clinical findings Listeria monocytogenes

A

Healthy adults asymptomatic
Pregnant woman flu like illness, risk for meningitis, fetal death, premature birth
Neonatal : early onset, abscesses, granulomas, death

145
Q

Lab diagnosis of Listeria monocytogenes

A

Isolation from sterile site
Weakly beta-hemolytic
Specific biochemical and serological tests

146
Q

Treatment and prevention of Listeria monocytogenes

A

Ampicillin or penicillin
safe food handling and consumption
no vaccine

147
Q

Important properties and structures of Enterobacteriaceae

A 
Gram-negative rods
Facultative anaerobes
Most have flagella and are motile
Oxidase negative, ferment glucose, some lactose
Grow on MacConkey agar
148
Q

Enterobacteriaceae virulence factors

A 
Endotoxin (LPS)
O polysaccharide
Some capsule
Antigenic phase variation
Type III Secretion Systems
Sequestration of Growth Factors
Plasmids
149
Q

Properties of Escherichia coli

A

Gram-negative rod
Facultative anaerobe
Encapsulated
Flagella

150
Q

Escherichia coli epidemiology and transmission

A

Part of normal flora
Endogenous infection when immune systems and barriers are compromised
Exogenous strains cause gastroenteritis

151
Q

Pathogenesis of Escherichia coli

A

Adhesins

Enterotoxins: ETEC and EHEC

152
Q

Clinical findings of Escherichia coli

A

UTI (most common cause in women)
Neonatal meningitis
Gastroenteritis

153
Q

Laboratory diagnosis for Escherichia coli

A

MacConkey agar: selective for gram neg, differential for lactose fermenters, E.coli produces red/hot pink color (Lac positive)

154
Q

Treatment and prevention of Escherichia coli

A

Supportive treatment for gastroenteritis
Antibiotics for disseminated infections, UTI septicemia, neonatal meningitis
No vaccine

155
Q

What do Proteus do on an agar plate?

A

Swarm

156
Q

What does Proteus cause?

A

Common cause of UTI

Pneumonia, wound infections, septicemia

157
Q

Properties of Pseudomonas aeruginosa

A 
Gram-negative rod, pairs
Motile, flagella
Obligate aerobe
Oxidase positive
Non-lactose fermenter
Some with capsule
Resistant to disinfectant
158
Q

Epidemiology and Transmission of Pseudomonas aeruginosa

A

Ubiquitous in environment
Not in normal flora
Opportunistic pathogen (burn patients, cystic fibrosis, catheters, etc)
Problem in hospitals

159
Q

Pathogenesis of Pseudomonas aeruginosa

A

Exotoxin A

Pyocyanin

160
Q

Clinical findings of Pseudomonas aeruginosa

A 
Pulmonary infection (can get aspiration pneumonia)
Skin infection
UTI: indwelling catheters
Ear infection
Bacteremia
161
Q

Lab diagnosis of Pseudomonas aeruginosa

A 
Gram stain for empiric therapy
Lac negative on MacConkey
Beta-hemolytic
Produces pyocyanin
Oxidase positive
Fruity aroma
162
Q

Treatment and prevent of Pseudomonas aeruginosa

A

Antibiotic resistance

Prevent via infection control, hand washing, etc

163
Q

Features of Klebsiella pneumoniae

A 
Encapsulated
Causes disease in those with predisposing condition
Cause of hospital-associated UTI
Thick, bloody sputum
Lactose ferment on MacConkey
Antibiotic resistance
164
Q

Systemic Inflammatory Response Syndrome

A 
2 of 4 criteria met:
Body temp >38.5 or less than 35
Heart rate >90
Respiratory rate > 20 or arterial CO2 <32 mm
WBC >12,000 or <4000 or 10% bands
165
Q

What is the definition of sepsis?

A

Life threatening organ dysfunction caused by a dysregulated host response to infection

166
Q

Septic Shock

A

Subset of sepsis patients with profound circulatory, cellular, or metabolic abnormalities associated with a greater risk of death

167
Q

Frequent pathogens causing sepsis

A

Escherichia coli
Streptococcus sp.
Staphylococcus sp.
Pseudomonas

168
Q

Hemorrhage

A

Blood outside the vessel

169
Q

Thrombus

A

Clotted blood within the vascular space composed of cellular elements from the blood and proteins from coagulation cascade

170
Q

Steps in normal hemostasis

A
  1. Vasoconstriction
  2. Primary hemostasis
  3. Secondary hemostasis
  4. Thrombosis and anti-thrombotic events
171
Q

Components of normal hemostasis

A

Vascular wall
Platelets
Coagulation cascade

172
Q

Anti-thrombotic properties

A

Anti-platelet: physical barrier, nitric oxide, prostacyclin PGI2
Anti-coagulant: heparin-like molecules, thrombomodulin, tissue factor pathway inhibitor
Fibrinolytic effects: tissue type plasminogen activator

173
Q

Anti-coagulant Mediates

A 
Heparin like molecule
Plasmin
Plasminogen activator
Thrombomodulin
Tissue factor pathway inhibitor
Protein C and S
174
Q

Pro-thrombotic effects

A

von Willebrand factor
Tissue factor
Plasminogen activator inhibitors
Thrombin

175
Q

What platelet reactions favor thrombus reaction

A

Adhesion (vWF and collagen)
Secretion (Ca++ and ADP)
Aggregation (ADP and thromboxane A2)

176
Q

Thrombus formation

A
  1. Endothelial cell injury
  2. Abnormal blood flow
  3. Hypercoaguable state
177
Q

Arterial thrombi

A

Arise at site of injury

Lines of Zahn

178
Q

Venous thrombi

A

Arise at sites of stasis
Less firmly attached
Veins of lower extremity

179
Q

Fate of thrombi

A

Propagate
Embolize
Dissolution
Organize and recanalize

180
Q

Pulmonary thromboemboli

A

Come from deep veins of legs or pelvis

181
Q

Fat emboli

A

After long bone fractures

182
Q

Air emboli

A

Decompression sickness

183
Q

Amniotic fluid emboli

A

following tear in amniotic membranes

184
Q

Septic embolic

A

Fragments of necrotic, infected tissue

185
Q

Hemorrhagic infarction

A

Dual blood supply such as lung
Reperfusion by unblocked vessel
Watershed areas

186
Q

White or anemic infarction

A

Occlusion of end arteriole

187
Q

What is increased in septic patients

A

TNF, IL-6, IL-8

188
Q

What happens to lymphocytes during sepsis

A

Accelerated apoptosis, anergic cells

189
Q

What happens to neutrophils during sepsis

A

Decreased apoptosis so they no longer persist in circulation

190
Q

What is in a quick SOFA

A

Respiratory rate >22/min
Altered mentation
Systolic blood pressure < 100 mm Hg
2/3 accurately screens

191
Q

Fungi characteristics

A

Lack chlorophyll

Eukaryotic

192
Q

Yeast

A

Form moist or waxy colonies, reproduce by budding or fission

Pseudohyphae are elongated yeasts

193
Q

Molds

A

Hyphae, branching tubular filaments

Aseptate or septa; reproduce when hyphae form spores

194
Q

Dimorphic

A

Grow as mold in environment and yeast in mammals

195
Q

Where should you plate fungi

A

Sabouraud fungi

196
Q

Labs for fungi

A

KOH prep, Silver and PAS stains

197
Q

Dermatophytes

A

Molds that can invade keratinized tissues

198
Q

Types of dermatophytosis

A

Tinea pedis, cruris, capitus, barbae, onychomycosis

199
Q

Tinea versicolor

A

Common, superficial fungal infection

Hypopigmented or hyperpigmented lesions on trunk/proximal limbs

200
Q

Seborrheic dermatitis and dandruff

A

Erythema and scaling on face, scalp, chest, back

Inflammatory reaction

201
Q

Subcutaneous mycoses

A

Madura foot

202
Q

Opportunistic mycoses

A

Causes disease in patients with defects in host defense system

203
Q

Candida

A

Yeast, with ability to form pseudohyphae and hyphae

204
Q

Oral thrush

A

Frequently the first sign in HIV+

205
Q

Disseminated candidiasis

A

Via GI tract or IV site

Risk: severe neutropenia, prior antibiotic therapy, GI surgery

206
Q

Lab diagnosis for candidiasis

A

Exam for endophtalmitis and skin lesions

Definitive requires pathologic evidence of tissue and positive culture

207
Q

What does cryptococcus neoformans cause

A

Meningitis

208
Q

Transmission of cryptococcus

A

Inhalation of airborne fungi (in soil by bird droppings and rotten wood); associated with AIDS (Africa/Asia)

209
Q

Diagnosis of cryptococcus neoformans

A

CSF, cryptococcal antigen
India ink smear
Positive culture
(yeast with capsule)

210
Q

Where is Aspergillosis found

A

Ubiquitous in nature, spores everywhere

INHALATION

211
Q

Allergic bronchopulmonary aspergillosis

A

Colonize respiratory tree; disease from allergic response to fungi
Fever, eosinophilia

212
Q

Aspergilloma

A

Growth in preexisting cavity

213
Q

Invasive aspergillosis

A

Invasion of blood vessels and tissues by hyphae with hemorrhage, necrosis, infarction
Immunocompromised patients
Lungs common site of infection

214
Q

Who is affected by Zygomycosis (mucormycosis)

A

Diabetics with ketoacidosis, neutropenia, bone marrow transplant
Diabetics get rhinocerebral mucormycosis (black necrotic lesions)

215
Q

Who commonly gets Pneumocytosis

A

HIV + in US

216
Q

Clinical features of Pneumocytosis

A

Pneumonia (insidious), diffuse interstitial infiltrates

217
Q

Where is Histoplasmosis

A

Ohio and Mississippi River Valley, Caribbean, Central America

218
Q

What does Histoplasmosis cause

A

Acute pulmonary disease
Most mild
Either completely recover or go to progressive (AIDS)

219
Q

Blastomycosis

A

Large year characteristic broad buds
Southeastern South Central States Great Lakes St. Lawrence River valley
Inhale spores

220
Q

Where does blastomycosis infect

A

Lung, skin, bone

221
Q

Coccidioidmycosis life cycle

A

In soil, every other cell dies and . remaining are airbone and inhaled; undergo a phase transition and develop into large thick walled spherules; hundreds of internal spores form and then it ruptures

222
Q

Where is Coccidioidmycosis found

A

Southwestern US and Latin America, common in AIDS

223
Q

Clinical manifestations of Coccidioidmycosis

A

60% asymptomatic
Rest primary infection symptoms ad most resolve without treatment. Some get progressive lung infections or disseminated disease

224
Q

Sporotrichosis

A

Found worldwide

Cutaneous disease and at site of minor trauma; secondary lesions common by lymphangitic spread

225
Q

Important properties of Rickettsia rickettsii

A

Very short rods
Similar to gram negative
Obligate intracellular parasites

226
Q

What transmits RMSF

A

Dog tick

227
Q

Symptoms of RMSF

A

HIGH fever and chills, SEVERE headache, myalgia, prostration.
Rash on hands/feet first and then move inward

228
Q

Treatment of RMSF

A

Doxycycline

Start treatment immediately

229
Q

How is Rickettsia prowazekii transmitted

A

person to person by lice, human reservoir

230
Q

Clinical findings of Epidemic typhus

A

Maculopapular rash on trunk and spreads peripherally

Not on face, palms, sole

231
Q

Coxiella burnetii properties

A

Coccobacillus
Stains poorly
Obligate intracellular parasite

232
Q

Transmission of Coxiella burnetii

A

To humans from animal reservoirs via inhalation of aerosolized materials contaimated with urine, feces, etc. Unpasteurized cow’s milk

233
Q

Clinical findings of Coxiella burnetii

A

Q fever

No rash

234
Q

Erhilichia and Anaplasma properties

A

Short rods, gram negative structure but not peptidoglycan or LPS
Form morulae
Obligate intracellular parasite

235
Q

How is ehrlichia chaffeenis (HME) transmitted

A

Lone star tick

236
Q

How is Anaplasma phagocytophilum transmitted

A

Ixodes scapularis

237
Q

Structure of Leptospira interrogans

A

Spirochete

238
Q

How is Leptospirosa transmitted

A

transmitted to humans by contact iwth urine or tissue from infected animals through cuts or abrasion
Farmers at risk, vets, exposure to flood water

239
Q

Clinical findings of Leptospira interrogans

A

Subclinical, self-limited
Abrupt onset
Hard to diagnose
Weil’s disease (kidney damage, meningitis, liver failure, respiratory distress, death)

240
Q

What does IgG antibodies in a convalescent serum indicate

A

Past infection

241
Q

Penicillin (narrow spectrum) prototype, beta lactam

A

Penicillin G (IV)

Narrow gram positive

242
Q

Penicillin (broad spectrum) prototype, beta lactam

A

Ampicillin (IV)
Amoxicillin (PO)
Narrow Gram positive and negative

243
Q

Mechanism of action of Penicillin G

A

Bind/inhibit enzymes (PBPs including transpeptidases)

Block cross-linking of peptidoglycan in cell wall

Activate autolytic enzymes

Bactericidal, time dependent

244
Q

Spectrum and clinical use for Penicillin G

A

Most gram positive aerobes

Good activity for streptococcus

Drug of choice for Streptococcus, group A strep pharyngitis, syphilis, meningoccal infections

Limited use for S. aureus due to resistance

245
Q

Penicillin G resistance

A

Penicillinase sensitive, cleaves beta lactam ring and inactivates antibiotic
Use beta-lactamase inhibitors to help reduce
Alterations in PBP (MRSA)
Alterations in outer membrane permeability or efflux (Gram negative)

246
Q

Pharmacokinetics and Interactions of Penicillin G

A

Absorption: moderate oral, PO for mild/moderate and IV for severe infection
CNS entry (better early)
Renal elimination, frequent dosing, dose adjustment
Minimal metabolism

247
Q

Adverse effects of Penicillin G

A

Well tolerated
Anaphylaxis/hypersensitivity with cross sensitivity with other beta lactams
GI disturbances, adverse renal effects (long course or IV)

248
Q

What does nafcillin cover?

A

S. aureus (MSSA)

Gram positive aerobes

249
Q

What is amoxicillin combined with?

A

Amoxicillin is a beta lactam combined with clavulanic acid to protect against destruction by beta lactamase

250
Q

What do Ampicillin (IV) and amoxicillin (PO) have greater activity for?

A

Gram negative bacteria!

251
Q

What do Ampicillin and Amoxicillin treat?

A

Enterococcus (Gram positive aerobe)
Listeria (Gram positive rod)
Enterobacteriaceae

Enterococcal endocarditis, respiratory tract infections, UTI
Endocarditis prophylaxis

252
Q

1st generation cephalosporin

A

Cefazolin (IV)

Broad gram positive, narrow gram negative, beta lactam

253
Q

Mechanism of action of cefazolin

A

Inhibit cell wall synthesis, less susceptible to penicillinases and beta lactamases
Bactericidal

254
Q

Spectrum and clinical use for cefazolin

A

Primarily gram positive aerobes
Streptococci, MSSA, limited gram negative
Skin infection, surgical prophylaxis, UTI
NOT against enterococci or Listera

255
Q

Cefazolin resistance

A

Less susceptible to penicillinase and beta lactamase

Alterations in PBPs

256
Q

Pharmacokinetics and interactions for cefazolin

A

Oral use for mild to moderate
IV for severe
Longer half life than penicillins

257
Q

Adverse effects for cefazolin

A

Well tolerated
GI disturbances
Hypersensitivity (cross-reactivity)
Renal adverse effects

258
Q

2nd generation cephalosporins

A

Cefuroxime (IV/PO)
Cefoxitin (IV)

Same mechanism of action and adverse effects of cefazolin

259
Q

Cefuroxime spectrum and use

A

Gram positive aerobes, less than 1st gen; retain strep, lose S. aureus
Gram negative: more than 1st

Respiratory infections, community acquired pneumonia

260
Q

Resistance of cefuroxime and cefoxitin

A

Similar to cefazolin but enhanced stability to beta lactamase

261
Q

Do cefuroxime and cefoxitin have short or long half lives?

A

short

262
Q

Spectrum and use for cefoxitin

A

Similar to Cefuroxime but has activity against gram negative ANAEROBES

Intrabdominal surgical prophylaxis, PID

263
Q

3rd generation cephalosporin

A

Ceftriaxone

264
Q

Spectrum and use for ceftriaxone

A

Gram positive aerobes, less than 1st gen
Gram negative aerobes, more than 2nd

Pneumonia and gram negative infections, gonorrhea, meningitis (at high doses)

265
Q

Resistance in ceftriaxone

A

Similar to cefuroxime but enhanced stability to beta lactamase

266
Q

Pharmacokinetics in ceftriaxone

A

3rd gen enter CNS

Longer half life, biliary excretion

267
Q

4th generation cephalosporin

A

Cefepime

268
Q

Spectrum and use of Cefepime

A

Gram positive aerobes, similar to 1st gen
Gram negative aerobes, more than 3rd gen, INCLUDES pseudomonas

Hospital acquired infections

269
Q

Resistance in Cefepime

A

Most stable cephalosporin against beta lactamases and efflux pumps (mainly found in pseudomonas)

270
Q

Prototype for Carbapenems

A

Imipenem/cilastin

271
Q

Mechanism of action of Imipenem

A

Combined with cilastatin to prevent breakdown of imipenem by renal dehydropeptidase to nephrotoxic product

272
Q

Spectrum and use for Imipenem

A

Last line of defense!
Broad spectrum
Reserved for resistance
Activity against gram positive, negative and anaerobic

273
Q

Resistance in Imipenem

A

Resistant to hydrolysis by beta lactamases

274
Q

Pharmacokinetics of Imipenem

A

Parental (IV) only; good distribution

Renal elimination, dosage adjustment in renal impairment

275
Q

Adverse effects of Imipenem

A

GI disturbnaces
Hypersensitivity
Lower seizure threshold

276
Q

Glycopeptide prototype

A

Vancomycin (IV)

277
Q

Mechanism of action of Vancomycin

A

Inhibits cell wall peptidoglycan formation and cell wall synthesis
Binds to terminus of cell wall precursor
Bactericidal (slower)
Time dependent

278
Q

Spectrum and use for Vancomycin

A

Gram positive aerobes and anaerobes, including MRSA

Suspected/documented gram positive infections resistant to beta lactams, infections in those with anaphylaxis to beta lactams
Second line for C. diff

279
Q

Vancomycin resistance

A

VRE (enterococci)

S. aureus resistance rare

280
Q

Pharmacokinetics of Vancomycin

A

Poor oral absorption; IV use for systemic and oral for C. diff
Moderate distribution, lower CSF, minimal metabolism
Renal excretion, dosage adjustment in renal dysfunction

281
Q

Adverse effects in vancomycin

A

Diffuse flushing (red man syndrome) with rapid IV infusion
Hypersensitivity
Rare –> ototoxicity, thrombophlebitis, nephrotoxicity

282
Q

Beta-lactamase inhibitor prototype

A

Clavulanic acid

283
Q

Mechanism of action of Clavulanic acid

A

Irreversible, noncompetitive beta lactamase inhibitor

Prevents destruction of penicillin, binds directly to PBPs

284
Q

Spectrum and use for clavulanic acid

A

Enhances spectrum of parent drug, such as amoxicillin, when decreased activity results from beta-lactamase production

285
Q

Aminoglycosides prototype

A

Gentamicin (IV), protein synthesis inhibitor

286
Q

Gentamicin mechanism of action

A

Inhibit protein synthesis by irreversible binding to 30S ribosome
Bactericidal, concentration dependent
Prolonged post antibiotic effect

287
Q

Spectrum and clinical use of Gentamicin

A

Gram negative aerobe, including Pseudomonas
Gram positive aerobes, limited activity alone but used with beta lactams
UTI, bacteremia

288
Q

Gentamicin resistance

A

Drug inactivation by plasmid mediated aminoglycoside modifiying enzymes
Reduced transport into cell
Reduced affinity for 30S

289
Q

Gentamicin Pharmacokinetics

A

Highly polar
Poor oral absorption, need IV/IM
Distributes to extracellular space
Renal excretion of unchanged drug; dose adjustment in renal patients

290
Q

Adverse effects of Gentamicin

A

Nephrotoxicity
Ototoxicity
Neuromuscular blockade at high doses

291
Q

Tetracycline prototype

A

Doxycycline (IV/PO)

292
Q

Mechanism of action of doxycycline

A

Reversibly binds 30S ribosome
Bacteriostatic, time dependent
Concentrates intracellularly

293
Q

Spectrum and use of doxycycline

A

Broad spectrum, acquired resistance common
Gram positive aerobes: Strep, Staph, H influenzae and other gram negative

Mild/moderate respiratory infection
Lyme, RMSF, Cholera, Syphilis, Chlamydia, Mycoplasma, Legionella, acne (low dose)

294
Q

Doxycycline resistance

A

Plasmid-encoded transport pumps decrease uptake or increase efflux out of bacterial cells
Enzymatic inactivation
Alteration of ribosomal target site

295
Q

Pharmacokinetics of doxycycline

A

Good oral absorption, decreased by binding cations
Distribution in most tissues
Hepatic metabolism, metabolites excreted into urine and bile
Long half life

296
Q

Adverse effects of doxycycline

A

PHOTOSENSITIVITY
Tooth/bone discoloration – contraindicated in children under 8
GI disturbances
Hepatotoxicity, renal toxicity

297
Q

Macrolides protypes

A 
Azithromycin (IV/PO)***
Also Erythromycin (IV/PO) and Clarithromycin (PO)
298
Q

Mechanism of action of Azithromycin

A

Reversibly binds 50S
Bactericidal/static depending on dose and organism
Time dependent

299
Q

Spectrum and use of Azithromycin

A

Gram positive aerobes: Streptococci and Stapylococci
Gram negative aerobes: H. influenzae, chlamydia, mycoplasma, legionella

Respiratory tract infections and patients with penicillin allergy

300
Q

Resistance to Azithromycin

A

Increasing (Staph, Strep)
Methylation of 50S prevents drug binding
Plasmid pumps decrease uptake or increase efflux
Enzymatic hydrolysis of drug

301
Q

Pharmacokinetics of Azithromycin

A

Good oral absorption (food interactions)
Distribution to most tissues except CSF
Distributes to neutrophiles and macrophages and has low serum levels and high Vd; eliminated into bile with minimal metabolism and renal clearance
Other macrolides: hepatic metabolism with many drug interactions; metabolites to urine and bile

302
Q

Macrolides/Azithromycin Adverse effects

A

GI disturbances
Nausea/vomiting
QT elongation

303
Q

Mechanisms of action of Clindamycin

A

Binds to 50S ribosome
Bacteriostatic
Time-dependent

304
Q

spectrum and use for clindamycin

A

Gram positive aerobes
Gram pos/neg anaerobes
Gram positive cocci

Pulmonary, abdominal, pelvic. Dental infections **; alternative for those with penicillin allergy

305
Q

Resistance in clindamycin

A

Cross resistance with macrolides
Inactivated by enzymatic hydrolysis
Ribosomal mutation alters target site

306
Q

Pharmacokinetics of Clindamycin

A

Good oral absorption
Distribution to most tissues except CSF
Hepatic metabolism; metabolites eliminated in bile with minimal urine excretion

307
Q

Adverse effects of clindamycin

A

GI disturbances
C. diff overgrowth
Metallic taste

308
Q

Quinolone prototype

A

Levofloxicin (IV/PO)

Nucleic acids/chromatin structure inhibitor

309
Q

Levofloxicin mechanism of action

A

Binds bacterial enzymes (topoisomerases) and inhibit DNA gyrase and topoisomerase causing arrest of DNA replication
Bactericidal, concentration dependent

310
Q

Spectrum and use for Levofloxicin

A

Moderate gram pos including S. pneumoniae
Broad gram neg, including pseudomonas and atypicals

Gram neg infections (limited due to resistance), respiratory infection, inhalation anthrax exposure, gastroenteritis, osteomyelitis, prostatitis, UTI

311
Q

Levofloxicin resistance

A

Target site altered (DNA gyrase)
Drug cannot reach target due to efflux pumps
Increaseing resistance with widespread use
Drug inactivation

312
Q

Pharmacokinetics of levofloxicin

A

Good oral absorption (impaired by antacids and multivitamins)
Distribution to most tissues
Minimal hepatic metabolism, mostly renal clearance
Dosage adjustment in renal dysfunction

313
Q

Adverse effects of Levofloxicin

A

GI upset, CNS, rash, photosensitivity, QT prolongation, hypo/hyperglycemia, tendo rupture
Tendinitis

314
Q

Nitroimidazole prototype

A

Metronidazole (IV/PO), nucleic acid/chromatin structure inhibitor

315
Q

Metronidazole mechanism of action

A

Enters cell and reduced to cytotoxic product that damages RNA, DNA and proteins
Bactericidal, concentration dependent

316
Q

Use and spectrum Metronidazole

A

Gram negative aerobe, many aerobic gram positives, protozoa

C. diff colitis, gold standar for anaerobic infections

317
Q

Pharmacokinetics of Metronidazole

A

Complete oral absorption, distribution into most tissues, CNS
Hepatic metabolism to active metabolites excreted to urine and bile
Dose adjust in severe hepatic or renal dysfunction

318
Q

Adverse effects of metronidazole

A

Well tolerated
Metallic taste
Unpleasant interaction with alcohol (disulfiram reaction, flushing, tachycardia, hypotension)
Peripheral neuropathy

319
Q

Antifolates

A

Sulfamethoxazole/trimethoprim

320
Q

Antimycobacterial agents

A

Isoniazid and rifampin

321
Q

Antifungals

A

Amphotericin B
Fluconazole
Capsofungin
Flucytosine

322
Q

Neuraminidase inhibitor

A

Oseltamivir (Tamiflu)

323
Q

Antiherpes nucleoside analog

A

Acyclovir

324
Q

NRTI

A

Emtricitabine/Tenovir

325
Q

NNRTI

A

Efavirenz

326
Q

Integrase Strand Transfer Inhibitor

A

Dolutegravir

327
Q

Protease Inhibitor

A

Darunavir

DRx Infectious Disease (1 decks)

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