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MAD > Bacteria > Flashcards

Bacteria Flashcards

1
Q

community acquired pneumonias

A

Strep pneumo, Haemophilus influenza, Moraxella catarrhalis, Legionella pneumophilia, Bordetella pertussis

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2
Q

nosocomial acquired pneumonias

A

Pseudomonas aeruginosa, Legionella pneumophilia

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3
Q

Streptococcus pneumoniae morphology

A

gram positive coccus
encapsulated
alpha hemolytic
sensitive to optochin

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4
Q

Streptococcus pneumoniae virulence factors

A

anti-phagocytic polysaccharide capsule
IgA protease
Teichoic acid (pro-inflammatory cell wall component)
Pneumolysin (ciliated and phagocytic cell wall lysis)

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5
Q

Streptococcus pneumoniae transmission

A

acquired by inhalation of droplet nuclei or direct contact with other persons
blood stream infection possible

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6
Q

Streptococcus pneumoniae clinical aspects

A

lobar pneumonia, sinusitis, otitis media, meningitis, endocarditis, bacteremia

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7
Q

Streptococcus pneumoniae host defense

A

serospecific antibodies

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8
Q

Streptococcus pneumoniae risk factors

A

smoking, lung disease, splenectomized, hypogamaglobinemia

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9
Q

Streptococcus pneumoniae diagnosis

A

gram stain, culture, PCR, serotype using specific antibodies

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10
Q

Streptococcus pneumoniae treatment

A

beta-lactam, macrolide or fluoroquinolone

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11
Q

Streptococcus pneumoniae prevention

A

vaccine given to children, elderly, immunocompromised or splenectomized

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12
Q

Haemophilus influenza morphology

A

gram negative bacillus/coccobacilli
encapsulated
requires Factor V and Factor X for growth

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13
Q

Haemophilus influenza virulence factors

A

anti-phagocytic capsule (contains polyribitol phosphate)
pili
lipooligosacaride cell wall (lipid A endotoxin)
IgA protease
beta lactamases

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14
Q

Haemophilus influenza transmission

A

acquired by inhalation of droplet nuclei or direct contact with other persons

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15
Q

Haemophilus influenza host defense

A

serospecific antibodies

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16
Q

Haemophilus influenza clinical aspects

A

lobar pneumonia, sinusitis, otitis media, meningitis, epiglottitis

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17
Q

Haemophilus influenza risk factors

A

smoking, lung disease, splenectommized, hypogammaglobinemia

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18
Q

Haemophilus influenza diagnosis

A

gram stain, culture, PCR, serotype using specific antibodies

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19
Q

Haemophilus influenza treatment

A

beta lactase stable beta-lactam, macrolide or fluoroquinolone

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20
Q

Haemophilus influenza prevention

A

conjugated HiB vaccine given to children and splenectomized adults
Rifampin is given to close contacts of patients with HiB infection

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21
Q

Moraxella catarrhalis

A

Haemophilus influenza “want to be”, but less virulent

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22
Q

Legionella pneumophilia morphology

A

gram negative rods
poor staining –> need silver stain to see
requires buffered charcoal yeast extract (BCYE) agar for growth
requires cysteine and Fe for growth

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23
Q

Legionella pneumophilia virulence factors

A

biofilm
lipopolysaccharide cell wall
facultative intracellular bacteria (produce proteolytic enzymes that kill the host when the vacuole is lysed)

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24
Q

Legionella pneumophilia transmission

A

acquired by inhalation of droplet nuclei from an infected aerosol (i.e. cooling towers, showers, spas, hot tubs)
blood stream infection is uncommon
organisms able to survive in hot water tanks (due to biofilm and intracellular ability)

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25
Q

Legionella pneumophilia clinical aspects

A

Pontiac fever (mild flu like illness)- fever, cough, lobar pneumonia

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26
Q

Legionella pneumophilia risk factors

A

increased age, lung disease, smokers, immunocompromised, alcoholics, concurrent kidney, liver or heart disease

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27
Q

Legionella pneumophilia diagnosis

A

culture of charcoal yeast extract agar, detection of antigens in urine

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28
Q

Legionella pneumophilia prevention

A

monitor water sources, hyperchlorination or superheating of water

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29
Q

Pseudomonas aeruginosa morphology

A

gram negative bacillus
obligate aerobe, oxidase positive
produces pyocyanin (green pigment)
characteristic musty grape odor

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30
Q

Pseudomonas aeruginosa virulence factors

A

pili (facilitate attachment)
exotoxin A
alginate

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31
Q

Pseudomonas aeruginosa transmission

A

acquired by inhalation of droplet nuclei from an infected aerosol or other environmental source
found in moist, warm environmental soils, plant materials and water
common nosocomial bacteria

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32
Q

Pseudomonas aeruginosa risk factors

A

chronicle ill or hospitalized patients

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33
Q

Pseudomonas aeruginosa clinical aspects

A

pneumonia, UTIs, bacteremia, wound infections, superficial “hot tub folliculitis”, bone and joint infection

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34
Q

Pseudomonas aeruginosa diagnosis

A

gram stain, culture, PCR

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35
Q

Pseudomonas aeruginosa treatment

A

anti-pseudomonas penicillin, cephalosporin or carbapenem

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36
Q

Pseudomonas aeruginosa prevention

A

hospital infection prevention (disinfection of medical devices, such as ventilators)

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37
Q

Bordetella pertussis morphology

A

gram negative coccobacilli

growth inhibited by unsaturated FAs (cotton swab and rayon swabs)

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38
Q

Bordetella pertussis virulence factors

A

fimbriae
tracheal cytotoxin (destroys mucocilliary cells)
adenylate cyclase toxin (acts like adenylate cyclase to increase cAMP which increases mucus production and respiratory secretions)
pertussis toxin (inactivates the protein that controls adenylate cyclase activity)

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39
Q

Bordetella pertussis transmission

A

highly contagious, person-to-person transmission through aerosolized large respiratory droplets

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40
Q

Bordetella pertussis clinical aspects

A

“whooping cough”
catarrhal phase- like a cold
paroxysmal phase- inspiratory whoop, coughing fits
convalescent phase

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41
Q

Bordetella pertussis diagnosis

A

PCR, serology

**culture is difficult and not sensitive

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42
Q

Bordetella pertussis treatment

A

macrolide or fluoroquinolone

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43
Q

Bordetella pertussis prevention

A

acellular vaccination of children

macrolide prophylaxis of close contacts

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44
Q

toxin food poisoning

A

Staph aureus, Bacillus cereus, Clostridium perfringens

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45
Q

watery diarrhea

A

mechanism- enterotoxin, adherence, superficial invasion

Salmonella, E. coli, Clostridium perfringens, Vibrio cholera

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46
Q

bloody diarrhea

A

mechanism- invasion and/or cytotoxin

Campylobacter, Shigella, Yersinia, Vibrio parahemolyticus, enteroinvasive E. coli (EIEC), EHEC

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47
Q

Campylobacter morphology

A

gram negative curved/helical bacillus
obligate aerobe- oxidase positive
invasive, thermophilic

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48
Q

Campylobacter virulence factors

A 
flagella (motile)
corkscrew shape (facilitates penetration)
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49
Q

Campylobacter clinical aspects

A

reactive arthritis, bloody diarrhea, post infection Guile-Barre syndrome (ascending flaccid paralysis due to acute inflammatory demyelination)

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50
Q

Campylobacter risk factors

A

developing countries

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51
Q

Campylobacter transmission

A

through contaminated poultry

fecal-oral, food borne or water borne transmission

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52
Q

Campylobacter treatment

A

macrolides

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53
Q

Enterobacter morphology

A

gram negative bacillus
lactose fermenter
motile

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54
Q

Enterobacter clinical aspects

A

nosocomial pneumonia, UTIs, wound infections, catheter related infections

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55
Q

Enterobacter risk factors

A

hospital patients, neonates, immunocompromised

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56
Q

Escherichia coli morphology

A

gram negative bacillus
sorbitol sensitive
lactose fermenter
catalase positive

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57
Q

Escherichia coli virulence factors

A

encapsulated- LPS lipid A (endotoxin)

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58
Q

Escherichia coli clinical aspects

A

UTIs, diarrhea

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59
Q

Escherichia coli treatment

A

treat with hydration

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60
Q

Escherichia coli diagnosis

A

can’t use culture, must use PCR

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61
Q

Escherichia coli transmission

A

EHEC- under cooked meat

ETEC- contaminated water

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62
Q

EHEC

A

serotype O157-H7, shiga toxin producing (cytotoxic to endothelial cells)

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63
Q

ETEC

A

traveler’s diarrhea, profuse watery diarrhea
heat labile toxin (LT1) increases cAMP production
heat stable toxin (STa) increases cGMP production

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64
Q

UPEC

A

virulence- PAP adhesion presents on tip of P fimbriae and binds to Gal-Gal receptor

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65
Q

EAEC

A

adherence via fimbrae, heat stable toxin and plasmid encoded toxin, forms biofilms, stack of bricks adherence of hep2cells

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66
Q

EPEC

A

intim- polymerizes actin and disrupts normal microvillus structures

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67
Q

Helicobacter pylori morphology

A

gram negative curved bacillus

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68
Q

Helicobacter pylori virulence factors

A

flagella- motility
acid inhibitory protein- blocks acid production
urease- neutralizes gastric acids and byproducts can cause local tissue damage

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69
Q

Helicobacter pylori clinical aspects

A

duodenal ulcers, gastric adenocarcinoma, mucosa associated lymphoid tissue (MALT) lymphomas, acute and chronic gastritis

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70
Q

Helicobacter pylori risk factors

A

low SES classes, developing countries

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71
Q

Helicobacter pylori transmission

A

humans are the primary reservoir, person to person spread (fecal-oral)

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72
Q

Helicobacter pylori diagnosis

A

blood antibody test, stool antigen test

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73
Q

Helicobacter pylori treatment

A

proton pump inhibitors, amoxicillin and clarithromycin (need all 3)

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74
Q

Klebsiella morphology

A

gram negative bacillus

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75
Q

Klebsiella virulence factors

A

capsule- mucoid appearance

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76
Q

Klebsiella clinical aspects

A

lobar pneumonia, UTIs, currant jelly sputum, abscess’

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77
Q

Klebsiella risk factors

A

alcoholics

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78
Q

Listeria morphology

A

gram positive coccobacillus, beta hemolytic, growth in cold and high salt environments

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79
Q

Listeria virulence factors

A

flagella- motile
facultative intracellular pathogen- actin directed intracellular motility
hemolysis

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80
Q

Listeria clinical aspects

A

meningitis

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81
Q

Listeria risk factors

A

pregnant women, elderly, neonates, immunocompromised

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82
Q

Listeria treatment

A

penicillin or ampicillin

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83
Q

Proteus morphology

A

gram negative bacillus

swarms on the culture (very motile)

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84
Q

Proteus clinical aspects

A

fishy odor, UTIs, kidney infection, pyelonephritis, struvite (Mg) and apatite (Ca) crystals, staghorn calculi

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85
Q

Salmonella morphology

A

gram negative bacillus
encapsulated
acid labile- which means you need a lot of the organism to infect the host

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86
Q

Salmonella virulence factors

A

type 3 secretion system
facultative intracellular- evades host’s immune response by blocking lysosome movement and then remaining and replicating in endocytotic vesicles

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87
Q

Salmonella clinical aspects

A

watery diarrhea, enteric fever (typhoid fever- rose spots, constipation, systemic illness with fever and abdominal symptoms), osteomyelitis, gastroenteritis, bacteremia, endovascular infection

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88
Q

Salmonella transmission

A

through food/water (poultry, eggs, milk) or through pets (turtles, snakes, ducklings)
colonizes in the gallbladder of chronic carriers

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89
Q

Salmonella treatment

A

only treat infants, adults over the age of 50 or high risk patients

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90
Q

Serratia morphology

A

gram negative bacillus, motile, produces a red pigment

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91
Q

Serratia clinical aspects

A

nosocomial pneumonia, UTIs, wound infections, catheter related infections

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92
Q

Shigella morphology

A

gram negative bacillus, immotile

Shigella dysenteriae- acid stable (low infective dose)

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93
Q

Shigella virulence factors

A

type 3 secretion system
facultative intracellular- enter M cells, evade host lysis in cell cytoplasm, multiply intracellularly, cell to cell spread using the host cell actin for locomotion

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94
Q

Shigella clinical aspects

A

watery diarrhea for 2-3 days and then bloody diarrhea

biphasic fever

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95
Q

Shigella treatment

A

ciprofloxacin

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96
Q

Vibrio morphology

A

gram negative bacillus (comma shaped/curved), requires salt for growth, susceptible to stomach acids but tolerable to a wide range of pH

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97
Q

Vibrio shared virulence factors

A

flagella (motility), pilli, LPS containing lipid A endotoxin

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98
Q

Vibrio treatment

A

rehydration

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99
Q

Vibrio cholerae virulence factors

A

cholera toxin (interacts with G protein controlling adenylate cyclase to increase cAMP production)

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100
Q

Vibrio cholerae clinical aspects

A

rice water stools, rapid onset diarrhea

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101
Q

Vibrio cholerae transmission

A

through contaminated food/water (fecal to oral)

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102
Q

Vibrio cholerae treatment

A

fluid and electrolyte replacement

single dose of azithromycin

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103
Q

Vibrio parahemolyticus virulence factors

A

acidic polysaccharide capsule- important for disseminated infections

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104
Q

Vibrio parahemolyticus clinical aspects

A

wound infection, bacteremia, watery diarrhea, n/v

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105
Q

Vibrio parahemolyticus transmission

A

shellfish and sea water

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106
Q

Vibrio parahemolyticus treatment

A

hydration and tetracyclines

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107
Q

Vibrio vulnificus virulence factors

A

polysaccharide capsule, RtxA toxin, iron acquisition systems

108
Q

Vibrio vulnificus clinical aspects

A

wound infections, primary sepsis

109
Q

Vibrio vulnificus risk factors

A

patients with chronic underlying disease (i.e. liver disease, hemochromatosis)

110
Q

Vibrio vulnificus treatment

A

combination of doxycycline and ceftriaxone

111
Q

Vibrio vulnificus transmission

A

shellfish and seawater

112
Q

Yersinia morphology

A

gram negative bacillus
encapsulated
needs factor V (NAD) and factor X (hemolin) to grow

113
Q

Yersinia virulence factors

A

type 3 secretion system- to resist phagocytic killing

114
Q

Yersinia pestis clinical aspects

A

bubonic plague, pneumonic plague

115
Q

Yersinia pestis diagnosis

A

safety pin appearance of gram stains

116
Q

Yersinia pestis treatment

A

gentamicin and fluoroquinolone

117
Q

Yersinia enterocolitica transmission

A 
food born (undercooked meats), contacts with pets
can grow in the cold
118
Q

Yersinia transmission

A

animal stools, fleas, carried in rodents

119
Q

Streptococci general characteristics

A

ubiquitous, rapidly growing, gram positive cocci
facultative anaerobes
alpha (viridian’s and pneumo), beta (pyogenes, agalaciae) or gamma (enterococcus) hemolytic
cocci form pairs on gram stain
catalase negative

120
Q

Streptococci pyogenes (Group A) virulence factors

A

lipoteichoic acid (cellular adhesion)
M protein (adheres to specific host cell receptors and interferes with complement and opsonization)
hyaluronic acid capsule (helps to avoid host defenses
streptococcal pyrogenic exotoxins (Spe)- a super antigen that causes scarlet fever, TSS, necrotizing fasciitis
streptolysin S and O- hemolysins
streptokinase- cleaves plasminogen (thus lyses blood clots)

121
Q

Streptococci pyogenes (Group A) clinical aspects

A

pharyngitis, cellulitis, pneumonia, bacteremia, necrotizing fasciitis, scarlet fever, pyoderma (pustules), erysipelas, streptococcal toxic shock syndrome, rheumatic fever (due to production of Ab against M protein), post streptococcal glomerulonephritis

122
Q

Streptococci pyogenes (Group A) transmission

A

direct contact and the environment (respiratory droplets)

123
Q

Streptococci pyogenes (Group A) diagnosis

A

gram stain, culture, swab of oropharynx, PCR

anti-streptolysin O, anti-hyaluronidase or anti-DNase antibodies in serum suggest recent infection

124
Q

Streptococci pyogenes (Group A) treatment

A

beta lactam, macrolide, tetracycline

antibiotic treatment for pharyngitis prevents rheumatic fever

125
Q

Streptococci agalactiae (Group B) virulence factors

A 
polysaccharide capsule (prevents opsonization)
sialic acid surface expression (inhibits alternate complement pathway)
126
Q

Streptococci agalactiae (Group B) clinical aspects

A

bacteremia, sepsis, meningitis, pneumonia

127
Q

Streptococci agalactiae (Group B) diagnosis

A

PCR of rectal or vaginal swab, culture

128
Q

Streptococci agalactiae (Group B) treatment

A

beta lactam/penicillin, clindamycin

129
Q

Streptococci agalactiae (Group B) prevention

A

test pregnant women between 35-37 weeks, give intrapartum penicillin if infected

130
Q

Enterococcus morphology

A

gamma hemolytic, NaCl and bile resistant (makes it very hard to kill)
normal flora of the large intestine

131
Q

Enterococcus virulence factors

A

biofilms, antibiotic resistance

132
Q

Enterococcus host defense

A

opsonization and phagocytosis

133
Q

Enterococcus risk factors

A

immunocompromised, neutropenic patients, comorbidities, GI surgery, hospitalizations, catheters

134
Q

Enterococcus clinical aspects

A

UTI, endocarditis, biliary tract infection

135
Q

Enterococcus diagnosis

A

PCR of blood, culture

136
Q

Enterococcus treatment

A

ampicillin (aminoglycosides in addition if severe infection because of the synergistic effect of the two antibiotics)

137
Q

Viridians streptococci virulence factors

A

no capsule but have dextran extracellular polysaccharides to facilitate adherence

138
Q

Viridians streptococci clinical aspects

A

dental caries, periodontal, head and neck infections, endocarditis, prosthetic joint infection

139
Q

Viridians streptococci treatment

A

beta lactams, vancomycin, macrolide, clindamycin

140
Q

Staphyococci general characteristics

A

gram positive coccus
facultative anaerobes
beta hemolytic
catalase positive

141
Q

Staphylococci aureus virulence factors

A

capsule, coagulase, hyaluronidase, biofilm, teichoic acid (pro-inflammatory), protein A (binds IgG receptors)
enterotoxins (superantigens), toxic shock syndrome toxin, exfoliative toxin A (EtA), quorum sensing

142
Q

Staphylococci aureus host defense

A

intact mucosa, antibody opsonization, phagocytosis, neutrophil mediated killing

143
Q

Staphylococci aureus risk factors

A

immunocompromised, splenectomized, phagocytic disorders, IV drug use

144
Q

Staphylococci aureus clinical aspects

A

toxin mediated food poisoning (from meats and mayonnaise), rapid onset, scalded scalp syndrome (due to exfoliative toxins A and B), toxic shock syndrome, impetigo, skin abscesses, endocarditis, bone infection, joint infection, heart valve infection
**post-influenz pneumonia

145
Q

Staphylococci aureus diagnosis

A

gram stain, culture, mannitol salt agar plates (turns yellow), PCR (to discriminate MRSA from methicillin sensitive)

146
Q

Staphylococci aureus treatment

A

beta lactam, macrolide, sulfa, tetracycline

vancomycin for MRSA

147
Q

Staphylococci aureus prevention

A

isolation in hospitals, hygiene and disinfection in the community

148
Q

Staphylococci epidermidis virulence factors

A

biofilm, less virulent

149
Q

Staphylococci epidermidis clinical aspects

A

commonly associated with medical device infections

common blood culture contaminant

150
Q

Staphylococci saprophyticus clinical aspects

A

UTIs especially in young sexually active females

151
Q

Treponema pallidum morphology

A

spirochete, need to use a silver stain, dark field microscopy or fluorescent antibody testing to observe

152
Q

Treponema pallidum virulence factors

A

minimal species specific antigens on surface (evade immune response)
fibronectin (adheres to host)
hemolysins, vasculitis

153
Q

Treponema pallidum transmission

A

direct sexual contact, transfusion through contaminated blood, congenital transmission

154
Q

Treponema pallidum clinical aspects

A

syphillis
primary- painless genital chancre
secondary- flu like syndrome, rash that includes the palms and soles of the feet, condyloma lata
tertiary- tabes dorsalis, Argyll Robertson pupil, aortitis, skin and bone granulomatous lesions, uveitis, deafness
congenital- hutchinson teeth, mulberry molars, saddle nose, saber shins, uveitis

155
Q

Treponema pallidum diagnosis

A

dark field or fluorescent microscopy
non treponema serology (RPR and VDRL) followed by treponema serology (fluorescent treponemal antibody absorption (FTA-ABS)

156
Q

Treponema pallidum treatment

A

penicillin!! desensitize pregnant women and immunocompromised instead of giving a different drug

157
Q

Borrelia burgdorferi morphology

A

spirochete, poorly stains with gram stain

158
Q

Borrelia burgdorferi virulence factors

A

outer surface protein A (OspA)- binds to gut proteins

outer surface protein C (OspC)- critical for transmission

159
Q

Borrelia burgdorferi transmission

A

via the Ixodes tick

160
Q

Borrelia burgdorferi clincal aspects

A

lymes disease
stage 1- erythema migrant, fever, headache
stage 2- muscle pain, neck pain, hepatitis, mild encephalopathy, motor or sensory radiculitis, AV block, myocarditis
stage 3- recurrent arthritis (especially in large joints like the knee), encephalomyelitis

161
Q

Borrelia burgdorferi diagnosis

A

disseminated infection- serologic testing; step 1- ELISA for IgM and IgG antibodies, step 2- western blot to confirm

162
Q

Borrelia burgdorferi treatment

A

early- oral doxycycline, amoxicillin

secondary lyme- ceftriaxone

163
Q

Leptospira interrogans morphology

A

observed by dark field microscopy or by direct fluorescent antibody testing or by silver stain

164
Q

Leptospira interrogans transmission

A

contaminated water; organism is shed in urine of infected mammals for weeks to months

165
Q

Leptospira interrogans clincal aspects

A

early symptoms- fever, headache, stiff neck, myalgia

2nd phase- Weil’s disease- conjunctival suffusion, thrombocytopenia, pulmonary hemorrhage, liver and kidney dysfunction

166
Q

Leptospira interrogans diagnosis

A

serology, dark field or silver stain of CSF

167
Q

Leptospira interrogans treatment

A

ceftriaxone, doxycycline

168
Q

Clostridium difficile morphology

A

obligate anaerobe

gram positive rods, spore forming

169
Q

Clostridium difficile virulence factors

A 
toxin A (enterotoxin)-stimulates infiltration of neutrophils, increases permeability of intestinal wall through disrupting tight junctions
toxin B (cytotoxin)- causes actin to depolymerize and destroy cellular cytoskeleton
170
Q

Clostridium difficile clinical aspects

A

acute onset of watery diarrhea, pseudomembranous colitis, fever, toxic megacolon

171
Q

Clostridium difficile risk factors

A

recent antibiotic exposure within a month (clindamycin and fluoroquinolone are highest), hospitalizations

172
Q

Clostridium difficile diagnosis

A

ELISA to demonstrate toxin A and B, PCR of stool to look for toxins

173
Q

Clostridium difficile treatment

A

oral vancomycin, stool transplant, colectomy if necessary

174
Q

Clostridium perfringens morphology

A

beta hemolysis (double ring)

175
Q

Clostridium perfringens virulence factors

A

alpha toxin- mediates massive hemolysis, increases vascular permeability
beta toxin- intestinal stasis, formation of necrotic lesions
enterotoxin- alters membrane permeability of ileum and jejunum, leads to increased loss of fluids and ions (acts as a super antigen)

176
Q

Clostridium perfringens clinical aspects

A

gas gangrene, cellulitis, fasciitis, often follows trauma/open wounds

177
Q

Clostridium perfringens diagnosis

A

gram stain and culture

178
Q

Clostridium perfringens treatment

A

high dose of penicillin

179
Q

Clostridium tetani virulence factors

A

tetanus toxin- inhibits inhibitory neurons (irreversible lack of inhibition of motor neuron produces tents- inhibits release of GABA through cleaving SNARE protein)

180
Q

Clostridium tetani clinical aspects

A

tetanus, uncontrollable muscle spasms, grinning face

181
Q

Clostridium tetani host defense

A

antibody against the toxin

182
Q

Clostridium tetani diagnosis

A

demonstration of seronegative state

183
Q

Clostridium tetani treatment

A

tetanus immunoglobulin (TIG), penicillin (to decrease organism number)

184
Q

Clostridium tetani prevention

A

vaccination with tetanus toxoid

185
Q

Clostridium botulinum virulence factors

A

botulinum toxin (inhibits the release of acetylcholine by the presynaptic cell by cleaving SNARE)

186
Q

Clostridium botulinum host defense

A

antibody against the toxin

187
Q

Clostridium botulinum risk factors

A

contamination and improper presentation of canned/stored foods, giving raw honey to infants

188
Q

Clostridium botulinum clinical presentation

A

descending flaccid paralysis, ptosis, blurred vision

189
Q

Clostridium botulinum diagnosis

A

clinical presentation, epidemiology, isolation of bacteria and toxin from food source, isolation of organism from stool

190
Q

Clostridium botulinum treatment

A

botulinum antitoxin

191
Q

Actinomyces morphology

A

branching gram positive rod
obligate anaerobe
dentate appearing colonies on agar
active infections tend to produce sulfur granules in pus

192
Q

Mycoplasma general characteristics

A

NO cell wall –> resistant to beta lactams (penicillin, cephalosporin, vancomycin, etc)
cell membrane contains sterols

193
Q

Mycoplasma treatment

A

macrolide, tetracycline, fluoroquinolone

194
Q

Mycoplasma pneumoniae virulence factors

A 
P1 adhesion (destroys ciliated epithelial cells)
functions as a super antigen to stimulate inflammatory cells to migrate to site of infection and release cytokines
rapidly changes expression of surface lipoproteins (allows it to evade host immune response)
195
Q

Mycoplasma pneumoniae transmission

A

via large respiratory droplets

196
Q

Mycoplasma pneumoniae clinical aspects

A

walking pneumonia

197
Q

Chlamydia general characteristics

A

obligate intracellular, gram negative
LPS with weak endotoxin activity (from lipid A)
life cycle- elementary bodies (infectious form) and reticulate bodies (metabolically active form)

198
Q

Chlamydia treatment

A

macrolid, tetracycline, fluoroquinolone

199
Q

Chlamydia pneumoniae clinical aspects

A

walking/atypical pneumonia, sinusitis, pharyngitis

200
Q

Chlamydophila trachomatis clinical aspects

A

serotypes A-C- trachoma, blindness, chronic inflammatory granulomatous of the eye
serotypes D-K- urogenital infections, commonly asymptomatic in women, inclusion conjunctivitis
serotypes L1-L3- lymphogranuloma venereum, painless ulcer followed by inflammation and swelling of the lymph nodes

201
Q

Chlamydophila trachomatis risk factors

A

sub-Saharan Africa (trachoma), impoverish areas, having another STI

202
Q

Chlamydophila trachomatis transmission

A

person to person, oral-genital contact

203
Q

Chlamydophila trachomatis diagnosis

A

nucleic acid amplification test (NAAT)

204
Q

Neisseria general characteristics

A

gram negative diplococci, oxidase positive, catalase positive, transferred from one person to another

205
Q

Neisseria meningitidis virulence factors

A

pili for attachment, IgA protease, LOS (from capsule)

206
Q

Neisseria meningitidis risk factors

A

kids, teenagers, young adults, sickle cell patients, splenectomized patients, immunocompromised, elderly, those who live in closed populations

207
Q

Neisseria meningitidis clinical aspects

A

meningitis, petechial rash, hypotension due to vasodilation and capillary leak, Waterhouse-Frederickson syndrome (bilateral adrenal hemorrhage)

208
Q

Neisseria meningitidis diagnosis

A

PCR, gram stain, culture on chocolate agar

209
Q

Neisseria meningitidis treatment

A

ceftriaxone or cefotaxime

210
Q

Neisseria meningitidis prevention

A

chemoprophylaxis for those with significant exposure to patients
vaccination for all strands but B (given to all adolescents prior to college entry and travelers to sub-Saharan africa during dry season)

211
Q

Neisseria gonorrhoeae virulence factors

A

opacity protein for attachment

212
Q

Neisseria gonorrhoeae risk factors

A

more common in SE US, minorities

213
Q

Neisseria gonorrhoeae clinical aspects

A

women are more likely to be asymptomatic

urethritis, cervicitis, PID, Fitz/Hugh Curtis (adhesions and inflammation around the liver and subdiaphragmatic space)

214
Q

Neisseria gonorrhoeae diagnosis

A

nucleic acid amplification test (NAAT), gram stain, culture on chocolate or Thayer Martin agar

215
Q

Neisseria gonorrhoeae treatment

A

ceftriaxone (with macrolide or doxycycline for chlamydia coverage)

216
Q

Chlamydia trachomatis treatment

A

macrolide or doxycycline (with ceftriaone for gonorrhea coverage)

217
Q

Rickettsiaceae general characteristics

A 
gram indeterminate but structurally similar to gram negative rods (have LPS in cell wall)
visualized best with Geimsa or Gimenez stain
obligate intracellular (have phospholipase to dissolve phagosome membrane)
218
Q

Rickettsiaceae rickettsia transmission

A

dermacentor ticks (dog ticks, wood ticks)

219
Q

Rickettsiaceae rickettsia epidemiology

A

southeastern US; peak season is May-July

220
Q

Rickettsiaceae rickettsia clinical aspects

A

infects vascular endothelium and causes small vessel vasculitis, Rock mountain spotted fever!!!, incubation period of 2-14 days, fever, headache, myalgia, petechial rash that spreads from the extremities to the trunk

221
Q

Rickettsiaceae rickettsia diagnosis

A

serology- usually takes 7-10 days after the onset of symptoms for seroconversion

222
Q

Rickettsiaceae prowazekii transmission

A

louse (lice transmit to humans)

223
Q

Rickettsiaceae prowazekii epidemiology

A

mountainous regions of central and eastern africa, central and south america, asia

224
Q

Rickettsiaceae prowazekii clinical aspects

A

epidemic typhus, meningoencephalitis, petechial rash that spreads from the trunk to the extremities (opposite RMSF), no eschar

225
Q

Rickettsiaceae prowazekii diagnosis

A

serology or PCR

226
Q

Rickettsiaceae treatment

A

doxycycline

227
Q

Brucella mophology

A

gram negative coccobacillus

non-motile, facultative intracellular

228
Q

Brucella epidemiology

A

developing world, US/Mexico border, bioterrorism agent

229
Q

Brucella transmission

A

from contaminated milk or cheese, spreads through the reticuloendothelial system and bloodstream

230
Q

Brucella clinical aspects

A

Brucellosis; fever, hepatomegaly, splenomegaly, lymphadenopathy

231
Q

Brucella prevention

A

pasteurize milk and cheese, vaccinate food producing animals

232
Q

Franciscella tularensis morphology

A

gram negative coccobacillus, non-motile, facultative intracellular

233
Q

Franciscella tularensis virulence factors

A

resistant to serum killing and phagocytosis

234
Q

Franciscella tularensis epidemiology

A

central US

235
Q

Franciscella tularensis transmission

A

rabbits, ticks, inhalation or ingestion

236
Q

Franciscella tularensis clinical aspects

A

Tularemia- fevers, chills, ulcerated painful skin lesions, regional lymphadenopathy

237
Q

Franciscella tularensis prevention

A

education of outdoorsmen, avoid reservoirs and vectors of infection

238
Q

Yersinia pestis virulence factors

A

facultative intracellular (in macrophages), type 3 secretion system

239
Q

Yersinia pestis transmission

A

rodents or fleas; direct contact with an infected animal, cat bite, scratch, airborne

240
Q

Yersinia pestis clinical aspects

A

plague- pneumonic, septicemic, bubonic

SOB, chest pain, GI symptoms

241
Q

Yersinia pestis prevention

A

rodent and flea control; antibiotic prophylaxis of contacts or exposures to infected individuals

242
Q

Bacillus anthracis morphology

A

gram positive bacillus, spore forming, non-motile

243
Q

Bacillus anthracis transmission

A

cattle, goats, sheep, contaminated hides, wool; contact, ingestion or inhalation of infective spores

244
Q

Bacillus anthracis virulence factors

A

edema factor (acts like adenylate cyclase to increase cAMP), lethal toxin (increases cytokines and leads to shock/cell death)

245
Q

Bacillus anthracis clinical aspects

A

Anthrax- lesion progresses to eschar, tissue necrosis, edema, widened mediastinum, pleural effusion

246
Q

Bacillus anthracis treatment

A

once exposed prophylaxis (60 day course) of ciprofloaxcin and doxycycline

247
Q

Coxiella brunetti morphology

A

pleomorphic rod, obligate intracellular (in macrophages)

248
Q

Coxiella brunetti virulence factors

A

antigenic variation, intracellular survival

249
Q

Coxiella brunetti epidemiology

A

more prevalent in Europe and northern Australia

250
Q

Coxiella brunetti transmission

A

cattle, sheet, goats, cats; often acquired during assisting with birthing or placental contact
aerosol transmission

251
Q

Coxiella brunetti clinical aspects

A

Q-fever, flu like symptoms, fever, pneumonia, hepatitis, splenitis

252
Q

Coxiella brunetti diagnosis

A

serology

253
Q

Coxiella brunetti prevention

A

education and safety

254
Q

Bartonella henselae transmission

A

cat bite, lick or scratch

255
Q

Bartonella henselae clinical aspects

A

cat scratch fever, fever with papule at inoculation site, regional adenopathy

256
Q

Pasteurella multocida morphology

A

gram negative coccobacilli

257
Q

Pasteurella multocida transmission

A

animal contact from dogs and cats (bites, scratches, shared food)

258
Q

Pasteurella multocida virulence factors

A

capsule and endotoxin

259
Q

Pasteurella multocida clinical aspects

A

pneumonia, systemic infection with bacteremia and septic shock in immunocompromised/liver disease patients

260
Q

Mycoplasma tuberculosis morphology

A

impermeable to staining, need acid fast staining to see –> resistant to acid, alkali, drying and germicides

261
Q

Mycoplasma tuberculosis risk factors

A

associated with overcrowding, poor hygiene, malnutrition, workers in congregate settings where disease is more prevalent and defects in cell mediated immunity (**HIV)

262
Q

Mycoplasma tuberculosis transmission

A

determinants of contagion = distance to source, duration of exposure, infectiousness of source
clinical factors enhancing infectiousness = presence of cough, production of sputum which is smear positive for acid fast bacteria, cavitary lesion on CXR

263
Q

Mycoplasma tuberculosis clinical aspects

A

primary TB- Ghon complex (focal caseation in parenchyma and hilarious nodes; undergoes fibrosis and calcification; can be seen radiologically); bilateral hilar lymphadenopathy
secondary (reactivation) TB- most commonly involves the apex of the lung; causes cavitary lesions with caseous necrosis
miliary TB- consequence of blood-borne spread; granulomatous inflammation with multinucleate giant cells; miliary usually in the liver and spleen

264
Q

Mycoplasma tuberculosis diagnosis

A

PCR, acid fast stain

265
Q

Mycoplasma tuberculosis treatment

A

long term treatment with a combination of drugs (two phases- induction and continuation)
active TB treatment- isoniazid, rifampin, pyrazinamide, pyridoxine and ethambutol
latent TB treatment- isoniazid and pyridoxine

MAD (7 decks)

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