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Micro Exam 10 Flashcards

1
Q

what is the major pathogen of osteomyelitis that is facultatively intracellular in osteoblasts

A

staph aureus

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2
Q

which pathogen must be considered for osteomyelitis in sickle cell patients

A

salmonella

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3
Q

which pathogen must be considered for osteomyelitis in children

A

kingella kingae

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4
Q

which pathogen must be considered for osteomyelitis in puncture wounds

A

pseudomonas

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5
Q

which pathogen must be considered for osteomyelitis in immunocompromised

A

aspergillus, mac, candida (Chronic agents)

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6
Q

what are the 3 ways osteomyelitis occurs from greatest to least

A

surgery/trauma
spread
hematogenous

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7
Q

what is the pathogenesis for osteomyelitis

A

inflammation at bone site, osteoclast activation, pus formation leading to vascular blockade

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8
Q

what are the 4 ways patients present with osteomyelitis

A

after surgery/trauma (systemic)
joint replacement
diabetes checkup
bacteremia (systemic)

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9
Q

what signs indicate osteomyelitis on physical exam in a pt with diabetic foot ulcer

A

ulcer area > 2cm squared

positive probe to bone test

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10
Q

what signs indicate chronic osteomyelitis

A

sequestra (dead/necrotic bone)

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11
Q

what is the tx for osteomyelitis

A

acute - abx parenterally for weeks

chronic - abx orally for months to years

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12
Q

how do you prevent osteomyelitis

A

give abx 30 mins before surgery

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13
Q

mycoplasma and ureaplasma may cause

A

septic arthritis

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14
Q

how long does it take for septic arthritis to occur

A

during prosthetic surgery up to 1 year after

after prosthetic surgery by hematogenous dissemination more than 1 year after

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15
Q

What causes dmg in septic arthritis

A

PMNs releasing degradative enzymes which damage cartilage

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16
Q

how is the damage in septic arthritis similar to osteomyelitis

A

effusion in septic arthritis can interfere with blood supply like the pus in osteomyelitis

both are from increased pressure

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17
Q

what are the 3 manifestations of septic arthritis

A

acute, disseminated gonoccocal, granulomatous

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18
Q

what is disseminated gonococcal infection and what does it cause

A

when gonococcal genital infxn spreads days after the infxn causing a rash, fever, and joint symptoms

septic arthritis

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19
Q

what is granulomatous arthritis

A

septic arthritis

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20
Q

what causes granulomatous arthritis

A

TB, coccidioides, blastomyces

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21
Q

which disorder has granuloma formation

A

granulomatous arthritis (a form of septic arthritis)

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22
Q

HLA B27 is not required but associated with

A

reactive arthritis

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23
Q

what precedes reactive arthritis

A

RT infxn, urogenital infn, Gi infxn

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24
Q

which gender is ReA more common in

A

males

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25
Q

what type of infxns cause reactive arthritis

A

G- mucosal infxn

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26
Q

which has autoantibodies form

A

ReA

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27
Q

Does septic arthritis have systemic signs

A

yes

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28
Q

does reactive arthritis have systemic signs

A

only if mucosal infection causes fever

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29
Q

how many joints are typically affected in septic arthritis

A

1

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30
Q

how many joints are typically affected in ReA

A

3-4

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31
Q

how many days does it take for reactive arthritis to occur

A

1 to 2 weeks

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32
Q

what diagnostic method is used to differentiate septic from reactive arthritis

A

arthrocentesis of SF

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33
Q

how does the arthrocentesis sample differ in SA vs ReA

A

Septic - Positive for agents. Reduced glucose level

ReA - Negative for agents. Normal glucose level

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34
Q

how does the tx for SA differ from ReA

A

Abx for sure in SA

Not for sure in ReA

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35
Q

whats the agent of syphils and describe it

A

treponema pallidum. G- spirochete. motile

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36
Q

why do you have to becareful when diagnosing syphilis

A

treponema may just be normal flora

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37
Q

which is hard chancre

A

syphilis

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38
Q

which are the GUDs

A

syphilis, chancroid, LGV, granuloma inguinale, and HSV

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39
Q

what is the virulence factor in treponema

A

lipoprotein that is similar to lps

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40
Q

how do you visualize treponema

A

darkfield microscopy. NOT gram stain

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41
Q

which pathogen is very sensitive to various environmental factors

A

treponema palllidum

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42
Q

which disorder has vascular pathologies including enarteritis obliterans and periarteritis

A

syphilis

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43
Q

which disorder has primary, secondary, latent, and tertiary stages

A

syphilis (LGV has primary secondary tertiary)

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44
Q

hard chancre

A

primary stage of syphilis

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45
Q

button like induration

A

primary stage of syphilis

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46
Q

how long before primary stage of syphilis starts

A

3-90 days

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47
Q

which can have regional lymphadenopathy

A

all GUDs

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48
Q

which dz has secondary disseminated form

A

syphilis

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49
Q

bilateral symmetrical rash of soles and palms

A

syphilis

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50
Q

condyloma lata mucous patches

A

syphilis

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51
Q

alopecia

A

syphilis

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52
Q

does syphilis have systemic signs

A

yes in secondary form

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53
Q

how long does it take for secondary syphilis to occur

A

2-6 weeks

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54
Q

what is the latent syphilis

A

post primary with positive serology bu asymptomatic

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55
Q

what is the diff between early and late latent syphilis

A

before 1 year and infectious bc relapse to secondary

after 1 year and rarely infectious bc rarely relapse to secondary

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56
Q

which are passed placentally

A

syphilis, herpes, toxoplasma, malaria

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57
Q

which is dz of thirds and what are they

A

syphilis
1/3 from secondary to 3
1/3 cured spontaneously from secondary
1/3 persistently infected but asymptomatic

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58
Q

how long does does it take for tertiary syphilis to occur

A

2-30 years later

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59
Q

what are the 3 forms of tertiary syphilis

A

cardiovascular, nerurosyphilis, and gumma syphilis

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60
Q

what is cardiovascular syphilis

A

destruxn of vasa vasorum in aortic arch

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61
Q

what is early vs late neruosyphilis

A

early may have meningitis

late has paresis (mnemonic) and tabes dorsalis

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62
Q

what is tabe dorsalis

A

destruxn of posterior columns with altered pain and temperature and argyll robertson pupil

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63
Q

what is robertson pupil

A

small, not responding to light, dilates imperfectly to mydriatics, not dilating to painful stimuli

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64
Q

what is gumma syphilis

A

benign granuomatous like lesions in many tissues (great immitator)

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65
Q

when does congenital syphilis occur

A

passed any time during pregnancy, but symptoms only 18-20th week b/c immune sys fomrs then

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66
Q

how does congenital syphilis present

A

stillborn, symptomatic newborn, infantile (secondary in adults), latent if they survive the first year, late congenital (tertiary in adults) which has Hutchinsons triad or stigmata

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67
Q

what does the late congenital syphilis form present with

A

hutchinsons triad (8th nerve deafness, corneal ulcers, hutchinsons teeth)

Also frontal bossing, bulldog jaw, higoumenakis sign, and saber shins

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68
Q

how is syphilis first seen and which is the first serology

A

darkfield microscopy and treponema SPECIFIC (FTA) is first one positive

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69
Q

where is treponema seen

A

not in blood. in lesion

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70
Q

what do non treponemal specific ab tests identify

A

Reagin

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71
Q

what are the screening tests for syphilis

A

the non treponemal specific ab tests

venereal VRDL
reagin RDR
and EIA

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72
Q

what is bad about the screening test for syph

A

low specificity

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73
Q

what are teh screening tests used for in syph

A

primary to early latent syphilis and monitor efficacy of tx

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74
Q

what are the confirmatory syphilis tests used for

A

late latent to tertiary but NOT to monitor therapy

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75
Q

which are the confirming tests for syph

A

fluorescent FTA
hemagglutination MHA-TP
EIA

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76
Q

tx for syphilis

A

benzathine penicillin G

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77
Q

backup syphilis tx

A

azithromycin but they may be resistant so tetracyclines also

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78
Q

when should you give mom tx for syphilis

A

more than 1 month before birth

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79
Q

what is jarisch herxheimer reaction

A

endotoxin like shock in response to syphilis tx that occurs within 12 hours due to dying treponema

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80
Q

in what disorder should you follow up for many months post tx

A

syphilis

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81
Q

which is a reportable dz

A

syphilis

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82
Q

cytolethal distending toxin

A

haemophilus ducreyi

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83
Q

most strongly associated with HIV transmission

A

chancroid (also chlamydia and gonorrhea)

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84
Q

bubos

A

chancroid, LGV

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85
Q

non indurated, purulent papule which ulcerate with ragged edges

A

chancroid

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86
Q

school of fish appearance on gram stain

A

chancroid

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87
Q

haemophilus ducreyi

A

chancroid

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88
Q

chlamydia trachonatis causes

A

lymphogranuloma venereum

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89
Q

L1, L2, and L3 serovars

A

LGV serovars of chlamydia trachomatis

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90
Q

homosexual males

A

LGV and herpes

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91
Q

bacteria infect macrophages and enter lymphatics

A

LGV

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92
Q

which disorder has primary, secondary, and tertiary stage

A

LGV (syphillis has latent stage also)

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93
Q

how long before the primary lesion of LGV occurs

A

3-30 days

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94
Q

how long for secondary lgv to occur

A

2-6 weeks

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95
Q

groove sign

A

lgv

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96
Q

tx for lgv

A

macrolide

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97
Q

donavanosis

A

granuloma inguinale

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98
Q

agent of granuloma inguinale

A

klebsiella granulomatis

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99
Q

how long does it take for signs of granuloma inguinale to occur

A

week to a year

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100
Q

how long does it take for signs of granuloma inguinale to occur

A

week to a year

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101
Q

what are the lesions of granuloma inguinale

A

nodular, ulcerovegetative, cicatrical, and hypertrophic/verrucous

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102
Q

pseudobubo

A

granuloma inguinale

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103
Q

elephantiasis

A

lgv and granuloma inguinale

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104
Q

safety pin bacteria

A

klebsiella granulomatis

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105
Q

dx of granuloma inguinale

A

wright or giemsa stain shows donovan bodies: clusters of organism in macrophages or monocytes

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106
Q

Agent of genital herpes

A

hsv 1 and hsv 2

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107
Q

highly infectious lesions

A

herpes

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108
Q

asymptomatic shed virus also

A

herpes, chlamydia trachomatis, and neisseria gonorrhea

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109
Q

life long latency in sacral root ganglion

A

herpes

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110
Q

incubation period for herpes

A

less than a week

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111
Q

follows nerve to skin to cause recurrent infxn

A

herpes

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112
Q

dewdrop on a rose petal lesion

A

herpes

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113
Q

often forgotten agent of urethritis

A

herpes

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114
Q

disseminated and constitutional symptoms on primary infxn

A

herpes

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115
Q

disseminated primary infxn more common in women

A

herpes

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116
Q

Multiple recurrences within a year that decrese over lifetime

A

herpes

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117
Q

what are the 3 herpes presentations in neonates that occur in the second week of life

A

SEM, disseminated, encephatlitis

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118
Q

what factors put you at greatest risk for congenital herpes

A

primary infxn, symptomatic, vaginal delivery

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119
Q

tzanck smear

A

herpes

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120
Q

syncitia formation can be seen in

A

herpes

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121
Q

viral culture is used for

A

herpes

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122
Q

only GUD caused by a virus

A

herpes

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123
Q

acyclovir doesn’t cure, but helps

A

herpes

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124
Q

medical personnel should wash hands and use protective barriers

A

herpes

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125
Q

genital warts

A

HPV

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126
Q

HPV morphology

A

nonenveloped icosahedral dsDNA virus

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127
Q

which HPV types cause genital warts

A

6 and 11

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128
Q

which HPV types cause cancer

A

16, 18, 31, 33, 45, 52, 58

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129
Q

condyloma acuminatum

A

HPV

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130
Q

cervical papillomas that may progress to neoplasms

A

HPV

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131
Q

head and neck SCC risk

A

HPV

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132
Q

Infect skin cells

A

HPV

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133
Q

affects p53 growth suppressors

A

HPV

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134
Q

infected cells have cytoplasmic vacuoles surrounded by dense cytoplasm

A

HPV

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135
Q

koilocytosis

A

HPV

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136
Q

how long for hpv

A

3-4 months

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137
Q

hard for CMI to access it due to location

A

HPV

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138
Q

cauliflower like raised lesion

A

HPV

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139
Q

pap smear shows koilocytic cells

A

HPV

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140
Q

acetowhite shows white patches

A

HPV

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141
Q

Tx of warts

A

excision, laser, chemical therapy, antivirals

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142
Q

imiquimod facilitates CMI

A

HPV

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143
Q

what is the vaccine available which covers 9 types and contains capsid but no DNA. Administer BEFORE

A

9vHPV

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144
Q

Serotypes D-K

A

Chlamydia trachomatis in urethritis/cervicitis

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145
Q

etiology of neisseria gonorrhea

A

gram - diplococcus, facultative intracellular

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146
Q

etiology of chlamydia

A

doesn’t gram stain, lacks cell wall, obligate intracellular

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147
Q

more common in women

A

GC and CT STD

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148
Q

agents of urethritis/cervicitis

A

neisseria, chlamydia, HSV sometimes

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149
Q

age groups 15-19 mainly and 20-24

A

chlamydia and GC STD

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150
Q

affects columnar cells

A

chlamydia trachomatis

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151
Q

what may asymptomatic cervicitis lead to

A

PID

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152
Q

Skenes and bartholins glands are involved with pus

A

gonococcal cervicitis

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153
Q

tender friable cervix with exudate, and dyspareunia

A

cervicitis

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154
Q

what agents cause PID

A

Chlamydia 1st
Gonorrhea 2nd
Normal flora
Can be polymicrobial

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155
Q

why does PID cause infertility

A

destruxn of fallopian tubes

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156
Q

chandelier sign +

A

symptomatic PID

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157
Q

lower abdominal pain and dysmenorrhea

A

symptomatic PID

158
Q

complications of PID

A

abscess, fitz hugh curtis syndrome and peritonitis, tubal scarring leding to ectopic pregnancy

159
Q

violin string fibrotic adhesions between liver and abdominal wall

A

fitz hugh curtis syndrome (complication of PID)

160
Q

How do you diagnose PID

A

Ultrasound/CT of fallopian tubes shows abscess or fluid filled tubes. Also violin string adhesions seen on laparascopy (gold standard)

161
Q

which gender has more asymptomatic cases of urethritis

162
Q

which has shorter incubation period, neisseria or chlamydia

163
Q

what is the difference between gonococcal urethritis vs chlamydial

A

purulent discharge in gonorrhea

more serous discharge in chlamydia

164
Q

what is uncomplicated gonorrhea

A

has not disseminated

165
Q

which are the signs of disseminated gonococcal infxn

A

fever, joint pain, rash days after a genital infxn

166
Q

what are the complications of urethritis/cervicitis that are common to men and women

A

DGI, reactive arthritis, proctitis, anorectal gonococcal dz, pharyngitis (gonococcal mainly), conjunctivitis, ophthalmia neanotorum (gonorrhea mainly)

167
Q

what leads to epididymitis

A

urethritis

168
Q

how do you diagnose gonococcal urethritis/cervicitis

A

gram stain and see G- diplococci in PMNs (careful in women b/c they have G- diplococci as NF)

Thayer martin low O2 media

169
Q

how do you diagnose chlamydial urethritis/cervicitis

A

won’t see on gram stain, but if you see more than 5 leukocytes on high power field, suspect it

170
Q

oxidase positive

A

Neisseria gonorrhea

171
Q

when treating urethritis/cervicitis, what organism must you cover

A

BOTH neisseria and chlamydia

172
Q

what is the tx for urethritis/cervicitis caused by neisseria

A

cefrtriaxone and azithromycin

173
Q

what is the tx for urethritis/cervicitis caused by chlamydia

A

tetracyclines and azithromycin

174
Q

what bacterial type predominates in the vagina as normal flora

175
Q

how is overgrowth of abcteria in the vagina prevented

A

lactobacillus produces H2O2 that maintains acidic environment

176
Q

what is the normal ratio of PMNs to vaginal epithelial cells

177
Q

what are clue cells

A

VECs covered with bacteria

178
Q

what is the order of most frequent cases to least of vaginal infxn

A

vaginosis, candidiasis, trichomoniasis

179
Q

what can alter vaginal flora

A

mensturation, oral contraceptives, douches, prolonged steroid/abx therapy, immunocompromised/diabetic

180
Q

what is trichomonas vaginalis

A

protozoan with 4 flagella and anaerobic (lacks mitochondria) that engulfs bacteria, RBCs, and PMNs

181
Q

herky jerky nondirectional motility

A

trichomonas vaginalis

182
Q

only protozoan that is transmitted sexually

A

trichomonas vaginalis

183
Q

what type of vaginal environment does trichomonas prefer

A

pH of 5-6 that occurs during menses

184
Q

what does trichomonas vaginalis infxn result in

A

asymptomatic in males usually. maybe urethritis

desquamation of vagina in females with itchy foamy discharge

185
Q

how long before vaginitis occurs from trichomonas

186
Q

what is a correlation with t vaginalis infections

A

preterm birth weights

187
Q

how do you diagnose t vaginalis

A

elevated pH, increased PMNs, negative sniff test

188
Q

what is the treatment for T vaginalis vaginitis

A

Metronidazole orally or douching to return normal flora

189
Q

what is the agent of vulvovaginitis

190
Q

which pathogen is NF of the vaginal tract

191
Q

which pathogen forms pseudomembranous patches that are yellowish white cottage cheese appearing on the external genitalia

192
Q

how do you diagnose candidal vulvovaginitis

A

normal pH, increased PMNs, negative sniff test

193
Q

how do you prevent candidal vulvovaginitis

A

probiotics of lactobacillus

194
Q

what is the tx for candidal vulvovaginitis

A

ketoconazole, nystatin, and miconazole

195
Q

whats unique about bacterial vaginitis as opposed to the previous 2

A

no inflammation

196
Q

what are the agents of bacterial vaginosis

A

mobiluncus, gardnerella vaginalis, and atopobium vaginae

197
Q

increased risk in homosexual females

A

bacterial vaginosis

198
Q

which forms biofilms

A

bacterial vaginosis, catheter associated bacteremias, infective endocarditis

199
Q

where are clue cells seen

A

bacterial vaginosis

200
Q

in vaginosis, what causes the destruxn

A

anaerobe production of carboxylase enzymes

201
Q

what has a malodorous gray discharge

A

bacterial vaginosis

202
Q

positive sniff

A

bacterial vaginosis

203
Q

how do you diagnose bacterial vaginosis

A

elevated PH, positive sniff, 20% clue cells

204
Q

which have elevated vaginal pH

A

trich and bacterial vulvovaginitis

205
Q

which have increased PMNs

A

trich and candidal vulvovaginitis

206
Q

which have negative sniff

A

trich and candidal vulvovaginitis

207
Q

what is the tx for vaginosis

A

clindamycin and metronidazole

208
Q

why is menstrual toxic shock not that common

A

gotta have the strain that produces toxin as NF in vagina, has to make enough toxin, host has to be non immunized

209
Q

what favors release of TSST1

A

menses where pH rises, decreased levels of Mg, increasd surfactant, higher O2 tension

Most of these are caused by menses and tampon use

210
Q

what is the toxin in menstrual toxic shock

A

toxic shock syndrome toxin 1

211
Q

what is the main agent of menstrual toxic shock

A

staph aureus

212
Q

what makes TSST1 toxin so devastating

A

it is a super antigen that links HLA 2 and TCR together without antigen specificity

213
Q

what are the signs of menstrual toxic shock

A

fever, hypotension, erythema on mucosal surfaces, diarrhea/vomiting, rash with desquamation, diarrhea, myalgia

214
Q

tampons

A

menstrual toxic shock syndrome

215
Q

what is a significant bacteriuria

A

more than 10^5 bacteria/mL of urine

216
Q

pyuria

A

leukocyte in urine

217
Q

what is lower uTI

A

bladder or urethral infection (cystitis/urethritis)

218
Q

what is an upper UTI

A

kidney infection (pyelonephritis

219
Q

what is a complicated UTI

A

UTI with a underlying condition that increases risk of failing therapy like diabetes or pregnancy

220
Q

what is the diff between recurrent, relapse, and refinection uti

A

recurrent - within 2 weeks

relapse - same organism within weeks or months

reinfection - different organism within weeks or months

221
Q

what is interstitial cystiti

A

bladder pain in the absence of other etiologies

222
Q

what are the types of utis

A

uncomplicated cystitis, uncomplicated pyeonephritis, complicated UTI, catheter associated UTI

223
Q

what is the most common agent of UTI

A

E coli. Candida yeasts in catheter associated

Also proteius, klebsiella, and staph saphrophyticus

224
Q

what are most UTis caused by

A

monomicrobial by gram negative rods

225
Q

which gender is more susceptible to UTI

A

females, shorter urethra

226
Q

why do neonates and infants get UTIs

A

structural defects

227
Q

why do school age women get UTIs

228
Q

why are UTIs bad during pregnancy

A

mental retardation, premature labor, neonatal death, growth retardation

229
Q

when is screening for UTI done in pregnant women (baacturia check)

A

12-16th week

230
Q

what things predispose to a uti

A

catheters, diabetes, obstruction, abx

231
Q

how do the uti agents get to the urinary tract

A

from the colon travel on skin by sweat, or more commonly hematongeously

232
Q

what is the protein that prevents pathogen attachment to the pithelium and prevents kidney stone formation

A

tamm horsfall or uromodulin

233
Q

what are the signs of UTI in children

A

fever, not feeding, suprabuci tenderness, vomiting

234
Q

what are the signs of UTI in adults

A

fever and vertigo

235
Q

what are the signso f uncomplicated cystitis

A

painful urination, blood in the urine, suprapubic pain

236
Q

what are the signs of uncopmlicated pyelonephritis

A

spiking high fevers, chills, headache, nausea and vomiting, flank pain, dysuria

237
Q

how is a complicated UTI associated with kidney stones

A

infectious agent produces urease that cleaves urea increasing the pH of urine where it precipitates magnesium ammonium phosphate and calcium carbonate

238
Q

what are the signs of complicate UTI with stone formation

A

flank pain, ammonia smelling urine, alkaline pH

239
Q

how do you diagnose a complicated UTI

A

microscopy will show magnesium ammonium phosphate crystals in urine. also can just do Xray/CT

240
Q

when might the urine appear cloudy

241
Q

how can you get a urine sample

A

mid stream clean catch, catheter, suprapubic bladder aspiration

242
Q

what is found in almost al lcases of UTI and in about half of all cases

A

pyuria

hematuria

243
Q

What should you treat UTI with

A

Sulfonamide (TMP SMX) if bacterial

Fluconazole if fungal

244
Q

what is the diff between bloodstream infxn and bacteremia

A

bacteremia is specifically bacteria in the blood

245
Q

what is the diff between spontaneous bacteremia and transient bacteremia

A

spontaneous is normal event like brushing your teet

transient is caused by trauma to mucosal surface

246
Q

what is intermittent/recurrent bacteremia

A

when a pt tests positive then negative

247
Q

what type of bacteremia occurs over a long period and is associated with infective endocarditis

A

continuous bacteremia

248
Q

what is an occult bacteremia

A

febrile kid without other symptoms but tests + for bactereia in the blood

249
Q

what is the diff between a primary and secondary blood stream infxn

A

primary has bacteria in the blood from IV or arterial line but NO DISTAL FOCI

secondary has bacteria in the blood subsequent to an infxn at another site

250
Q

what in our body fights off bactermeia

A

liver and spleen

251
Q

what are the main agents of bacteremia

A

staph aureus (not polyclonal), coag negative staph (polyclonal), enterococci, GNR, strep

252
Q

what are some causes of bacteremia

A

catheters, UTIs, dz

253
Q

what are the leading causes of bacteremia in neonates and elerly

A

Neonates is Strep agalactiae followed by E coli

Elderly is GNR

254
Q

how do you diagnose bacteremia

A

take large blood samples at least twice separated by time and from 2 different sites

255
Q

why do you have to take multiple samples of blood in cases of bacteremia

A

they could have an intermittent form where it goes and comes

also they probably don’t have that much in their blood or they would be in shock so just to make sure you don’t miss any

256
Q

what are the definition of sepsis

A

life threatening organ dysfunction due to a dysregulated host response to infxn

patients having 2 of the 3: tachypnea, AMS, low BP

257
Q

what is septic shock and how is it defined

A

septic shock is a subset of sepsis in which vasopressors must be administered to maintain BP and lactate levels are elevated after fluid resuscitation

258
Q

what is infective endocarditisi

A

microbial invasion of the heart endothelium or valve with continual shedding of organism into the bloodstream

259
Q

what are the three forms of infective endocarditis

A

native valve endocarditis, prosthetic valve endocarditis, intravenous drug abuse

260
Q

which is the most common form of infective endocarditis

A

native valve endocarditis

261
Q

what are the agents of native valve endocarditis

A

staphs, strep, bacteroides, enterococci, GNR, etc.

262
Q

what are predisposing factors for native valve endocarditis

A

prior heart conditions

263
Q

what causes a native valve endocarditis

A

bacteremia

264
Q

which valves are most commonly affected in native valve endocarditis

A

mitral and aortic

265
Q

what causes a prosthetic valve endocarditis

A

early form is caused by a recent valve surgery

late form is caused by bacteremia

266
Q

what area is at greatest risk for iv drug abuse related infective endocarditis

A

inner city peeps

267
Q

which valve is typically involved with iv drug abuse infective endocarditis

268
Q

what causes a iv drug abuse infective enedocarditis

A

bacteremia from drug use

269
Q

what are the main agents of prosthetic valve endocarditis

A

staph, strep, GNR etc.

270
Q

what are the main agents of IV drug abuse infective endocarditis

A

staph and coag negative staph

271
Q

which is the most common to least common form of infective endocardiits

A

native, prosthetic, IV drug abuse

272
Q

which valves are most commonly involved in endocarditis from greatest to least

A

mitral, aortic, tricuspid

273
Q

what do bacteria colonize on in infective endocarditis

A

nonbacterial thrombus that forms from fibrin deposition on an arterial defect

274
Q

what are the comlications of infective endocarditis

A

embolus flicking off, impaired valvular function, continuous bacteremia, type 3 vasculitis

275
Q

what are the two major forms of infective endocarditis

A

subacute and acute

276
Q

what are the signs and symptoms of subacute

A

weeks to months long infection before death with fever, murmurs, janeways lesions, oslers nodes etc. due to type 3 hypersensitivityu in vessels

277
Q

what is the main agent of subacute IE

278
Q

what is a janeway lesion

A

painless petechial lesons on palms and soles

279
Q

what are oslers nodes

A

painful petechial lesions on fingers and toes

280
Q

what are the signs and symptoms of acute IE

A

may be asymptomatic or symptomatic but it progresses over days until death

signs are frequently embolic stuff causing ischemia like stroke, heart attack, liver failure etc. with fever of course and heart murmur

281
Q

how do the signs and symptoms of subacute differ from acute

A

acute doesn’t have weight loss, anemia, splenomegaly, etc. b/c it happens so fast

282
Q

what agents cause acute IE

A

high virulence bacteria (not strep) but staph aureus, coag negative strep, and GNR

283
Q

what requires 10x the MBC parenterally for 4-6 weeks to get rid of

A

infective endocarditis, meningitis, osteomyelitis

284
Q

how do you diagnose infective endocarditis

A

transthoracic or transesophageal echo

285
Q

what are the unique oropharyngeal flora that may cause infective endocarditis

A

HACEK

haemophilus
aggregatibacter
cardiobacterium
eikenella
kingella
286
Q

what agent causes leishmaniasis

A

Leishmania donovani

287
Q

what is leishmania donovani

A

obligate intracellular protazoan

288
Q

what can make leishmania donovani more virulent and less susceptible to treatment

A

the leishmania virus

289
Q

who is susceptible to leishmaniasis

A

travelers to middle east or immigrants from there

290
Q

which is divided into old world and new world

A

leishmaniasis

291
Q

which is passed by sandflies

A

leishmaniasis

292
Q

which has dogs as a reservoir

A

leishmaniasis and chagas

293
Q

what cells are infected by leishmania donovani

A

reticuloendothelial (macrophages, monocytes, Langerhans)

294
Q

what is the pathogenesis of leishmaniasis

A

sandfly bites. promastigote goes into macrophage cytoplasm and turns into amastigote. macrophage lyses and amastigote released. disseminates via lymphatics to spleen, liver, and bone. new sandfly bites and gets the amastigote

295
Q

how can leishmaniasis be passed

A

congenitally, transfusions, sexual intercourse

296
Q

what immunity is necessary for leishmaniasis

297
Q

what are the 3 forms of leishmaniasis in regards to immunity

A

cutaneous (Th1)
diffuse (Th2)
mucocutaneous (mononuclear)

298
Q

what can be grouped by dz it causes or geographic location

A

leishmaniasis

299
Q

what are the 3 clinical forms of leishmaniasis

A

visceral dz, mucocutaneous dz, and cutaneous dz

300
Q

how long does it take for visceral leishmaniasis to occur

A

months to years

301
Q

how does visceral leishmaniasis present

A

fever, weakness, hemorrhaging, anemia, diarrhea

302
Q

what is post kala azar dermal leishmaniasis

A

skin lesions present months to years after a patients recovery from visceral leismaniasis

303
Q

who is susceptible to viscerotropic leishmaniasis

A

GIs from desert storm

304
Q

how do cutaneous and mucocutaneous leishmaniasis differ from visceral

A

they lack systemic signs

305
Q

what is the incubation period for cutaneous leishmaniasis

A

1-3 months

306
Q

what does the lesion of cutaneous leishmaniasis look like

A

a painless non pruritic papule that increases in size

307
Q

what are the two types of cutaneous leismaniasis

A

localized, diffuse (has multiple widespread), recidivans

308
Q

what is leishmaniasis recidivans

A

recurrence of infxn years later at the site of original infxn. Usually on the face

309
Q

how does mucocutaneous leishmaniasis differ from cutaneous

A

cutaneous lesion that spreads to oral and nasal mucosa causing a disfigurement

310
Q

what is present in the lesions of mucocutaneous leishmaniasis

A

mononuclear cells but few parasites

311
Q

how do you diagnose leishmaniasis

A

travel history and biopsy of bone marrow, spleen, lymph node, liver, or other tissue with giemsa stain showing amastigotes in macrophages. Also leishman intradermal skin test

312
Q

which has a monocytopenia occur followed by a pancytopenia

A

leishmaniasis

313
Q

what is the tx for leishmaniasis

A

combination therapy of amphotericin B, pentavalent antimony, miltefosine, paromomycin etc.

314
Q

what is the agent of Chagas

A

Trypanosoma cruzi

315
Q

what is another name for Chagas

A

american trypanosomiasis

316
Q

who is susceptible to trypanosomiasis

A

central and south americans

317
Q

what is the etiology of trypanosome cruzi

A

C or U shaped protozoan hemoflagellate that is obligate intracellular

318
Q

what has a vector that is the reduvid bug

A

trypanosome cruzi

319
Q

what ist he pathogenesis of chagas

A

reduvid bug bites you and poops at the same time. invade cytoplasm of local host cells. replicate and turn into trypomastigotees. lyse the cells they are in and disseminate to the myocardium and CNS. new bug bites and gets the trypomastigotes

320
Q

what are the complications of chagas

A

megadisease (megacolon/megaesophagus)

321
Q

which organ is most commonly affected in chagas

322
Q

what are the 3 forms of chagas disease

A

acute, intermittent, and chronic

323
Q

how does acute chagas present

A

asymptomatic or

with local nodule called a chagoma, romanias sign (conjunctivitis with edema), and fever, myocarditis, etc if parisitemia

324
Q

when does chronic chagas disease occur

A

years after the acute dz

325
Q

how does chronic chagas present

A

biventricular enlargement and megadisease

326
Q

how is chagas diagnosed

A

motile parasites seen in blood exam

327
Q

what is thet x for chagas

A

nifurtimox and benzidiazole

328
Q

what is the agent of African trypanosomiasis and its etiology

A

trypanasoma brucei is a S shaped protozoan hemoflagellate that is obligately EXTRACELLULAR

329
Q

what is another name for African trypanosomiasis

A

African sleeping sickness

330
Q

which pathogen is obligately extracellular

A

trypanosome brucei

331
Q

what is the vector for African sleeping sickness

A 
tsetse fly
subspecies gambiense (west)
subspecies rhodesiense (east)
332
Q

what is the pathogenesis of African sleeping sickness

A

tetse fly bites you and injects into blood. parisetemia occurs after local multiplication. long slender form changes to short stumpy form and new insect bites

333
Q

which form of trypanosome btrucei does not divide and is adapted to the insect

A

short stumpy form

334
Q

what is the immunity against trypanosome brucei

A

antibodies against the variant surface glycoprotein

335
Q

which pathogen creates antigenic variants of its surface proteins

A

trypanosome brucei

336
Q

what are the different stages of African sleeping sickness caused by the gambiense fly

A

primary lesion, hemolymphatic stage, and meningoencephalitic stage

337
Q

what are tye symptoms of gambiense fly associated African sleeping sickness

A

primary lesion - painful chancre at bite site
hemolymphatic stage - posterior cervical lymph nodes involved (winterbottoms sign)
Meningoencephalitic stage - meningoencephalitis with kerandels sign and difficulty arousing

338
Q

what is kerandels sign

A

prolonged sensation to pain present in African sleeping sickness caused by gambiense fly

339
Q

what is winterbottoms sign

A

posterior cervical lymphadenopathy seein in African sleeping sickness caused by gambiense fly

340
Q

when can trypanosomes be found in the blood in African sleeping sickness

A

during the fever

341
Q

how does rhodesiens version of African sleeping sickness differ from gambiense

A

more rapid progression with myocarditis and severe febrile CNS illnesses occurring in weeks with early deathj

342
Q

How do you diagnose African sleeping sickness

A

collect blood during fever and examine under microscope

343
Q

what I tx for African sleeping sickness

A

prior to CNS involvement: suramin or pentamidine

after CNS involvement: malasoprol or eflornithine

344
Q

which has a toxic tx

A

African sleeping sickness

345
Q

What is the etiology of the agent of Toxoplasmosis

A

toxoplasa gondii an obligate intracellular protazoan

346
Q

what cells does toxoplasma gondii invade

A

nucleated cells

347
Q

what are the three forms of toxoplasma gondii

A

trophozoite - actively proliferates in all tissues
tachyzoite - actively proliferates in macrophages
bradyzoite - found in pseudocysts in muscle and brain

348
Q

what is the 2nd most common cause of CNS infxn in AIDS pts

A

Toxoplasma gondii

349
Q

what is the leading cause of death attributed to foodborne illness in the US

A

Toxoplasma gondii

350
Q

Toxoplasma is found in what animals

A

rodents and birds
Felines - definite host
humans - intermediate host

351
Q

what are some of the main ways toxoplasma gondii is passed

A 
undercooked meat
inhalation (children)
blood transfusion
direct spread
transplacentally
352
Q

where is toxoplasma commonly found

A

US and europe

353
Q

how does toxoplasma usualy present in an immune competent host

A

asymptomatic

354
Q

what is the life cycle of toxoplasma

A

cat eats trophozoite/tachyzoite which replicates in the intestinal epithelium and is pooped out. Human eats cat fece or cysts in meat which go to epithelium and replicate and convert to trophozoites. These multiply and infect adjacent cells and macrophages. They may spread by lymph or blood to other organs. They are encysted for years and come out when CMI wanes.

355
Q

What organs are affected by toxoplasma

A

CNS mainly
eyes
lungs
skeletal muscle

356
Q

what does the CMI response do to toxoplasma gondii

A

encysts it in the visceral organs where it may stay for years. Also mainly CD8 and CD4 handle it by producing IFN gamma that prevent replication

357
Q

how does symptomatic toxoplasmosis present like

A

mononucleosis like syndrome of fever, myalgia, splenomegaly, and lymphadenoathy

358
Q

how does severe toxoplamosis present

A

posterior uveitis and myocarditis,

359
Q

how logn does it take for severe toxoplasmosis to occur

360
Q

what has to occur in order for toxoplasmosis to occur congenitally

A

the mom has to be affected DURING the pregnancy. NOT before

361
Q

when is the risk of toxoplasma infection to the child in utero greatest

A

during the 2nd and 3rd trimester

362
Q

when is the risk of toxoplasmma disease to the child in utero greatest

A

1st trimester

363
Q

what is the result of congenital toxoplasmosis

A

90% asymptomatic most of the time or vision/hearing problems later

10% death or severe disease of the newborn with the tetrad of:
retinochoroiditis (most common)
hydrocephalus
convulsions
intracerebal calcifications
364
Q

how is toxoplasmosis diagnosed

A

IgM and IgG presence

Sabin-Feldman dye test

TORCH

365
Q

tx for toxoplasmosis

A

pyrimethamine and sulfonamides target tachyzoites

spiramycin also for pregnant peeps

366
Q

how do you prevent toxoplasmosis

A

throw cat feces away promptly and cook meat

367
Q

what is the agent of schistosomiasis

A

schistosoma

368
Q

what is schistosoma

369
Q

what are the 3 schistosoma agents and their differences

A

schistosoma mansoni - release eggs in feces
schistosoma japonicum - release eggs in feces
schistosoma haematobium - release eggs in URINE

370
Q

What is the life cycle of schistosoma mansoni

A

snail releases cercariae which penetrate human through hair follicle. Schisosomula migrate through the lungs to the the inferior mesenteric veins where male and female worms reside. Ova are produced and leave in feces. Ova go to fresh water and release miracidum where it penetrates a snail

371
Q

what is the immune response to schistosomiasis

372
Q

What is the main problem with schistosomiasis

A

eggs deposit and host has a granulomatous response that causes fibrosis and tissue destruction

373
Q

What are the clinical manifestations of schistosomiasis

A

schistosomal dermatitis - itchy rash at penetration site
katayama fever
Trapped in liver veins with granulomatous response

374
Q

how long does it take for katayama fever to occur and what is it

A

4-8 weeks

an infxn usually by s japonicum that results in fever, myalgia, headache, N/V/D, a cough from lung invasion, toxic hepatitis, and intestinal hemorrhaging with pseudodysentery

375
Q

what is the tx for schistosomiasis

A

praziquantel

376
Q

what is another name for schistosome dermatitis

A

swimmers itch or claim diggers itch

377
Q

what animal is associated with schistosome dermatitis

378
Q

what occurs in schistosome dermatitis

A

larvae penetrate human tissue and die there causing a severe allergic dermatitis

379
Q

what are the agents of malaria

A 
plasmodium vivax
plasmodium falciparum
plasmodium malaeriae
plasmodium ovale
plasmodium knowlesi
380
Q

what cells do plasmodium infect

381
Q

what is the vector for plasmodium

A

anophele mosquito

382
Q

what confers resistance to p falciparum

A

Fetal Hb, Hb S, Hb C, Sickle cell, G6PD Deficiency

383
Q

what confers resistance to p vivax

A

duffy blood group negative

384
Q

what is the lifecycle of plasmodium

A

mosquito bites and it invades the liver. they invade hepatic cells and transofrm into trophozoites and then schizonts. incubation period occurs and then liver cells rupture releasing merozoites. merozoites infecct RBCs and become trophozoites.RBC becomes a schizont containing many merozoites. RBC ruptures and releases merozoites causing malaria symptoms. new mosquito bites and ingests male and female gametocytes

385
Q

when does immunity develop to malaria

A

after multiple exposures to the same strain

386
Q

what are the clinical manifestations of malaria

A

high fever with chills and rigors when RBCs rupture

387
Q

what are the complications of malaria

A

p malariae - nephrotic syndrome

p falciparum - sticky rbcs causing ischemia. Blackwater fever. Stillbirths. Cerebral malaria. Algid malaria

p vivax and p ovale - relapse

388
Q

what is blackwater fever

A

Sudden massive hemolysis which results in hemoglobinuria and ischemia in several organs

389
Q

what is algid malaria

A

characterized by low temperatures, feeling cold, severe diarrhea, and weakness

390
Q

what is the diagnosis for malaria

A

blood smears to ID species and see the percent of RBCs infected

Antigen dipstick to check LDH levels

391
Q

what is the tx for malaria

A

antimalarials like Chloroquine (falciparum is resistant) which destroys parasites in blood and Primaquine which destroys parasites in liver

P falciparum is what you want to make sure you treat for if you are not sure what it is

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