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Quarter 3 Finals > Micro > Flashcards

Micro Flashcards

1
Q

Cryptococci

A

Can resolve on own in normal pts, PROBLEMATIC in immunocomp

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2
Q

Cryptococci reservoir

A

Soil, bird poop

Not communicable person to person

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3
Q

Cryptococci

A

Skin or pulm –> CNS Meningoencephalitis (fatal)

Inhalation of desiccated yeast cells

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4
Q

Cryptococci

A

India ink on direct exam(yeast)
Sabaroud’s & Potato dextrose agar (SDA or PDA culture)
Growth on CGB medium

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5
Q

Crypto most likely pathogen

A

Cryptococcus Neoformans

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6
Q

Cryptococcus neoformans: Virulence Factors

A

Diphenol oxidase forms melanin from phenol containing subst
Ability to grow at 37C
Capsule evades phago

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7
Q

Crypto clinical sx

A

Pulmonary: No sx, OR flu-like
Disseminated: Meningitis, Crypto skin lesions

(C. Gattii: more extensive infections)

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8
Q

Toxoplasmosis Gondii

A

Foodborne illness

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9
Q

Toxoplasmosis Gondii

A

Usually not a problem in normal pts, PROBLEMATIC in Immunocomp and Pregnant

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10
Q

Triad of sx in Congenital Toxoplasmosis

A

Chorioretinitis (eye)
Hydrocephalus
Intracranial calcifications

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11
Q

Toxoplasmosis has 2 forms

A

Trophozoite (Tachyzoite and Bradyzoite)

Cyst (INFECTIOUS)

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12
Q

Toxoplasmosis subtypes of Trophozoites: Tachyzoite and Bradyzoite

A

Tachyzoite: acute dz, actively proliferating
Bradyzoite: chronic dz, slowly replicating

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13
Q

Toxoplasmosis subtypes of Cysts: Zoitocyts and Oocyst

A

Zoitocyst: tissue type that contains bradyzoites
Oocyts: sexual stage in Cats

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14
Q

How does Toxoplasmosis generally spread through Foodborne illness?

A

Via Zoitocyst (the tissue type containing bradyzoites)

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15
Q

Toxoplasmosis Gondii dx

A

Difficult to get samples
ELISA: IgG, IgM in pregnant mother
PCR: detect parasite DNA in amniotic fluid

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16
Q

Prevent Toxoplasmosis

A

Cook meat thoroughly
Wear gloves/ wash hands after gardening
Keep sandbox covered
Do not allow pregnant mothers to clean litter box- stay away from cats bc they are evil

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17
Q

Naegleria Fowleri

A

Soil and Fresh water
Lake Havasu- rare brain infection
Amoeboid is the DANGEROUS form

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18
Q

N. Fowleri

A

Cyst and

Trophozoite (flagellate and amoeboid*)

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19
Q

N. Fowleri

A

Can cause PAM in HEALTHY pts

Travels olfactory nerves –> brain, eats RBC, WBC, olfactory bulbs, and brain tissue

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20
Q

N. Fowleri

PAM!

A

1-14 d post exposure

Often death within 2 wks of sx onset

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21
Q

N. Fowleri dx

A

Clearing zone on E.Coli agar (takes long)- Flagellated form is confirmation

Wet mount for motile Amoeba
CSF findings
PCR test in the making

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22
Q

N. Fowleri, Trophozoite subtypes

  • Flagellate
  • Amoeboid
A

Flagellate: INFECTIOUS, enters nasal passage then transforms into–>
Amoeboid: DANGEROUS, DESTRUCTIVE, travels along olfactory bulb to brain

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23
Q

Acanthamoeba spp

A

Enter through break in skin OR Lower respiratory tract

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24
Q

Acanthamoeba spp

A

Soil and Contact lens

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25
Q

Acanthamoeba spp

A

Trophozoite (INFECTIVE, spiked pseudopodia) and

Cyst (3 layered wall, resistant to environment)

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26
Q

3 clinical syndromes of Acanthamoeba spp

A
  1. GAM/GAE- Granulomatous Amoebic Meningoencephalitis (100% mortality)
  2. Ocular Acanth/ Keratitis and Uveitis
  3. Disseminated dz
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27
Q
  1. GAM/GAE of Acanthamoeba
A

Frm break in skin or inhaling cyst

Sx: CNS, flu-like, Parenchymal (lung) edema, DEATH

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28
Q
  1. Ocular Acanthamoebiasis
A

After trauma to eye
Ulcer and pain (might look like Herpes)
Blurred vision, FB sensation

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29
Q

Acanthamoebiasis

A

Most ppl are resistant

Mostly PROBLEMATIC for Immunocompromised

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30
Q

Acanthamoeba dx

A

Both forms (Tropho and cytst) can be seen in tissue sections
Corneal scrapings
GAE-post mortem brain biopsy

NO POINT to examine CSF

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31
Q

Balamuthia Mandrillaris

A

Baboon dz

AGGRESSIVE, both forms (Tropho and Cyst) are INFECTIOUS

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32
Q

Balamuthia Mandrillaris

A

Can infect healthy person

Enters via Skin break or Respiratory

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33
Q

Balamuthia Mandrillaris infections

A

Healthy person: PAM

Immunocompromised: GAE

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34
Q

Balamuthia Mandrillaris sx

A

Face paralysis, difficulty swallowing
Seizures
Double vision

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35
Q

Balamuthia Mandrillaris feeds on other Amoeba… co-infection

A

With Legionella, you are screwed

Allows Legionella to txr to be 1000x more virulens–> CNS and Respiratory complications

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36
Q

Forms of Balamuthia Mandrillaris (Both are infectious)

A

Trophozoite: flat pseudopodia for locomotion
Cyst: 3 layered wall

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37
Q

Balamuthia Mandrillaris

A

Soil organism

Southern states and Latin america

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38
Q

Balamuthia Mandrillaris dz

A

Cyst and Tropho can be seen in tissue sections

Culture only works as Co-culture with Primate liver cells or Human brain cells

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39
Q

Tetanus

A

“Lowjaw” and “Trismus”

Death usually d/t Respiratory or Cardiac failure

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40
Q

Tetanus vaccine

A

Routine DTap and Td

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41
Q

Tetanus tx

A

Human tetanus immunoglobulin (HTIG) will neutralize toxin

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42
Q

Clostridial infections (2 subtypes)

A

C. Tetani-Tetanus
C. Botulinum- Botulism

Both are Neurotoxins and ANAEROBES

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43
Q

Clostridial infections: Tetanus and Botulinism

A

Gram (+) Bacilli
Environmentally resistant spores
Exotoxins: imp in dz progression

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44
Q

Tetanus spores

A

“tennis racket” appearance

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45
Q

Tetanus dz can arise from

A

Contaminated soil or Human/animal feces

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46
Q

Ppl at risk for Tetanus

A

Newborns, IVDU

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47
Q

Tetanus pathogenesis

A

Trauma to skin allows entry of spore

Extent of dz depends on site of infection and infectious dose

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48
Q

Tetanus

A

Bacteria remains local but if multiplies and releases Tetanospasmin (potent exotoxin), this can be absorbed by local nerve endings and transported thru neurons, blood, and lymph

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49
Q

Clinical forms of Tetanus (3 subtypes)

A

Generalized (most common)
-includes neonatal infection of umbilical stump
-broken skin
Localized (uncommon)
-muscle spasm confined close to injured area, immunocompromised
Cephalic (rarest)
-assoc w/lesions to head/face/ear. only affects face, but can progress

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50
Q

Tetanus clinical sx

A

Severe dz, toxin –> cramping, twitching, spasm of muscles

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51
Q

Tetanus clinical sx

A

HA, trouble swallowing, fever, sweating, Clenched jaw: “Risus Sardonicus”, arched back

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52
Q

Tetanus extremity sx

A

Flexed arms

Extended legs

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53
Q

Dx of Tetanus (early is vital!)

A

Clinical findings more reliable than labs

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54
Q

Botulism

A

Bacillus has distended shape
Great heat resistance

Spores in soil, GI tract of birds, fish, mammals

Food poisoning assoc w/contaminated foods

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55
Q

Botulinim toxin (A-H)

A

A and B: Human dz

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56
Q

Botulinum toxin is Neurotoxic on chromosome

A

Prevents ACh from being released –> Flaccid paralysis

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57
Q

Botulinum toxin type H

A

Considered the most deadly substance ever
Inhaling only 13 ng or injecting ONLY 2 ng will kill adult

NO standard anti-toxin
(found in a strain that also produces type B)

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58
Q

3 Clinical forms of Botulism

A

Infant: ingest spores, 70% cases, colonize in intestine that has no established gut flora yet

Foodborne: ingested toxin, canned foods

Wound: spores reproduce in Anaerobic environment, IVDU

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59
Q

Botulism sx

NO FEVER

A

Infant: lethal (sudden infant death)

Foodborne: Gi disturbance, Toxemia, Eventual neuroparalysis

Wound: Neuroparalysis

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60
Q

Do you have a fever with Botulism?

A

NO

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61
Q

Dx of Botulism

diff bc similar presentation to many other dz

A

Confirmation related to toxin presence- stool sample

Tx: Antitoxin to neutralize

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62
Q

Dx of UTI

A

Microscopy: 2-5 WBC or 15 bacteria per high power

Dipstick test

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63
Q

E. Coli

A

Most common cause of UTI

Caused by UPEC: Uropathogenic E. Coli strains

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64
Q

E. Coli

A

Gram (-) bacillus, flagellated

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65
Q

UPEC E. Coli virulence factors

A

P. Fimbrae (pili) and Dr adhesins bind to uroepithelial cells and RBC

Produce a and b-hemolysins which lyse both types of cells

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66
Q

UPEC E.Coli

A

can produce K (capsular) antigen- typically in upper UTI and Chronic UTI d/t increased biofilms

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67
Q

Proteus spp (UTI)

A

Proteus vulgaris most common for UTI

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68
Q

Proteus Vulgaris cause of UTI

A

Nursing home/hospitals
(nare of hospital staff)
Can be part of normal flora

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69
Q

Proteus Vulgaris

UTI

A

“Swarming” on culture agar

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70
Q

Proteus causing UTI

A

Organism spread –> Sepsis

Produces UREASE and makes urine more Alkaline

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71
Q

Proteus causing UTI

A

Urease makes urine more alkaline –> Struvite Stones

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72
Q

Proteus UTI

A

Struvite stones

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73
Q

S. Saprophyticus causing UTI

A

Gram (+)
coag negative

Sexually active females
“Honeymoon cystitis”

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74
Q

S. Saphrophyticus causing UTI

A

2nd leading cause of UTI
sexually active Females
(normal flora of female genital tract)

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75
Q

S. Saphro causing UTI

A

Organism not very virulent
Has ADHESINS (lactosamine)
No exotoxins
Difficult to dx bc little number of bacteria present

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76
Q

How to differentiate S. Saphro causing UTI from other Coag negative organisms

A

Novobiocin resistance

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77
Q

S. Agalactae causing UTI

A

AKA Group B strep (GBS)

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78
Q

S. Agalactae (Group B Strep) causing UTI

A

Gram (+) coccus

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79
Q

S. Agalac (GBS) causing UTI

A

Gray-white colony w narrow zone of Beta-hemolysis

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80
Q

S. Agalac (GBS) causing UTI

A

infections in adults mostly only affects IMMUNODEFICIENT

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81
Q

S. Agalac (GBS) virulence factors

A

Capsular polysacch
Hyaluronidase
Collagenase
Hemolysin

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82
Q

Dx of S. Agalac (GBS)

A

Detection of CAMP factor

Definitive: isolation from blood, urine, CSF

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83
Q

Ulcerative STDs

A

Syphilis
Chancroid
Herpes

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84
Q

Non-ulcerative STDs

A

Gonorrhea
Trich
Chlamydia

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85
Q

Trepenoma pallidum causes:

A

Syphillis

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86
Q

Haemophilus Ducreyi causes:

A

Chancroid

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87
Q

Syphillis

A

Requires mammal host

Spirochete with slow rotational motility

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88
Q

Syphillis virulence factors

A

Fibronectin coat

Lesions are result of Inflammatory Respone

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89
Q

Syphilis

A

Only a HUMAN pathogen

Spread: usually STD, also needle sharing, lesion near mouth, MOTHER TO BABY

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90
Q

Clinical stages of syphillis

A

Primary: Chancre, if untreated heals in 3-8 wks w/ Fibrosis
Secondary: Maculopapular rash, Condyloma lata (warts)
LATENCY?? Or–>
Tertiary: NEURO, CARDIO, and Skin GUMMAS

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91
Q

Chancre (Primary Syphillis)

A

Thin, gray exudate
Base smooth
Border raised, firm, and indurated

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92
Q

Tertiary Syphillis

A

Neurosyph: cortical degeneration
Cardiovasc syph: aneurysm of ascending aorta
Gumma: skin, bones, joints

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93
Q

Congenital syphilis

A

Maculopap rash
Nasal obstruction w/mucoid discharge (infectious)
Osteitis of nasal bone
Neurosyphilis

+HUTCHINSONs TRIAD

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94
Q

Congenital syphilis

“Hutchinson’s Triad”:

A

Notched incisors, interstitial keratitis, 8th nerve deafness

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95
Q

Hutchinsons triad of Congenital Syphilis

Simple version

A

Incisors, Keratitis, Deaf

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96
Q

Dx of Syphillis

A

Darkfield microscopy

Most diagnosed w Serology: Trepenomal test- specific antibodies are confirmatory

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97
Q

Dx of Syphillis

A

Non-trep: used as screening. If (+), then move on to Trepenomal test… FTA-ABS, MHA-TP

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98
Q

N. Gonorrhea

A

Gram (-) diplococcus w kidney bean shaped cell

PICKY (fastidious) growing requirements

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99
Q

N. Gonorrhea virulence factor

A

Plasmid and Chromosome mediated RESISTANCE to PCN, Tetracycline, Specto, and Fluoroq

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100
Q

More N. Gonorrhea virulence factors

A

Attachment via Pili
Surface proteins can dodge phagocytic activity
Bacteria alter surface property
Antigenic variation of pili

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101
Q

Gonorrhea epidemiology

A

Presence of b-lactamase positive strains (increasing #s of cases)
Major reservoir is Asymptomatic pt

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102
Q

Gonorrhea

A

Injury to cells d/t released Lipooligosacch and Peptidoglycan

Spread to other tissues via PILAR ATTACHMENT

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103
Q

Gonorrhea clinical spectrum

A

Can enter/exit any mucosal service

Female: endocervix, urethra
Male: anterior urethra with THICK mucopurulent d/c

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104
Q

Complications of Gonorrhea

A

Acute salpingitis

PID

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105
Q

DGI- Disseminated Gonorrhea Infection

A

Fever, rash, Endocarditis, Meningitis

Purulent arthritis is MOST COMMON

106
Q

Dx of Gonorrhea

A

Nucleic acid amplification (PCR): Gold standard

107
Q

Non-gonn urethritis

A

Chlamydia
Ureaplasma
Mycoplasma

108
Q

The Chlamydial diseases

A

STD
PNA
Conjunctivitis

109
Q

Chlamydia characteristics

A 
Infectious (elementary body) and 
Fragile intracellular (reticulate body)
110
Q

Chlamydia

A

Complication in female –> Salpingitis and PID

111
Q

Cervicitis, Salpingitis, and PID in women probably caused by

112
Q

Dx of Chlamydia

A

Isolation in culture: Gold standard (detect Intracellular inclusions)

113
Q

Dx of Chlamydia, non culture based test

A

NAAT preferred

114
Q

Ureaplasma urealyticuum

A

NGU
Main reservoir: genital tract of sexally active
Responsible for 50% of non-gon, non-chlam urethritis in men
Cause of Chorioamnionitis and postpartum fever in women

115
Q

Trich

A

Flagellated protozoan
Extracellular anaeroba
Trophozoite only

116
Q

Life cycle of trich

A

Establishes on the mucosa and multiplies

117
Q

Clinical sx of Trich

A

M: often no sx
F: Profuse vaginal d/c, frothy and malodorous

118
Q

Trich often leads to

119
Q

Trich dz

A

Wet mount: most commonly used

Culture: more sensitive

120
Q

BV

A

Not STD

Overgrowth of opportunistic pathogen in vagina d/t change in pH

121
Q

Criteria for BV (any combo of 3)

A 
Homogeneous secretions
Clue cells
Release of amine oder with addition of 10% KOH
pH >4.5
Curved gram (-) variable rods
122
Q

Etiology of Vulvovaginitis Candidiasis “yeast infection”

A

Usually Candida Albicans

123
Q

“yeast infection” Candidiasis

A

Thick, white, frothy d/c with NO odor

Itching, irritation, vaginal pain, soreness

124
Q

H. ducreyi

Chancroid

A

Tropical country
Typical lesion: TENDER papule with sharp margins
Soft, ragged edge

125
Q

Soft chancre of Chancroid

A

Develops quickly (3-5d)
Vesicle –> pustule/ulcer
Enlarges quickly, and multiple form
PAINFUL, bleeds readily, no induration

126
Q

Dx of H. Ducreyi (chancroid)

A

ID from ulcer or swollen lymph node

PCR method commercially available

127
Q

PID usually caused by

A

Gonorrhea or Chlamydia

128
Q

Clinical sx of PID

A 
Lower abd pain
Abnormal d/c
Painful sex
Increased menstrual pain/irregular menses
Scarring
129
Q

Dx of PID

A

Clinical +

Inflammation, fever, leukocytosis, elevated ESR

130
Q

Cholera

A

gram (-)
sensitive to acid
LARGE NUMBERS must be ingested to cause infection

131
Q

Cholera

A

A-B toxin
B(attachment)
A(enter cell)

132
Q

Cholera

A

high CAMP causes cells to secrete Cl ions, Na, other ions, water follows, outpouring from cells

133
Q

Cholera

A

rice water diarrhea
TONS of diarrhea- 20 L per day
(bacterial load in diarrhea is HUGE)

134
Q

Cholera concern

A

Severe dehydration

135
Q

Cholera most common source

A

Fecal contaminated water

136
Q

Dx and Tx of Cholera

A

Dx: Culture stool specimen
Tx: Oral rehydration
Tetracycline, Erythromycin (severe cases)

137
Q

Clostridium Difficile (C.Diff)

endospores

A

Severity ranges widely
Diarrhea, fever, abd pain, Colitis*
*pseudomembranous colitis, life threatening

138
Q

C. Diff

endospores

A

Gram (+)
Anaerobic rod
DANGEROUS bc: Forms ENDOSPORES

139
Q

Endospores of C.Diff are:

A

Highly RESISTANT to disinfectants, environment, abx

140
Q

C. Diff toxins

A

A and B disrupt ACTIN and Cell signaling, cause pseudomembranes to form

141
Q

C. Diff tx

A

Vancomycin, Metronidazole x 10d

142
Q

Campylobacter

A

Most common cause of Bacterial gastroenteritis in US (mostly C. Jejuni)

143
Q

Campylobacter

A

requires special gas concentrations

144
Q

Campylobacter

A

Usually self-limiting

PROBLEMATIC usually in HIV/immuncompromised

145
Q

Campylobacter

A

contaminated chicken

146
Q

Campylobacter

A

Low infectious dose! (not as low as E.Coli and Shigella)

147
Q

Rare complication of Campylobacter

A

Guillain-Barre syndrome
(symm weakness)
d/t Campylobacter LOS resembles human neuronal ganglioside- infection creates antibodies to this

148
Q

Dx of Campylobacter

A

Microscopy: S shaped antigen in stool sample

Antigen detection

149
Q

H. Pylori

A

Imp virulence factor: UREASE, allows it to colonize in stomach (one of the only that can do this) by making environment BASIC

150
Q

H. Pylori

A

Gastric ulcer, Gastric CA

151
Q

H. Pylori virulence factors

A

VacA- kills epithelial cell, forms pores, inflamm response

CagA- cytoxin assoc

152
Q

CagA (+) strains of H. Pylori show higher incidence of

A

Gastric CA

153
Q

30% of strains of H.Pylori in Europe are

A

Cag A negative

154
Q

Dx of H. Pylori

A

Tissue biopsy

Antigen detection* stool sample

155
Q

H. Pylori Tx

A

Omeprazole
Clarithromycin
Amoxicillin
7-10 d

156
Q

C. perfringens

A

FOODBORNE
ingest toxins contaminated meat
Toxin short incubation period: SHORT dz, 24-48 hours

Abd cramps, nausea, diarrhea, no fever

157
Q

C. Perfringens

A

24-48 hrs

Potluck meals

158
Q

Bacillus

SOIL, water, human microbio, everywhere

A

most are harmless, BUT B. Anthracis is very dangerous (ANTHRAX)

159
Q

B. cereus more common

A

Gastroenteritis
Vomiting: heat stable enterotoxin
Diarrhea: heat labile enterotoxin

160
Q

Bacillus

A

imp for creation of many Abx

161
Q

Emetic dz of Bacillus Cereus

NO FEVER

A

Heat stable (cant be killed from heat)

Contaminated rice

162
Q

Toxin bacillus stuff usually means

A

NO FEVER

not infectious, just the toxin causing issue

163
Q

Diarrheal Bacillus cereus

A 
contaminated Veggies or meat
INFECTIOUS
fever
2-3 days
Heat labile
164
Q

Bacillis cereus infections

A

No abx necessary

165
Q

Staph

A

Non motile
Enterotoxin
FOOD POISONING
Heat labile, resistant to gastric enzymes

166
Q

Staph GI food poisoning

A

Rapid onset, within 4 hrs of ingestion

Deli meat, potato salad

167
Q

Staph- food poisoning

A

Severe diarrhea, vomiting, abd pain

NO FEVER

168
Q

Giardia

A

Cross infectivity b/w animals and humans

More problematic in immunocomp

169
Q

Giardia

A

Most common intestinal parasite in world

Flagellate

170
Q

Giardia simple llfestyle

A

Trophozoite: teardrop, feeds on mucous only (does not destroy tissue/RBC)

Cyst: Infectious, passed into environment, oval

171
Q

Giardia lifestylee

A

Ingest cyst
Cysts escapes in stomach –> Trophozoite form in small intestine, replicate
Back to cyst in large intestine, passed to environment

172
Q

Where is highest incidence of Giardia in US?

A

Western states (rocky mountains) contaminated water

173
Q

Giardia

A

Can be STI
Diarrhea- no blood
Vit B12 deficiency dt malabsorption

174
Q

Dx of Giardia

A

Stool sample

ELISA detect Giardia antigen 65

175
Q

Amoebiasis

A

Can –> Colitis and liver abscess

Most cases asympto

E. Histolytica is most common form

176
Q

E. Histolytica

A

Ingest Cyst and then Trophozoite colonizes mucosa of colon- can pass in feces OR INVADE mucosal barrier and disseminate into bloodstream

177
Q

Amoebiasis: E. Histolytica

A

Fecal contamination of food and water

High risk: children, pregnant, malnourished, immunocompromised, oral-anal sex

178
Q

E. Histolytic can be caused by a small number of cysts

A

BLOODY stools–> d/t ulcers in RUQ

Death: peritonitis, cardiac failure, exhaustion

179
Q

Amobeba: E. Histolytica is pretty dangerous

A

Ulcers
Bloody stool
Death

180
Q

Amoeba: E. Histolytica Virulence Factors

A

Lectin: adhesion
Phospholipase: disrupt membrane
Amoebapore: lysis
Cysteine protease: degrade everything

181
Q

Crypto diarrhea

A

Mainly affects children

Self limiting in normal healthy pts

182
Q

Cryptosporidium diarrhea

A

Oocyts: infectious
Sporozoites: bind to intestinal cells

183
Q

Crypto diarrhea

A

Thin walled oocyst: Asexual reinfeciton

Thick walled ooccyst: Sexual, shed into environment

184
Q

Crypto diarrhea

A 
SERIOUS in immunocompromised
Highly infecitous
Severely wasted
~2 weeks
Bad prognosis 
Watery diarrhea cardinal sx (dehydration, weight los, fever, abdominal ipain)
185
Q

Dx of Crypto diarrhea

A

Oocyts in stool sample

186
Q

Cyclosporiasis diarrhea

A

Autofluourescent Oocyts
LARGE
Contaminated foods and veggies

187
Q

Cyclosporiasis clinical sx

A

EXPLOSIVE, NON-bloody diarrhea, rapid weight loss, profound fatigue

188
Q

Dx of Cyclosporiasis

A

LARGE oocyst in stool sample

Acid-fast, autofluorescent

189
Q

Nematode (roundworm)

A

Elongated cylindrical, tapers at both ends

Separate sexes

190
Q

E. Vermicularis (pinworm)

A

Most common worm in US

Small, whitich colored worm

191
Q

E. Vermicularis (pinworm)

A

eggs become infectious very quickly!

life cycle direct and short

192
Q

E. Vermicularis (pinworm)

A

Humans only host (children mostly affected)

Person to person, or frm environment

193
Q

E. Vermicularis (pinworm) lifecycle

A

Eggs ingested and hatch in small intestine

Pregnant female MIGRATES AT NIGHT to peri-anal region to deposit eggs

194
Q

E. Vermicularis (pinworm) clinical sx

A

Mostly no sx
Itching anal region at night
can –> Secondary Bacterial Infections, distrubed sleep, abd pain

195
Q

E. Vermicularis (pinworm) dx

A

Scotch tape method

196
Q

Soil transmitted worms- ingesting contaminated soil

A 
Ascaris lumbricoides (roundworm)
Trichuris trichiura (whipworm)
197
Q

Ascaris lumbricoides

“Roundworm”

A

LARGEST intestinal roundworm

198
Q

Ascaris lumbricoides “roundworm” life cycle

A

Ingested, travel via blood to LUNGS, then travel up trachea to OROPHARYNX, swallowed and then mature in SMALL INTESTINE (duodenum)

199
Q

Ascaris Lumbricoides “roundworm” clinical sx

A

Worm burden
BLOCKAGE
“Pulmonary Loefflers sydnrome”
Abd pain

200
Q

Pulmonary “Loefflers syndrome”

A

Ascaris Lumbricoides

“roundworm”

201
Q

Ascaris Lumbricoides “roundworm” dx

A

Stool sample (eggs)

202
Q

Trichuris trichiura “Whipworm”

ingesting soil

A

Small worms whiplike morphology

egg capsules

203
Q

Trichuris trichuria “whipworm” life cycle

A

Eggs ingested, larvae released into duodenum

Mature in colon

204
Q

Trichuris trichuria “whipworm” clinical sx

A

depends on worm burden
Heavy: painful passage of stool, Rectal PROLAPSE
Children: growth retardation, anemia

205
Q

Hookworm

A

Small worm, Adult FEEDS ON BLOOD of intestinal mucosa

206
Q

Hookworm, feeds on blood –>

207
Q

Hookworm get into body by

A

Can penetrate skin!!

208
Q

Hookworm life cycle

A

Penetrate skin, travel to LUNG, up trachea to OROPHARYNX, swallowed and mature in SMALL INTESTINE (duodenum)

209
Q

Worms that travel via blood to LUNGS, swallowed, then mature in DUODENUM

A

Hookworm
Roundworm (Ascaris lumbricoides)
Threadworms (Strongy)

210
Q

Hookworm clinical sx

A

Blood filled pruritic lesions (penetrate skin)
“Ground itch”
Continuous blood loss

211
Q

Strongyloides stercoralis “threadworms”

A

2 multiplication cycles (host or soil)

Poor sanitation

212
Q

Strongyloides stercoralis “threadworms” lifecycle

A

LUNGS, swallow, SMALL INTESTINE (Duodenum)

213
Q

Strongyloides “threadworm” clinical sx

A

Larval migration under skin
funny looking squiggly pattern
Intestinal diarrhea, pain, constipation, chronic infection

Life threatening in pts with defect in cell mediated immunity

214
Q

Strongyloides “threadworm” dx

A

Stool sample, SPUTUM of hyperinfected pt, or duodenal aspirate

215
Q

Trematude (fluke)

A

FLATTENED, leaflike
Suckers
Hemaphrodite (M and F)

216
Q

Tapeworm

A

Large worms
SCOLEX face
Eggs are IMMEDIATELY INFECTIOUS once released

217
Q

Tapeworm

A

“Taenia”

Humans are only host

218
Q

Tapeworm “Taenia”

A

Cattle, pigs
Larvae develop in muscle
UNDERCOOKED MEAT

219
Q

Tapeworm “Taenia” clinical sx

A

Most pts no sx, only one worm

Mild GI but if serious–> BLINDNESS, SEIZURE

220
Q

Cystigercosis

A

seizures, bad form of Tapeworm “taenia”

221
Q

Diphyllobothrium latum (fish tapeworm)

A

Worms VERY LONG
thousands of Proglottids
SERIES OF HOSTS required for life cycle completion

222
Q

Diphyll (fish tapeworm)

A

Great lakes, Alaska
Humans and other fish eating mammals

Infectious larvae are in the MUSCLES OF FISH

223
Q

Diphyll (fish tapeworm) clinical sx

A

Mostly asx

BUT adult worm COMPETES FOR B12

224
Q

Dx of Diphyll (fish tapeworm)

A

Anemia
stool sample
ID of worm

225
Q

Two types of Viral Gastroenteritis (acute watery diarrhea, anorexia, vomiting)

A

Norovirus

Rotavirus

226
Q

Norovirus

A

TOP CAUSE in US of gastroenteritis (90% of viral)

227
Q

Norovirus

A

Cruise ship

out of both ends

228
Q

Norovirus

A

Persistent in environment and very easily spread

NAKED virus is more persistent (protein capsule)

229
Q

Norovirus and Rotavirus dx

A

RT-qPCR (identify the RNA)

sensitive and specific

230
Q

Rotavirus

A

Common cause of Infant gastroenteritis- hospitalizations

231
Q

Rotavirus

A

5-7d of Fever and Vomiting

232
Q

Which one is more common: Norovirus or Rotavirus?

A

NOROVIRUS (cruiseship)

Rotavirus is assoc w/ infants

233
Q

Enterobacteria

A

Gram (-) rods

Fimbrae
Flagella: H antigen
Capsule: K or Vi
LPS: O antigen
Peptidoglycan
234
Q

Enterobacteria

A

Most ferment carbs –> lactid acid, how we differentiate b/w a wide array of organisms

235
Q

Enterobacteria

A

70% of UTIs

1/3 Bacteremia

236
Q

Subcategories of Enterobacteria

A

Salmonella
Shigella
E. Coli
(all gram negative)

237
Q

Enterobacteria, most are motile EXCEPT

A

Yersinia
Klebsiella
Shigella

238
Q

Enterobacteria

A

Fimbrae
Cell attachment
Horizonal sex gene transfer

239
Q

Common virulence factors of Enterobacteria

Salmonella, Shigella, E.Coli

A

Endotoxin (A component of LPS) –> septic shock

Capsule (protect from phago)

240
Q

Type 3 Secreteion System

A

Widely used by gram negative

241
Q

Salmonella (a type of Enterobacteria)

A

Primary source: contaminated food/water
Chicken
Veggies
Honey smacks

242
Q

Salmonella methods of transmission (secondary sources, after food)

A

Pet reptiles/birds
Pet chickens
Person to person

243
Q

Serotyping Salmonella

A

Based on Flagellar (H) or LPS (O) antigens

244
Q

Non-typhoidal salmonella

A

Foodborne gastroenteritis

245
Q

Salmonella Typhimurium

A

Self limiting gastroenteritis in humans

246
Q

Type 3 secretion system- Salmonella

A

How it gets in?

Actin cytoskeleton changes, bacterium engulfed, thru epithelium layer and now access to systemic sites

247
Q

Types of E.Coli

A

ETEC (entero-toxigenic)
EHEC (entero-hemorrhagic)
EIEC (entero-invasive)
UPEC (uro-pathogenic)

248
Q

ETEC: Entero-toxigenic E.Coli

A

underdeveloped countries
children or travelers
Contaminated food/water

Watery diarrhea/cramps
lasts 3-5 days, then clears

249
Q

ETEC: Entero-toxigenic E.Coli

Virulence

A

LT1- heat labile toxin
(increase cAMP)

STb- heat stable toxin
(increase cGMP)

250
Q

EHEC: Entero-hemorrhagic E.Coli

A

Foodborne intestinal illness
Aka “STEC” Shiga-toxin producing E.Coli
O157:H7 (most common serotype)

251
Q

Cattle are important reservoir for

A

EHEC, aka shiga toxin prducing E.Coli

O157:H7

252
Q

EHEC (shiga toxin producing E.Coli) virulence factor

A

Stx (shiga like toxin)
Intimin (binding)
Tir (type 3 secreted protein, inserts into cell membrane then acts as receptor for intimin)

253
Q

EIEC: Entero-invasive E.Coli

A

basically same as shigella

PROFUSE BLOODY DIARRHEA

254
Q

The Lactate (+) or (-) is what differentiates Shigella from other E.coli

A

Shigella is lac (-)

255
Q

Shigella sx

A

Severe diarrhea with blood and mucus

256
Q

Shigella spread

A

Leaves gut via M cells or dendritic cell engulfment
Replicate inside macrophage, killing cell
Invades membrane of epithelial cell

can also spread cell to cell

257
Q

Shigella virulence factor

A

Shiga toxin 1 (identical to O157:H7)

Shiga toxin 2

258
Q

Shigella and EHEC strain

A

Low infectious dose

ONLY takes 10 cells!!!

259
Q

Shigella, Salmonella, E.Coli diagnosis

A

Isolate from fecal sample

Mackonkey agar

260
Q

Shigella and Salmonella

A

Lactate (-)

261
Q

E.Coli

A

Lactate (+)

262
Q

D+ HUS

Diarrheal Hemolytic Uremic Syndrome

A

10% infections by shiga toxin producing Shigella and E.Coli

Abx use actually WORSENS infection

Quarter 3 Finals (10 decks)

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