Micro Exam 3

Front 1

The group fungi include what organisms?

Back 1

• Yeasts
• Molds
• Mushrooms

Front 2

What are aflatoxins?

Back 2

naturally occurring mycotoxins that are produced by many species of Aspergillus
One of the strongest carcinogens known

Front 3

What is the significance of ergot alkaloids?

Back 3

They come from moldy grains and rye and can cause severe health issues. they are a type of mycotoxicosis

Front 4

What does it mean for a fungi to be opportunisitc?

Back 4

It means they result from a secondary infection.

Front 5

What patients are most suseptible to opportunisitc mycoses?

Back 5

cancer (leukemia, lymphoma)
transplant
AIDS
autoimmune (lupus, arthritis)
diabetes
long-term hospital

Front 6

What risk factors increase mycoses?

Back 6

broad spectrum antibiotics
radiation
chemotherapy
corticosteroids
surgery
catheterization
Hormones

Front 7

What mycoses colonized quickly after birth can become opportunistic if not heald in check by the body?

Back 7

Candida albicans (thrush or cheilitis)
Pityrosporum ovaled (druff-producing microbe)

Front 8

What is Cheilitis?

Back 8

is a medical condition involving inflammation of the lip
Often seen with oral candidiasis patietns

Front 9

What is an example of a primary fungal pathogen? (they aren't vary common)

Back 9

Coccidiomycosis
Most considered environmental

Front 10

Are fungi eukaryote of prokaryotes? What other cellular features do they have?

Back 10

Eukaryotes
Contains erogosterol and zymosterol (in cell membrane)
Cell wall with chitin, glycan and mannin (but no peptidoglycan)

Front 11

What is Thermal dimorphic conversion?

Back 11

The ability of some fungi to grow as yeast at 37*C but as a mold at 25*C.

Front 12

How do yeast reproduce? What is their structure?

Back 12

(1) Single oval to round cell that buds to reproduce.
(2) Pseudohypha or an elongated yeast cell.

Front 13

What is a germ tube?

Back 13

(1) Elongated appendage (ie, hypha) growing from a yeast cell.
(2) Virulence factor that has adhesive and invasion functions.

Front 14

What is the structure of mold?

Back 14

Multicellular filamentous colony with potential for hyphae

Front 15

What is a hypha?

Back 15

long filament or strand of cells, which are often defined by
septa

Front 16

What organisms are classically know to have hyphe? Which do not?

Back 16

Aspergillus is septate hyphe, Rhizopus and Mucor are not hyphe-nated

Front 17

What is the name for a mat of hyphae?

Back 17

Mycelium

Front 18

What yeast is know to be polysaccharide encapsulated?

Back 18

Crypyococcus neophormins

Front 19

What is the significance of a germ tube?

Back 19

It adds virulemce bby its adherence qualities and it also has proteases which penetrate surfaces (tissues) making it hard to get rid of. can be used to identify candida

Front 20

Where do you see the following structures: germ tube
pseudohypha?

Back 20

Yeast! A budding structure

Front 21

Where do you see the features: mycelium
hypha
septum
sporangiophore
sporangium
sporangiospore
conidiophore
conidia?

Back 21

In MOLD

Front 22

What are the two asexual spore types?

Back 22

Sporangiospore
Conidium (Conidiospore)

Front 23

Describe a Sporangiospore

Back 23

Sporangium is the sack that the sporangiospores are held in. Like ballons in a bag that sits on a stalk

Front 24

Describe a Conidium (Conidiospore)

Back 24

Conidiophore: hyphal branch that bears conidia. Not in a "bag" like the sporingiospores. Tree like branching: Hypha to condidophore to phialide to conidium

Front 25

What fungi produce conidiospores?

Back 25

Penicillium and Aspergillus

Front 26

What is the appearance of athroconidium?

Back 26

Fragmented hypha of jointed spores
ex: ringworms, Coccidioides

Front 27

What is the appearance of a bloastoconidium?

Back 27

it is budding

Front 28

What does as Chlamydoconidia look like

Back 28

It has swollen hypha

Front 29

How does Microcondium appear?
Example:

Back 29

Unicellular
Trichophyton (dermatophyte)

Front 30

How does Macrocondium appear? Example:

Back 30

Multicellular: Looks like a banana or fusiform shape
Microsporum (Dermatophyte)

Front 31

What two fungi are nonseptate?

Back 31

Rhizopus, Mucor— assocaited with DM and ketoacidosis

Front 32

What are the three fungal pathogenicity typpes?

Back 32

granulomas,
hypersensitivities, or
mycotoxicoses

Front 33

What fungus is responsible for Systemic or endemic mycoses (extremely serious)?

Back 33

coccidioidomycosis

Front 34

What fungi are responsible for Superficial infestations?

Back 34

thrush and dermatophytes

Front 35

What ate the two dermatophytes learned and their classifciation?

Back 35

Macroconidia—Microsporum
Microconidia—Trichophyton

Front 36

What fungi are responsible for Subcutaneous mycoses?

Back 36

sporotrichosis and mycetoma.

Front 37

What are the main opportunisitc mycoses?

Back 37

candidiasis and cryptococcosis.

Front 38

What are candidias virulence attributes

Back 38

Adherence to tissue & prosthesis (biofilms)
Form germ tubes & hyphae (tissue invasion)
Extracellular enzymes (break down tissue)

Front 39

What mycoses is an Encapsulated pathogen?

Back 39

Cryptococcus neoformans

Front 40

What yeast could you see living inside a macrophage?

Back 40

Histoplasma capsulatum

Front 41

What type of respiration do most yeast use?

Back 41

Most are obligate aerobes (some are facultative but none are anaerobes)

Front 42

What is the difference between working with mold and yeast in the lab?

Back 42

Yeasts can be safely handled on the bench in the laboratory but working with molds usually require an isolation safety cabinet (ie, never smell a mold culture because spores may become airborne).

Front 43

What are the most common isolation media for fungi that do not readily support the growth of bacterial contaminants?

Back 43

Sabouraud and potato dextrose agars

Front 44

What are the growth rates of molds and yeasts

Back 44

• Yeasts grow rapidly
• Molds may require weeks to mature

Front 45

What stains can be done easily on yeasts?

Back 45

Gram stain & Chlorazol Black
(India ink & KOH)
10% KOH—direct observation

Front 46

What therapy might you use for Candida?

Back 46

Ketoconazole-itraconazole - it inhibits ergosterol synthesis

Front 47

what therapy might you use for systemic fungi and why?

Back 47

amphoteracin B
Targets ergosterol, causing membrane damage

Front 48

What therapy is used for dermatophytes because it tragets micrtubules interfering with mitosis?

Back 48

Griseofluvin

Front 49

how does Flucytosine work

Back 49

Interferes with DNA & protein synthesis in fungal organisms

Front 50

What therapy for dermatophytes inhibits ergosterol synthesis and targets the cell membrane?

Back 50

Terbinafine

Front 51

What antifungal can be used for both candida and spergikkus that inhibits glycan synthesis (targets cell wall)?

Back 51

Caspofungin

Front 52

What are the most common and invasive candida species?

Back 52

C. albicans
C. dubliniensis

Front 53

What is unique about Candida glabrata?

Back 53

is the only species that
forms only yeast cells
(not able to form pseudohyphae or hyphal structures)
It is resistant to AZOLES!

Front 54

When are pseudohyphae formed?

Back 54

produced when budding cells
fail to detach from each other

Front 55

What is a true hyphae?

Back 55

A germ tube formed in serum and at 37*C
Seen in (C. albicans, C.dubliniensis)

Front 56

How can you distinguish between differenf species of candida?

Back 56

Grow it on chrome argar and they grow different colors

Front 57

eWhat are the asexual reproductive features of candidia?

Back 57

Chlamydospores or
Blastocinidia

Front 58

What are the pathogenic factors of candida/

Back 58

They are great attachers if they use their germ tubes!
The secreteproteases
Phospholipases and heat shock proteins

Front 59

True or False: Candidiasis is communicable

Back 59

FALSE

Front 60

When would you see chronic mucocutaneous candidiasis?

Back 60

With a genetic defect that impaired cellular immunity. Persons would present in early child hood and experience infections in the skin and mucous membranes

Front 61

What areas would you test for candida based on where it can infect?

Back 61

– Blood-systemic candidiasis
– CSF
– Materials from removed catheters
– Tissue samples
NOT SPUTUM as it is a normal flora

Front 62

How does candidiasis stain?

Back 62

gram positive even though they aren't really gram positive organisms

Front 63

What newly emerging fungal pathogen is able to infect immuocompetient hosts?

Back 63

Cryptococcus neoformans

Front 64

What is resivoir for Cryptococcus neoformans?

Back 64

Natural reservoir Soil, bird droppings
Must be inhaled

Front 65

What mycoses lives CSF?

Back 65

Cryptococcus neoformans
It can result in meningeoencepalitis which contributes to its lethality

Front 66

What are the general gross and microscopic features of Cryptococcus neoformans?

Back 66

mactoscopically it forms creamy mucoid colonies
microscopically it shows encapsulated

Front 67

What are the pathogenicity factors of cryptococcus neoformans?

Back 67

Capsule
Diphenol Oxidase that forms melanin from phenol cotainging substances
Its ability to grow at 37*C

Front 68

What mycoses is isolated in mixed ifections by growing it on birdseed agar?

Back 68

CRYPTOCOCCOSIS

Front 69

How can you distinguish between CRYPTOCOCCOSIS gatti and CRYPTOCOCCOSIS neoformans in the lab?

Back 69

Grow them on CGB agar. Neoformans will stay yellow, gatti will turn blue

Front 70

What is the treatment for Cryptococcosis?

Back 70

Amphotericin B and Fluconazole (it can cross CNS!)

Front 71

What are the risk factors and pathogenisis of Aspergillosis?

Back 71

Immunosuppressed and DM
Spores inhaled
Can contain mycotoxicosis that cans hepatocellualr and colon carcinomas

Front 72

What mycoses forms a powdery moled that produces many small cinidia that aerosilize that can cause sever allergic reactions?

Back 72

Aspergilliosis

Front 73

What are the microscopic features of aspergillus?

Back 73

septate, hyaline hyphae (dichotomous branching), vesicule,
microconidia

Front 74

What are the pathogenicity factors of Aspergillus?

Back 74

Hyphae
Phospholipase

Front 75

Describe allergic aspergillosis

Back 75

Two Types:
1. Asthma (Type I)
2. Allergic bronchopulmonary aspergillosis (Types I, III)

Front 76

Describe An aspergilloma

Back 76

It is a fungus ball that forms in the lungs or paranasal sinuses by conidia that enter the cavity, germinate and produce hyphae in the cavity. They must be surgically removed.

Front 77

Besides the lungs, where else can you commonly find aspergillosis infections?

Back 77

Otomycosis (external otitis)
Onychomycosis
Eye inf. (conjunctival, corneal, intraocular)

Front 78

What is invasive aspergillosis?

Back 78

FATAL IF UNTREATED
Starts in the heart and disseminates to GI, brain, liver, kidney, skin and eye.

Front 79

What is the best way to diagnose Aspergillosis?

Back 79

Sputum or tissue samples

Front 80

What are the treatments for
Allergic
Aspergillioma
Superficial and
Invasive Aspergilliosis infections?

Back 80

Allergic: Steroids
Aspergillioma: surgery and amphotericin B
Superficial: Nystatin
Invasive Aspergilliosis: Dibridnment and posaconazole

Front 81

What is the main cause of Pneumocystic Pneumonia? What is the resivoir?

Back 81

Pheumocyctis jirovechi
No know resivoir

Front 82

What are the 2 morphologies of Pneumocystis jiroveci?

Back 82

– Trophozoite (Thin walled)
– Cysts (Sphericules with thiick wall that is multinucleated)

Front 83

Describe the life cycle of pneumocystis jiroveci

Back 83

1) Mature cyst has 8 intracyystic bodies
2) Cyst ruptures releasing the bodies
3) Bodies develop into trophozoites
4) Trophozoites divide
5) Each trophozoites develop into a mature cyst

Front 84

What are the sx of Pneumocystis Pneumonia?

Back 84

– Fever
– Non-productive cough
– Shortness of breath
– Weight loss
– Night sweats
– CXR shows diffuse bilateral
infiltrates

Front 85

Is pneumocystis pneumonia communicable?

Back 85

Yes, we think so

Front 86

how do you make a dx od PCP?

Back 86

CXR shows widespread infiltrated
Can finf in lung biopsy and sputum

Front 87

What is the tx for PCP

Back 87

TMP-SMZ (Trimethoprim-Sulfamethoxazole)
and possible steroids for inflammation

Front 88

When does PCP show disease?

Back 88

When humoral and cell mediated immunity fails

Front 89

Where is Coccidioidomycosis seen regionally? Where is it found?

Back 89

Southwest USA - in Soil

Front 90

Coccidioides immitis is known by what other names?

Back 90

Valley fever
San Juaquin Valley fever
and "the great imitator"

Front 91

What is the morphology of Coccidioides immiti?

Back 91

• Dimorphic spherule and mold
• Spherule w/ endospores
• Arthroconidium

Front 92

How does Coccidioides immitis look cultured?

Back 92

• White, gray, or brown colony
• Powdery or wooly colony

Front 93

Waht two antigenic factors can be usedul for immunodiagnosis of coccidiodes?

Back 93

Coccidioidin
Spherulin

Front 94

Describe the pathogenicity of coccidioides imitis

Back 94

Primay pulmonary involvement, but can look like flu or pneumonia
persons can be asymptomatic
most infections are self limited

Front 95

What is the phase like manner coccidioises crosses though after inhilation?

Back 95

Upon inhalation, the arthroconidia are transformed into
pulmonary spherules (contain endospores).
Endospores are released from spherules, and then,
endospores produce new spherules.
Septate hyphae and arthroconidia are sometimes associated
with the spherules in the pulmonary cavities.

Front 96

What is Erythema Nodosum?

Back 96

Allergic response that is marked by tender red cutaneous nodules. Delayed hypersensitivit that develops abotu 1 month after coccidiodes immitans infection. Indicator of a good prognosis because the cell-
mediated immunity is functional.

Front 97

How is Coccidioides spread?

Back 97

Not communicable (ie, no person-to-person transmission).
Airborne transmission

Front 98

What does it mean to have Disseminated coccidioidomycosis?

Back 98

systemic infection in which 15-20% of people develop skin lesions

Front 99

Waht groups are at greater risk forDisseminated
Coccidioidomycosis

Back 99

American Indians, Asians,
African Americans, & Hispanics
Preggers
Immunodificient

Front 100

What is the best way to identify Coccidioides immitis?

Back 100

• KOH for fresh samples (Athrocondia culture)
• PAS for fixed tissue (pathology lab)
• Microscopic – spherical form
• Culture – mold 25°C
• Caution – arthrospores
• IgM/IgG to coccidioidin/spherulin

Front 101

What is the treatment for Coccidioides immitis?

Back 101

• DOC – fluconazole or amphotericin B (IV for months in priary or disseminated)
Supportive care

Front 102

What is the best way to control Coccidioides immitis?

Back 102

• Dust protection
• Pave roads
• Plant vegetation
• No vaccine available :(

Front 103

What is the morphology of Histoplasma capsulatum?

Back 103

Dimorphic:
Yeast is Uninucleate budding cells
Mold is Microconidium and also shows Tuberculate macroconidium.

Microconidium
(infective stage)
Mold is White or brown cottony colony that is Slow growing – up to 12 wk

Front 104

What is the antigen for immunodiagnosis for Histoplasma capsulatum

Back 104

Histoplasmin
Produced in broth in which mycelium grows

Front 105

What it the pathogenicity/phases that Histoplasmin goes through once inhaled?

Back 105

Inhaled microconidia convert to a yeast cells. Yeast cells may be phagocytosed by alveolar macrophages and transported deeper into the body.
Often described as an intracellular mycosis of the reticulo-endothelial system.

Front 106

What are the virulence factors of Histoplasma/

Back 106

Yeast releases urease to raise pH
Interferes w/ phagolysosome killing
activity of phagolysosome

Front 107

Where is Histoplasma capsulatum seen most frequently regionally?

Back 107

Ohio & Mississippi River Valleys

Front 108

What is the best way to ID Histoplasma capslatum?

Back 108

• Microscopic – intracellular yeast
• Isolation – site of infection
• Serologic – latex agglutination

Front 109

What is the DOC for Histoplasma capslatum?

Back 109

DOC – itraconazole or amphotericin B
• Supportive

Front 110

What is the best way to control Histoplasma capslatum?

Back 110

• Dust protection
• Formaldehyde soil spraying

Front 111

What mycosis is known for its lung and cutaneous granuloma formation

Back 111

Blastomyces dermatitidis

Front 112

What is the morphology of Blastomyces dermatitidis in tissue or exudate?

Back 112

it appears as a multinucleate, budding cell (1 broad-based bud each cell).

Front 113

What is the morphology of Blastomyces dermatitidis in culture?

Back 113

hyphae bear conidia
Production of chlamydospores is possible.

Front 114

How does one get infected with Blastomyces dermatitidis?

Back 114

inhaling the microconidia soil

Front 115

What is the best way to diagnose Blastomyces dermatitidis?

Back 115

Direct microscopic examination: wet mount may show
broadly attached buds on thick walled cells (KOH smear of
sputum, pus, exudate, urine, skin, and biopsy material).

Front 116

What is the DOC for Blastomyces dermatitidis?

Back 116

DOC: itraconazole or amphotericin B.

Front 117

Where is Paracoccidioides brasiliensis prevalent?

Back 117

Predominant systemic mycosis in Latin America

Front 118

What does Paracoccidioides brasiliensis look like??

Back 118

Dimorphic.
Resembles B dermatitidis.
Yeast is characterized with thick walls and multiple buds.

Front 119

Cultures of Paracoccidioides brasiliensis at 25°C produce?

Back 119

conidia and chlamydospores.

Front 120

What it the pathogenicity of Paracoccidioides brasiliensis?

Back 120

Basically a chronic, granulomatous disease that begins in
the lungs (infective stage is inhaled) but is usually benign
and self-limited in the young. Can disseminate

Front 121

What is the virulence factor of Paracoccidioides brasiliensis?

Back 121

Virulence factor: cell wall α-glucan stimulates granulomas.

Front 122

How is Paracoccidioides brasiliensis transmitted and what is the resivoir?

Back 122

Not communicable (transmission is airborne) hides out in soil

Front 123

What is the DOC for Paracoccidioides brasiliensis

Back 123

DOC: itraconazole or amphotericin B for up to2 years

Front 124

What are dental caries caused by?

Back 124

Localized destruction of the teeth due to ACIDS produced during bacterial
fermentation of carbohydrates

Front 125

A high incidence of caries is associated with?

Back 125

High carb intake
low SES
Meth use (causes dry mouth)

Front 126

Describe Early Childhood Caries
(Baby Bottle Tooth Decay)

Back 126

Predominantly affects the front
teeth
Repeated ingestion of sweetened
liquids sugar sticks to teeth

Front 127

What Plaque Microorganisms is blamed as being an initiator of caries? Why?

Back 127

Streptococcus mutans
It has Glucosyltransferase which changes sugar to glucan which sticks strongly to teeth

Front 128

How does Lactobacillis contribute to caries

Back 128

Small part of normal flora (~1%) but when the ph is reduced by s. mutans it is able to grow even better.
Know PROGRESSOR of caries

Front 129

What is the role of Actinomyces viscosus in dental disease.

Back 129

Role is still unclear, but currently
implicated in root surface caries

Front 130

How does lactobacillis gram stain?

Back 130

Postive as do many of the other dental caries related bacteria

Front 131

What bacteria that is part of the normal mouth flora is anticarigonetic?

Back 131

Veillonella spp.
it RAISES pH in the mouth

Front 132

What is the most cariogenic sugar?

Back 132

Sucrose
It is what s. mutans uses

Front 133

What is the progression of tooth decay?

Back 133

White spot which is first sign of
demineralization
Sticky lesion
Demineralization
Fracture

Front 134

What four factors must come to together for caries to form?

Back 134

Microorganism
Diet
Host Factors
Time

Front 135

What two organisms can be used to measure/diagnose caries?

Back 135

S. mutans
Lactobacillus spp.

Front 136

What are the new preventative treatments for dental caries and what bug are they direct for?

Back 136

– Vaccination against dental caries
– Passive immunization
– Replacement therapy (probiotic therapy)

Directed at s. mutans

Front 137

What are the stages of periodontal disease?

Back 137

Healthy
Gingivitis/Periodontitis
Advanced Periodontitis

Front 138

What is the morphology of the flora in a healthy mouth?

Back 138

Mainly gram + cocci with few
spirochetes or motile rods
Predominantly facultative

Front 139

What is the morphology of the flora in a mouth with Chronic gingivitis?

Back 139

About 55% of the cells are gram + with
occasional spirochetes and motile rods

Front 140

What is the morphology of the flora in a mouth with Chronic periodontitis?

Back 140

About 75% are gram –
90% are strict anaerobes
Motile rods and spirochetes present

Front 141

What is the morphology of the flora in a mouth with aggressive periodontitis?

Back 141

About 65-75% are gram – bacilli. Few spirochetes or motile rods are present.
May be associated with cellular immune or genetic defects

Front 142

Describe Chronic gingivitis

Back 142

Inflammatory response limited to the marginal gingiva without bone loss or deep periodontal pockets
_REVERSIBLE
_Halitosis
Patients asymptomatic

Front 143

What specific organism changes do you see in ginigivits?

Back 143

Increase in Actinomyces (+),
Capnocytophaga (-),
gram – obligate anaerobes

Front 144

What specific bug changes do you see in Periodontitis?

Back 144

Increase in
Porphyromonas gingivalis (-)
and Prevotella intermedia (-)

Front 145

What is Periodontitis?

Back 145

Progression of gingivitis to include loss of collagen attachment to the tooth and bone, loss of bone, and to deep periodontal pockets
– Cause of most tooth loss in adults

Front 146

What are the two types of Periodontitis?

Back 146

Chronic periodontitis (95%_
Aggressive periodontitis (rare, may be inherited)

Front 147

What percentage of adults have periodontitis?

Back 147

70-80% of adults

Front 148

What is Porphyromonas gingivalis associated with?

Back 148

Chronic Periodontitis

Front 149

how does Porphyromonas gingivalis look stained and what does it need to grow>

Back 149

• Gram negative coccobacilli
• Black-pigmented anaerobe
Requires hemin to porphyrin pigment
vitamin K and peptides

Front 150

What are the virulence factors of Porphyromonas gingivalis?

Back 150

Fimbriae
Hemagglutinins
Hemolysins
Proteases
Polysaccharide capsule (K antigen)
Outer membrane vesicles

Front 151

What is the respiration of Porphyromonas gingivalis?

Back 151

anaerobe

Front 152

What are the organisms of Chronic periodontitis? (4)

Back 152

Porphyromonas gingivalis
Prevotella intermedia
Tannerella forsythia
Capnocytophaga spp.

Front 153

What treatment may be necessary for patients with chronic periodontitis?

Back 153

– Removal of plaque by scaling or planing
– Surgical removal of inflamed tissue
Antimicrobial agents like:
– Mouthwashes
– Antibiotics

Front 154

When do you see Aggressive periodontitis?

Back 154

Teens usually present and more females than males. genetic/autoammunte component

Front 155

Aggressive periodontitis usually presents how?

Back 155

– Associated with bone loss around teeth
Often does NOT present with inflammation, bleeding, or plaque accumulation

Front 156

Aggregatibacter actinomycetemcomitans is associated with what disease?

Back 156

Aggressive periodontitis
Looks like a star fish

Front 157

What is another name for Acute Necrotizing Ulcerating Gingivitis (ANUG)?

Back 157

Trench Mouth

Front 158

How does (Acute) Necrotizing Ulcerating Gingivitis present?

Back 158

– Gingivae that are red, inflamed, shiny, bleeding, with ulcers
– Lesions are painful and covered by a pseudomembrane
– Halitosis
– Patient may notice a metallic taste
– Usually no lymph node involvement, fever, or malaise

Front 159

What bacteria contribute to trench mouth?

Back 159

Fusobacterium nucleatum
Treponema spp.
both obligate anerobes
Both gram negative

Front 160

What three factors are needed to diagnose trench mouth?

Back 160

– Fusobacteria
– Spirochetes
– Leukocytes

Front 161

What is the treatment for trench mouth (ANUG)?

Back 161

– Removal of plaque and local debridement
– Improvements in oral hygiene, use of antiseptic mouth rinses
- Antibiotics

Front 162

What is Noma?

Back 162

Cancrum oris, gangrenous stomatitis
Basically Extremely severe form of ANUG

Front 163

When/where do you see NOMA

Back 163

– Severe malnourishment
– Recent infection, usually viral infection or TB
Young kids under 10 in developing countries

Front 164

What are dentoalveolar infections?

Back 164

Pyogenic infections of the teeth and
supporting structures

Front 165

What is Ludwig’s angina?

Back 165

A type of dentoalveolar infection that is a swelling of the tissue at the front of the neck accompanied by fever
Bullneck appeareance
Must make sure airway remains open

Front 166

What is a Periodontal abscess?

Back 166

type of dentoalveolar
Painful!
Polymicrobial infection

Front 167

What are the features of Cervicofacial Actinomycosis?

Back 167

Associated with trauma or invasive oral procedures. Common for actinomycosis
"Lumpy jaw"
Swelling is fibrosed and Pus is gritty/sand-like and
contains visible, yellow granules
(called “sulphur granules,” but
do not contain sulphur)

Front 168

What bug causes Cervicofacial Actinomycosis?

Back 168

Actinomyces israelii
Look grains look like teeth

Front 169

What is candicia-associated denture stomatitis?

Back 169

Common in full-time denture wearers or other orthodontic appliances,
 Erythema and edema of mucosa in contact with surface of upper denture

Front 170

What is Gentian Violet used for?

Back 170

OTC treatment for candida

Front 171

What is the HSV Epidemiology?

Back 171

NO season
Humans only reservoir - fluid spread
80% have HSV1
20% have HSV2

Front 172

What are the HSV Characteristics?

Back 172

 Linear dsDNA genome
 Large, enveloped virus with
an icosadeltahedral capsid
 Envelope contains:
– Attachment proteins
– Fusion proteins
– Structural proteins
 Persistant infections in neurons
 Lytic infections in epithelial cells/fibroblasts

Front 173

What is a HSV finger lesion called?

Back 173

Herpetic whitlow
Primary lesion on finger

Front 174

VZV Reactivation presents how?

Back 174

Herpes virus (HHV-3)
 May show sharp lines
of demarcation, especially at midline

Front 175

Coxsackie A causes what problems?

Back 175

Herpangina
Hand-foot-and-mouth disease
Aspetic meningitis

Front 176

Coxsackie A Characteristics (morphology, genome,etc.)

Back 176

 Enterovirus—also includes poliovirus
 +ssRNA genome
 Small, non-enveloped
 Icosahedral capsid
Totall opposite of HSV

Front 177

What is the epidemiology of Coxackie?

Back 177

 Infections highest in the summer
 Seen mainly in children
 Associated with areas of poor sanitation and crowding
 Humans are the only reservoir
 Spread primarily by fecal-oral route

Front 178

What virus associated with infant/childhood diarrhea?

Back 178

rotavirus
adenovirus

Front 179

What virus associated with feces contaminated food?

Back 179

Norovirus

Front 180

What is the makeup of Rotaviruses?

Back 180

ds RNA
nonenveloped,
icosahedral capsid
Segmented genome

Front 181

Does Rotavirus have seasonality?

Back 181

Yes. Winter outbreaks expected in
temperate zones called
“winter vomiting disease”

Front 182

How would a patient with Rotavirus present?

Back 182

They would be an INFANT
5-7 day course of fever, vomiting, diarrhea
10-20 diarrhea episodes per day

Front 183

What is the Rotavirus Enterotoxin?

Back 183

NSP4
It is seccteted form infected cells and binds to neighboring cells causing Ca++ to be released which stimulates secretion

Front 184

What are the ways to detect rotavirus?

Back 184

ELISA screen for presence
of viral antigens in stool
Latex agglutination test is
available for type A rotaviruses

Front 185

Describe the Rotasheild vaccine

Back 185

Live, attenuated preparation for infants administered at 2, 4, and 6 months of age from
Tetravalent

Front 186

Which rotavirus was voluntarily withdrawn from the market

Back 186

Rotasheild due to intussusception

Front 187

Describe the Rotarix vaccine

Back 187

Live, attenuated monovalent G1 strain
2 doses over 2 months (~80% efficacy)

Front 188

Describe the RotaTeq Vaccine

Back 188

Live, oral vaccine containing
5 reassortant viruses derived
from human and bovine viruses
– Express human virus
serotype proteins G1-4 and
P1A
– Three doses starting at 6-12 weeks
– Licensed in US

Front 189

Describe the structure of Enteric Adenoviruses

Back 189

Double stranded DNA virus
Acid resistant capsid

Front 190

What population get Enteric Adenoviruses?

Back 190

Endemic diarrhea of infants
Extended period 5-12 days
of diarrhea, fever, and
vomiting

Front 191

What are the two Caliciviruses? Where are they found?

Back 191

Sapporovirus
Noroviruses
marien environmetns

Front 192

Describe the structure of norovirus?

Back 192

ssRNA genome
These viruses are small

Front 193

What population gets noroviruses? How does it present?

Back 193

Older children and adults
Epidemics of diarrhea
and vomiting, Typically mild and self-limited
24-48 hours
Associated with food/shellfish

Front 194

Why is it difficult to trace a norovirus outbreak?

Back 194

because not only is it transferd by food, but also many secondary cases from person to person

Front 195

Which viruses are unculturable, and extraordinarily resistant to inactivation?

Back 195

norovirus

Front 196

Describe the structure os astrovirus

Back 196

ss RNA genome, star-
shaped aspect on capsid
visible by EM

Front 197

Does astrovirus have a seasonal link?

Back 197

No

Front 198

Where are tou most likley to see an epidemic of astovirus?

Back 198

young children, pediatric
wards, day care centers,
and nursing homes

Front 199

What is cholera?

Back 199

Cholera -- acute diarrheal disease due to Vibrio cholerae infection.
Cauess massive morbitity and mortality

Front 200

What is the main feature of cholera?

Back 200

Acute and massive watery diarrhea is the main feature

“Rice water” stools

Front 201

What is the cardinal sign of cholera

Back 201

Abrupt Massive volume watery diarrhea (1 liter /hour)

Front 202

Describe the morphology of cholera

Back 202

• Gram negative, bent rod shaped (vibrio) bacterium
• Nonspore-former
• Facultative anaerobe
• Motile, polar flagellum
• Classified by O (somatic) antigens

Front 203

What is the significance of Serogroup O-1 cholera?

Back 203

It is the one seen in classic cholea epidemics - contains Biotype El Tor
(1930s pandemic)

Front 204

What is the significance of the cholera Serogroup O-139?

Back 204

Seen in India in 1992
O-139 can cause disease in individuals who have recovered from a previous O-1 infection

Front 205

What disease is a frequent attender of disasters?

Back 205

Cholera

Front 206

What is interesting about how cholera colinizes?

Back 206

The colonized mucosa shows
NO change in physical
integrity

Front 207

What is choleragen?

Back 207

Cholera toxin
Phage encoded AB toxin

Front 208

Describe the AB toxin mechanism for cholera

Back 208

B Binds
A causes cAMP to inctrease causing hyper secretion of water and electrolytes causing the diarrhea

Front 209

Besides cholera toxin, what is the other main virulence factor?

Back 209

toxin coregulated pilus gene product – needed for attachment to host.

Front 210

How are cholera toxin genes aquired?

Back 210

Lisogenic Conversion
CTX is a mobile genetic element, a filamentous virus related to M13.
The CTX receptor is on the tcp gene.

The ctx and tcp genes are in effect environmentally regulated

Front 211

How id cholera diagnosed

Back 211

Direct microscopic examination of stool shows large numbers of vibro shaped bacteria that are motile

Front 212

What strains of V. choleraemay cause diarrheal disease but not
cholera?

Back 212

O-1

Front 213

What are some cholera suseptitbility factors

Back 213

Type O
achlorohydria (High pH- they love acid!)

Front 214

What are the features of V. parahaemolyticus

Back 214

, infection most common in summer
Consumption of raw or undercooked shellfish has been a recurrent source of human infection.
Oxidase positive, will form green colonies on TCBS agar

Front 215

What are the features of V. vulnificus

Back 215

frequently associated with oysters or exposure to seawater harboring oysters,
other shellfish or marine life
more common when warm weather!
The bacterium is a serious threat primarily to patients with underlying disease or immune compromise.

Front 216

What is the treatment of V. vulnificus?

Back 216

Treat with tetracycline

Front 217

Describe Shigellae morphology

Back 217

• Gram negative rod
• Nonspore-former
• Facultative anaerobe
• Nonmotile (usually)
• Lactose non-fermenter

Front 218

Describe Shigella clinical

Back 218

the large bowel- Incubation 72 hours
Initial symptoms - fever, cramps, vomiting, watery diarrhea
can progress to dysentary

Front 219

What allows shigella to be distinguised from e-coli?

Back 219

It is a Lactose non-fermenter

Front 220

What is the differnence bewteen diarrhea and dysentery?

Back 220

dysentery is classic - blood,
mucous and PMN’s in stools, fever, cramps, tenesmus

Front 221

Describe the surface o antigen of shigellas virulence

Back 221

Induce endocytosis into follicle-associated M (microfold) cells
Shigella will lyse phagosome
and escape to cytoplasm on basolateral side allowing for cell to cell transmission

Front 222

What virulence factors does shigella have?

Back 222

Surface O antigen
Actin binding protein (promotes movement)
Shiga toxin

Front 223

Describe the shiga toxin

Back 223

It causes Disruption of protein synthesis and damage to the intestinal epithelium

Front 224

How do you diagnose shigelliosis

Back 224

Microscopic examination of feces - Normal diarrhea wont have RBCs and PMNs
Culture Quickly so other species dont overgrow
Look for blood tinged flecks of mucus to plate
Immunoflourencesns
Sigmid colon exam to look for ulcers

Front 225

What is the treatment of Shigelliosis?

Back 225

This is a self-limiting disease

Fluid replacement

Effective antibiotic therapy may shorten course, eliminate carriers (there are a lot of resistant strands though)

Front 226

What are the complications of shigella?

Back 226

bacteremia is UNCOMMON however
Potential to become a carrier

Front 227

What is reiters syndrome

Back 227

(urethritis, polyarthritis, inflammatory eye disease, skin lesions)

Nonspecific acute inflammatory arthritis that ranges from slight to severe

Strong association with HLA B27 individuals and shigella

Front 228

What is Hemolytic uremic syndrome (HUS)

Back 228

S. dysenteriae, type 1 infection (Shiga toxin production) but can be seen with others like ecoli and samonella that damage cells

Acute renal failure with poor prognosis

Front 229

How is shigella apread? What is the resivoir?

Back 229

Humans
Person to person

Front 230

Does it take a lot of shegella to get sick?

Back 230

Nope

Front 231

What is the significance of the group types of shigella?

Back 231

Groups A-D
A most severe. D least

Front 232

Where is Salmonella found naturally?

Back 232

Normal gut flora of many birds and animals

Front 233

how does Salmonella persent clinically?

Back 233

Incubates for 12-48hrs
Sudden onset of disease - fever, chills, cramps, diarrhea, vomiting

2-3 days duration in normal host

Front 234

What host is samonella more sever in

Back 234

infants and elderly

Front 235

What is the morphology of Samonella

Back 235

• Gram negative rod
• Nonspore-former
• Facultative anaerobe
• Motile
• Lactose non-fermenter

Front 236

What is the proble with treating S. dysenteriae with antibiotics?

Back 236

It may provoke hemolytic uremic symdrome

Front 237

What age has the highest incidence of shigella?

Back 237

kids 1-4

Front 238

What are the four types of salmonella infection

Back 238

1. Gastroenteritis
2. Bacteremia or septicemia without GI symptoms
3. Enteric fever
4. Carrier state

Front 239

What are the virulence factors of salmonella?

Back 239

Enterotoxin
Mucosal invasion genes (enters both M and epithelial cells!)
LPS
Others:
Resistance to serum killing
Acid resistance
phoPQ-controlled genes for intra-phagocyte
survival
Virulence plasmid factors (spv genes)

Front 240

How do you make the diagnosis for salmonella?

Back 240

Microscopic-Fecal leukocytes
Culture
FA tests
Serological confirtmation

Front 241

What ate the reservoirs of salmonealla

Back 241

Animal reservoirs
primarily
 Eggs
 Beef products and cattle
 Pigs and pork products
 Also dogs, cats, pet
reptiles

Front 242

Does it take a lot of salmonella to get infected? How?

Back 242

Yes
Usuall by contaminated food or water

Front 243

What is the hiset incidence range for salmonella

Back 243

Infacnts and children 6 months to 5 years

Front 244

Does salmonella have a seasonality?

Back 244

Yes summer and fall

Front 245

What is the best prevention of salmonella?

Back 245

Animal reservoirs
primarily
 Eggs
 Beef products and cattle
 Pigs and pork products
 Also dogs, cats, pet
reptiles

Front 246

What are the recent outbreaks from salmonella?

Back 246

Tomatos
Alfalfa
frozen rodents???
Eggs!
Ground Turkey
Cantaloupe

Front 247

What does the pink tube indicate?

Back 247

Urease Activity

Front 248

Back 248

A: Indole Production
B: H2S Production shows as black percipitate

Front 249

What bugs can cause lactose fermenting as shown?

Back 249

E-coli and Klebsellia

Front 250

What is evidenced by the color change on the left? What organism from lab can do this?

Back 250

Lactose fermentation on MacConkeys
Klebsellia and E.Colu

Front 251

What is being tested? Which side is positive?

Back 251

Oxidase
the Right shows a positive result

Front 252

What does a RED slant on A TRIPLE SUGAR IRON AGAR indicate?

Back 252

does not ferment either lactose or sucrose

Front 253

What does a Yellow slant on A TRIPLE SUGAR IRON AGAR indicate?

Back 253

ferments lactose and/or sucrose

Front 254

What does a RED butt on A TRIPLE SUGAR IRON AGAR indicate?

Back 254

no fermentation, the bacterium is an obligate aerobe

Front 255

What does a YELLOW butt on A TRIPLE SUGAR IRON AGAR indicate?

Back 255

some fermentation has occurred, acid has been produced, it is a facultative anaerobe.

Front 256

What does a Black butt on A TRIPLE SUGAR IRON AGAR indicate?

Back 256

H2S has been produced

Front 257

What is know about the organism in tube a?

Back 257

Yellow Slant: ferments lactose and/or sucrose
Wellow Butt: some fermentation has occurred, acid has been produced, it is a facultative anaerobe. It also makes gas

Front 258

What enterics make H2S?

Back 258

Proteus and Salmonella

Front 259

What enteric is positive for indole production?

Back 259

E.Coli

Front 260

What enterics are lactose non-fermenters?

Back 260

Proteus and salmonella

Front 261

What does the oxidase test distinguish between?

Back 261

Enterobacteriaceae,
which are oxidase-negative, and members of the genus Pseudomonas, which are
oxidase-positive.

Front 262

What is the Indole Production test looking at?

Back 262

the ability to degrade the amino acid tryptophan to indole
E. Coli does this

Front 263

Alkaline slant (red) and alkaline butt (red) or no change (orange-red) indicates what?

Back 263

No carbohydrate fermentation has occurred

Front 264

What enteris are motile?

Back 264

E. Coli, Proteus, Samonella

Front 265

What does VPI mean?

Back 265

Vibrio cholerae pathogenicity island

Front 266

Where and what is the gene for the cholera toxin (CTX) virus receptor?

Back 266

– The gene for the CTX virus receptor (tcp) is in the VPI

Front 267

What are Two lysogenic conversions are required for cholera?

Back 267

First converstion makes the receptor
Secondconversion makes the A-B CTX toxin that can now bind to the made receptor.
This is cool because one virus is actually promoting an infection by another virus

Front 268

Scraping of a candida specimine under the microscope would show what formation?

Back 268

Budding yeast and pseudohyphae

Front 269

What are dermatophytes?

Back 269

Ringworm Fungus
Microsporum & Trichophyton most common

Front 270

Which candida can from germ tubes?

Back 270

albicans & dublinensis
(gabralta cannot!!!)

Front 271

what organism is found in bird droppings?

Back 271

Cryptococcus neoformans

Front 272

Cryptococcus serotypes a & d?
Cryptococcus serotypes b & c?

Back 272

neoformans
gattii

Front 273

What organism is seen here?

Back 273

histoplasma capsulatum

Classic Tuberculate macroconidium present

Front 274

Whose life cycle is illustrated?

Back 274

Coccidioides immitis
Spherule and Athroconidia

Front 275

Whose life cycle is illustrated?

Back 275

Coccidioides immitis
Spherule and Athroconidia

Front 276

What organism is associated with bat droppings?

Back 276

Histoplasma capsulatum

Front 277

What organism is shown here?

Back 277

Blastomyces dermatitidis
note wide base and budding

Front 278

What organism is shown here?

Back 278

Paracoccidioides brasiliensis