Microbiology: Block 3: Pathogenic Organisms Po22 - Po28

Front 1

Characteristics of the exoerythrocytic (EE) stage of blood protoza?

Back 1

No hepatic inflammation, no symptoms.

Front 2

What procedures must be careful about not transmitting prions?

Back 2

Neurosurgery, tonsillectomy

Front 3

What are prions?

Back 3

Self-propagating, infectious, misfolded proteins

Front 4

What can be done to reduce the transmission of prions in the OR

Back 4

Appropriate cleaning of surgical instruments

Front 5

PrP is made of stacked sheets of __ sheets

Back 5

β sheets

Front 6

What type of amyloid is associated with alzheimer's disease?

Back 6

Aβ

Front 7

Prions bind to the plasma membrane via what?

Back 7

GPI (glycophosphoinsositide)

Front 8

What percentage of proteins don't fold properly?

Back 8

Up to 25%!

Front 9

How are prions transmitted?

Back 9

By injection or, less efficiently, ingestion.

Front 10

What is the general progression of prion disease?

Back 10

Very slow. Can take 50 years to kill.

Front 11

What are some things that will sterilize surgical instruments of prions?

Back 11

1. 1 molar NaOH
2. Bleach + strong proteases + SDS

Front 12

What is the prion infectious dose?

Back 12

Very small

Front 13

What causes vCJD?

Back 13

vCJD is due to infection by BSE prions.

First diagnosed in the UK in 1994

Front 14

What are some anatomical locations that carry prions?

Back 14

Dental pulp
Tonsils
Corneal transplants

Front 15

True or false: scrapie cannot be transmitted via blood transfusion.

Back 15

False

Front 16

(extra credit)

What drugs have been used to retard the progress of vCJD?

Back 16

Quinacrine and chlorpromazine.

Front 17

What is the most prevalent human prion disease?

Back 17

Creutzfeld-Jacob disease. 85% of CJD are sporadic.

Front 18

(Extra credit)

What is kuru?

Back 18

Fatal neuropathy in the Fore people of New Guinea. Transmitted by ritual cannibalism.

Front 19

Prions exhibit ___ - ___ transmission

Back 19

species - species. But do see cow --> human transmission despite greater than 10% difference

Front 20

Median age of variant CJD?

Back 20

Age 27!

Front 21

If you take hamster PrPSc and inject it into a normal mouse, will the mouse be affected?

Back 21

No

Front 22

If you take hamster PrPSc and inject it into a mouse expressing hamster PrPc, will the mouse get infected?

Back 22

Yes, but this mouse will produce prions that can only affect HAMSTERS.

Front 23

Subclinical prion disease

Back 23

While taking hamster PrPSc and injecting it into a normal mouse does not cause disease in that mouse's lifetime, transplanting the brain tissue 3 times (for 3 mouse lifespans) will show symptoms.

The species barrier is merely a delay in progression of the disease.

Front 24

vCJD happens in humans carrying what Prnp polymorphism?

Back 24

M/M. V/V may be carriers

Front 25

PrPc

Back 25

The normal form of the prion gene

Front 26

PrPSc

Back 26

The infectious prion form

Front 27

____ activation is seen in neurons infected with prions.

Back 27

ASTROCYTE activation is seen in neurons infected with prions.

Front 28

What allows prions to travel from the GI tract to the brain?

Back 28

Travelling in macrophages or dendritic cells.

Front 29

True or false: a PrP negative mouse cannot be infected with prions?

Back 29

True

Front 30

Mad Cow disease was a special concern in this country.

Back 30

The UK

Front 31

(extra credit)

What is the name of a familial prion disease?

Back 31

Gerstmann-Straussler-Scheinker disease (GSS)

Front 32

What proved that BSE causes vCJD?

Back 32

Infectivity of the human vCJD prion for mice expressing the bovine PrP.

Front 33

Why are neurons particularly susceptible to prion disease?

Back 33

Because probability of amyloid formation is directly related to cell age.

Front 34

What is a unique aspect of cryptococcus neoformans?

Back 34

It has a polysaccharide capsule

Front 35

How do you test for cryptococcus neoformans?

Back 35

Look for cryptococcal antigen in blood/CSF

Front 36

Strong association of C. neoformans with what kinds of immune disorders?

Back 36

T cell deficiencies. Especially with AIDS

Front 37

What is the most common clinical presentation of C. neoformans?

Back 37

Insidious meningitis. See Inc protein 50% of time see dec glucose, WBCs , mostly lymphocytes.

Front 38

What should be offered to a patient with no history of immunosuppression but has cryptococcosis?

Back 38

An HIV test.

Front 39

Where are spores of Aspergillus found?

Back 39

Everywhere

Front 40

The form of aspergillosis seen in patients depends on what?

Back 40

On the underlying immune status of the patient

Front 41

Disease with aspergillosis is a result of what?

Back 41

Because of an allergic response to the fungus

Front 42

What is the most common site of invasive aspergillosis?

Back 42

Lungs

Front 43

Invasive aspergillosis is seen in patients with what immune deficiency?

Back 43

With neutropenia (often post transplant)

Front 44

What is an aspergilloma?

Back 44

Non-invasive ball of fungus within a preexisting cavity (from TB bullae, sarcoidosis). Can rupture and cause hemoptysis. Antifungals generally are not effective here.

Front 45

Invasive aspergillosis clinical manifestations?

Back 45

Hemorrhage
Necrosis
Infarction

Front 46

Mucormycosis

Back 46

Only medically significant fungi that are aseptate

Front 47

Mucormycosis is associated with what disease

Back 47

Diabetes
like the low pH of DKA.

Bone marrow transplant recipients

Recipients of iron-chelation therapy with deferoxamine

Front 48

Mucormycosis: progression

Back 48

Very rapid case

Front 49

Mucormycosis: treatment

Back 49

Agressive surgical debridement
Correction of acidosis
Amphotericin B

Front 50

Mucormycosis is associated with what underlying disease?

Back 50

Diabetic ketoacidosis

Front 51

PCP

Back 51

Pneumocystis pneumonia

Front 52

Presentation of PCP on chest x-Ray

Back 52

Diffuse interstitial infiltrates

Front 53

What is the most common presentation of infection with P. jiroveci?

Back 53

Pneumonia

Front 54

P. jiroveci: detection

Back 54

DFA (direct fluorescent antibody)

Front 55

When do you see PCP in HIV patients?

Back 55

CD4 count less than 200.

Front 56

What should be given to HIV patients with CD4 counts below 200?

Back 56

Prophylaxis against PCP (bactrim). This also protects against toxoplasmosis.

Front 57

What are dimorphic fungi?

Back 57

Fungi that exists as a mold in nature and a yeast in tissue.

Front 58

When does "phase conversion" occur?

Back 58

At 37 degrees

Front 59

Histoplasmosis

Back 59

No capsule
intrcellular, inside macrophage
endemic in Ohio/Mississippi river basin, Caribbean, central america
bat/bird droppings

Front 60

Immune response to histoplasmosis

Back 60

Cell-mediated immunity
granulomas with subsequent calcification is common

Front 61

You can get pericarditis with what fungal infection?

Back 61

Histoplasma capsulatum

Front 62

Histoplasmosis: detection

Back 62

Antibodies in immunocompetent
Histoplasmosis antigen in urine in immunocompromised

Front 63

Yeast cells inside macrophages

Back 63

H. capsulatum

Front 64

Blastomycosis

Back 64

Broad-based buds
Thermally dimorphic fungi. Mold in nature, yeast in tissue.

Front 65

Blastomycosis - who does it effect?

Back 65

Affects those with apparently normal immune systems.

Front 66

Coccidioidomycosis

Back 66

Thermally dimorphic fungus with a unique life cycle.
Hyphae in soil, spherulus with endospores in tissues. Each endospore can grow into a spherule.

Front 67

Endemic regions of coccidioidomycosis

Back 67

SW USA, some parts of Latin america.

Front 68

Fungus with erythema nodosum and erythema multiforme.

Back 68

Coccidioidomycosis. Can also see with sarcoidosis and TB.

Front 69

Paracoccidioidomcosis

Back 69

Pilot-wheel buds. Endemic to south america. Lungs oral mucosa, skin. Treat with itraconazole (expensive)

Front 70

Sporotricosis

Back 70

Rose-gardener's disease
not geo resistricted
roses, sphagnum moss. Cutaneous disease --> spreads via lympangitics
Doesn't like elevated temp --> stays on skin

Front 71

Penicilliosis marneffei

Back 71

Northern Thailand
sim to histoplasmosis
Yeasts reproduce by binary fission (unique)

Front 72

What does saprophytic mean?

Back 72

Uses non-living organic material to survive.

Most fungi are saprophytic

Front 73

What is a commensal fungi?

Back 73

A fungi that uses organic material from living organisms in such a way that is beneficial to the fungi, but is neither harmful nor beneficial to the host.

Front 74

What is the sexual state of a fungi called?

Back 74

The teleomorph or the "perfect" state)

Front 75

What is the asexual state of a fungi called?

Back 75

The anamorph or the "imperfect" state.

Front 76

Are fungi eukaryotic or prokaryotic?

Back 76

Eukaryotic.

Have a nucleus with a nuclear membrane
80S ribosomes
Golgi apparati

Most pathogenic fungi have a rigid cell wall containing chitin, mannan, and β-glucan.

Front 77

What is an example of a prototypical yeast?

Back 77

Cryptococcus neoformans

Front 78

What are two ways that a yeast can reproduce?

Back 78

1. Budding
2. Fission

Front 79

What are hyphae?

Back 79

Branching tubular filaments.

A mass of hyphae is called a mold.

The protoplasm in the hyphae can be either septate (be separated by walls) or aseptate.

Front 80

What is a prototypical mold?

Back 80

Aspergillus fumigatus

Front 81

What are three examples of dimorphic fungi?

Back 81

1. Histoplasma capsulatum
2. Blastinomyces dermatitidis
3. Coccidioides immitis (grows as spherules rather than yeasts in tissues)

Front 82

Result of gram stain with fungi?

Back 82

Not useful. (Candida stains positive)

Front 83

What are four lab techniques that are helpful for detecting fungi?

Back 83

1. KOH prep
2. India ink (Cryptoccocus neoformans negative stain)
3. PAS stain (Fungi stain red)
4. Silver stain (Fungi stain black)

Front 84

What is a type of agar especially suited to growing fungi?

Back 84

Sabouraud agar

(Have to specially order this. Most bacteria will not grow on this agar)

Front 85

What are four fungal virulence factors that contribute to immune evasion?

Back 85

1. Large size prevents phagocytosis.

2. Capsules inhibit phagocytosis (Cryptococcus neoformans)

3. Cell wall structure - chitin, mannans, glucans (provides complement resistance, but can also provide antigens for antibodies)

4. Proteinases - elastases that break down lung tissue, keratinases that break down hair, skin, and nails.

Front 86

What is a prototypical example of a superficial mycoses?

Back 86

Dermatophytosis (ringworm, tinea)

Front 87

General characteristics of dermatophytosis.

Back 87

Molds that can invade keratinized tissues because they can metabolize keratin.

Can occur at any skin site

Feet - tinea pedis, "athelete's foot"
Groin - tinea cruris, "jock itch"
Scalp - tinea capitis
Beard - tinea barbae
Nails - onychomycosis

Front 88

Dermatophytosis: diagnosis

Back 88

Fluoresce under UV light (Wood's lamp)

Front 89

Dermatophytosis: treatment

Back 89

Topical therapy
Azoles
Widespread infection is treated with oral drugs (terbinafine or itraconazole)

Front 90

Describe Tinea versicolor

Back 90

Common superficial fungi
Caused by Malassezia species
Produces hypo/hyperpigmented lesions on the trunk and proximal limbs

Front 91

Describe Seborrheic dermatitis and dandruff

Back 91

Erythema and scaling on face, scalp, chest, back.

Likely due to a reaction to Malassezia species.

Dandruff is seborrheic dermatitis of the scalp

Front 92

(extra credit)

What is mycetoma?

Back 92

Also known as madura foot.
Chronic bacterial (actinomyces)/fungal infection in foot
Seen in tropics

Front 93

50% of all diseases cause by Candida are caused by what species?

Back 93

Candida albicans

Front 94

What is unique about how Candida is acquired?

Back 94

Candida infections are usually acquired endogenously. The skin, mucous membranes, and GI tract is normally colonized. Breakdown of host defenses --> infection spread

Front 95

What types of patients are at risk of developing a candida infection?

Back 95

1. Diabetics
2. Burn patients
3. Those receiving broad-spectrum antibiotics.

Front 96

Prevalence of vulvovaginal candidiasis?

Back 96

Over half of women will experience at least one episode.

Front 97

Candidiasis: treatment

Back 97

If caused by eradication of normal flora, discontinue anitbiotics.

Fluconazole for more extensive infection.

Front 98

What is often one of the first clinical symptoms of HIV?

Back 98

Thrush

Front 99

Patients with unexplained thrush should get what?

Back 99

An HIV test

Front 100

Disseminated Candidiasis: transmission

Back 100

Transmission of Candida on the skin to the bloodstream via IV injection.

Front 101

Disseminated Candidiasis: diagnosis

Back 101

Blood cultures are positive in fewer than 50% of patients.

See endophthalmitis (white, cotton ball-like lesions on the chorioretina) and skin lesions

Front 102

(extra credit)

How do you distinguish between Candida albicans and other Candida species?

Back 102

The germ-tube test. When incubated in serum at 37 C, C. albicans will begin to germinate.

Front 103

Disseminated Candidiasis: treatment

Back 103

An echinocandin or
fluconazole.

Front 104

Do AIDS patients show WBCs in their CSF?

Back 104

No - they don't have any WBCs!

Front 105

Cryptococcus neoformans: treatment

Back 105

Amphotericin B plus flucytosine for 2 weeks followed by fluconazole.

Patients with AIDS need maintenance therapy with fluconazole as long as CD4 counts remain low.

Front 106

Invasive Aspergillosus: treatment

Back 106

Voriconazole.

Sometimes used in combination with amphotericin and echinocandins

Front 107

What types of patients get rhinocerebral mucormycosis?

Back 107

Diabetics (especially those with DKA)

Front 108

Pneumocystis jiroveci was formerly called what?

Back 108

Pneumocystis carinii

Front 109

What is pneumonia caused by Pneumocystis jiroveci called?

Back 109

PCP (PneumoCystis Pneumonia)

Front 110

See both cysts AND trophozoites during human infection.

Back 110

Pneumocystis jiroveci. (Hence formally classified as a parasite)

Front 111

(extra credit)

Why are amphotericin and azoles not effective with P. jiroveci?

Back 111

Because P. jiroveci lacks ergosterol in its cell membrane.

Front 112

What are two important characteristics of thermally dimophic fungi?

Back 112

1. They can infect immunocompetent patients

2. They are restricted to certain geographic locations.

Front 113

Histoplasmosis: treatment

Back 113

Most immunocompetent patients don't require therapy

With progressive disease, try amphotericin B and switch to itraconazole.

Front 114

Blastomycosis: treatment

Back 114

Itraconazole. For severe disease, start with amphotericin B

Front 115

Coccidioidomycosis: manifestations

Back 115

About 60% will be asymptomatic or will have mild flu-like symptoms

40% will develop symptoms of a primary infection 1 to 3 weeks after exposure.

Front 116

Coccidioidomycosis: treatment

Back 116

Primary infection in immunocompetent patients is self-limiting and requires no therapy.

Progressive disseminated disease is treated with amphotericin, fluconazole or itraconazole.