Microbiology: Neisseria Meningitidis, Cryptococcus, & Mycobacterium: Block Ii

Front 1

Group of gram negative diplococci whose stained cells appear chractreristically kidney shaped:

Back 1

Neisseria

Front 2

This species of Neisseria causes septicemia and meningitis

Back 2

N. Meningitids

Front 3

This species of Neissera causes gonorrhea and disseminated infections

Back 3

N. gonorrhea

Front 4

Is normal flora of the upper respiratory tract, the third most common cause of otitis media in children and causes chronic bronchitis (occasional pnuemonis and bacteremia in adults)

Back 4

Moraxella Catarrhalis

Front 5

This genus is gram negative diplococci, obligate parasites of the respiratory and genital tract of humans, are obligate aerobes, catalase and oxidase positive, require special growth media and have increased CO2 requirements:

Back 5

Neisseria

Front 6

What is the major virulence factor of N. Meningitidis (meninigococcus)?

Back 6

Has a capsule that is antiphagocytic - major surface antigen

Front 7

How is N. Meningitidis transmitted?

Back 7

Person to person through respiratory droplets. There is a carrier state that is important in transmission.

Front 8

What are the groups most susceptible to N. Meningitidis?

Back 8

6-24 months and college students - also military recruits

Front 9

This serotype of N. Meningitidis causes a rare pneumonia and local infection of the nasopharnyx:

Back 9

Serogroup Y

Front 10

When N. meningitidis spreads to the bloodstream via lymphatics resulting in sepsis. Can cause endotoxic shock and DIC

Back 10

Meningococcemia

Front 11

When N. Meningitidis spreads from the blood to the meninges and can cause permanent CNS damage with auditory, neurological, and behavioral abnormalities - may also lead to amputations

Back 11

Meningitis

Front 12

What organism should be considered when a patient goes from healthy to near death in 24 hours?

Back 12

N. Meningitidis

Front 13

How would N. Meningitidis be detected?

Back 13

With a gram stain of the CSF. CSF often shows nothing early in the disease, and must be repeated.

Front 14

How would N. Meningitidis look on a gram stain of the CSF?

Back 14

Gram negative diplococci with neutrophils

Front 15

How would bacterial meningitis be treated?

Back 15

With IV penicillin - there are no penicillinase producing strains

Front 16

How is bacterial meningitis prevented? Is there a vaccine?

Back 16

Yes. It has two vaccines for different populations, the MSPV4 purified polysaccharide capsule is used for persons >55 and the menactra conjugate vaccine is used for 11-12 y/o and college students.

Front 17

What is Menomune MPSV4? When is it used?

Back 17

It is a vaccine for bacterial meningitis that is made of purified capsule polysaccharide for N. Menigitidis and is used for people 55 years old or older.

Front 18

What is Menactra or MCV4 and when is it used?

Back 18

It is a vaccine for bacterial meningitis made of purified polysaccharide capsule that is conjugated to a protein. It is used in 11-12 year olds and college students.

Front 19

What is the problem with the vaccination available for meningitis?

Back 19

There is no vaccine effective against serogroup B capsule and it is a common type of N. Meningitidis found in the US.

Front 20

This yeast is described as basidiomycete filamentous fungi:

Back 20

Cryptococcus

Front 21

This yeast is only encapsulated when found in the human host:

Back 21

Cryptococcus

Front 22

This crytococcus has recently emerged as a significant cause of disease in normal immunocompetent individuals in the Pacific Northwest:

Back 22

C. gatti

Front 23

Infection with this crytococcus is primarily thought of as meningoencephalitis in AIDS patients, is occasionally seen in immunocompetent patients and may involve pnemonia as the primary infection with dissemination to different body sites.

Back 23

C. Neoformans

Front 24

The most commonly considered method of transmission of this pathogen is through exposure to pigeon droppings:

Back 24

C. Neoformans

Front 25

This variant of C. Neoformans is seen in the northern hemisphere and is a major cause of meningitis in immunocompromised people:

Back 25

C. Neoformans var. grubii

Front 26

This type of cryptococcus is historically seen in australia and southern california and causes pneumonia/meningitis in immuno-competent individuals and animals

Back 26

C. Gatti

Front 27

The formation of ______ during the sexual stage of C. neoformans likely makes the organism more transmissable airborne:

Back 27

Basidiospores

Front 28

In the host and laboratory, C. neoformans replicates only as a ______ with typical _______.

Back 28

Yeast with typical budding

Front 29

Why is C. neoformans not considered dimorphic?

Back 29

Because only the yeast phase is observed clinically in patient samples or laboratory cultures

Front 30

What is the main virulence factor of C. neoformans?

Back 30

It has a capsule that is antphagocytic and inhibtis opsonization and phagocytosis similar to bacterial capsules.

Front 31

Which yeast has a polysaccharide capsule composed of mannose, xylose, and glucuronic acid?

Back 31

C. Neoformans

Front 32

What is C. Neoformans usual habitat?

Back 32

Found in the soil (organic material) or in pigeon droppings.

Front 33

How is C. Neoformans transmitted?

Back 33

It is airborne from the environemental source and travels as basidiospores.

Front 34

Is found in the dust from eucalyptus and other tree material and is transmitted to normal, immunocompetent individuals.

Back 34

C. gattii

Front 35

These necrotizing or fibrosing granulomas are seen in normal people with infections with C. gattii:

Back 35

Cryptococcomas

Front 36

This is the primary presenting pathology for C. gattii in normal persons:

Back 36

Pneumonia

Front 37

What does pulmonary symptoms does cryptococcal infection cause in immunocompromised individuals, especially patients with organ transplant or chemotherapy?

Back 37

Causes pneumonia with ARDS.

Front 38

These variants of cryptococcus may become latent in the lungs of immunocompromised patients with activation of the disease when the immune system is diminished:

Back 38

C. neoformans and C. gattii

Front 39

This is the primary presentation of 80% of the observed cryptococcal disease in AIDS patients:

Back 39

CNS cyrptococcosis

Front 40

Most HIV patients show symptoms of what when infected with C. neoformans?

Back 40

Will show symptoms of meningitis without respiratory symptoms

Front 41

How do meningitis and meningoencephalitis commonly manifest?

Back 41

Subacute or chronically - symptoms appear over a period of 2-4 weeks.

Front 42

In infections with cryptococcus, in addition to meningitis, inflammation of the brain (encephalitis) may occur with brain lesions called ________.

Back 42

Cryptococcomas

Front 43

What is the prognosis for untreated CNS cryptococcosis?

Back 43

It is invariably fatal without therapy (2 weeks to several years)

Front 44

This cytococcus causes infection in normal people, can disseminate showing meningitis or cryptococcomas of the brain and can be fatal if untreated:

Back 44

C. gattii

Front 45

How is cryptococcus infection of the CNS diagnosed?

Back 45

Direct examination of the CSF. May also use cryptococcal antigen but it does not distinguish between neoformans and gattii.

Front 46

These are rod shaped aerobic bacteria that are acid fast. They are widespread in soil and water where they replicate within free living amoebae and other protozoa. In the human host they replicate intracellularly within macrophages. Causes tuberculosis and leprosy.

Back 46

Mycobacterium

Front 47

Where does mycobacterium replicate?

Back 47

Intracellularly within amoebae and protozoa in the environment and within macrophages in the human host.

Front 48

Does mycobacterium affect immunocompromised or competent persons?

Back 48

Immunocompetent

Front 49

This form of mycobacterium causes necrotic lesions in the skin and subcutaneous tissue:

Back 49

M. ulcerans

Front 50

This kind of mycobacterium is found free living in soil and water, grows within amoeba, transmits to humans from the environment and causes chronic diseases and opportunistic infections only (healthy people are resistant)

Back 50

Atypical mycobacteria

Front 51

This type of atypical mycobacterium casues superficial skin lesions known as swimming pool granulomas that come from the environment, usually through a break in the skin. It causes a slow growing granulomatous skin lesions:

Back 51

M. marinum

Front 52

This species has to be differentiated from M. marinum, is found in soil and water, is a filamentous aerobic, and acid fast. Causes skin and tissue granulomas.

Back 52

Nocardia

Front 53

This type of mycobacterium is a slow growing, extracellular pathogen (does not replicate within the macrophage) and has a potent lipophilic toxin

Back 53

M. ulcerans

Front 54

How do you distinguish M. marinum from M. ulcerans?

Back 54

M. ulcerans has a potent lipophilic toxin called mycolactone

Front 55

This type of mycobacterium is cytotoxic causing tissue necrosis leading to spreading ulceration and is also anti-inflammatory/immunosupressive causing little fever and no early granulomas.

Back 55

M. ulcerans

Front 56

What is the habitat of M. ulcerans?

Back 56

It has an aquatic environment similar to M. marinum and other atypical mycobacterium

Front 57

How is M. ulcerans transmitted?

Back 57

From water habitat, following trauma and usually involving the arms and legs

Front 58

Can cause Buruli ulcer disease, and is usually seen in children less than 10 years old swimming in rivers. Infects otherwise healthy people but not commonly seen in the US.

Back 58

M. ulcerans

Front 59

What is the incubation period for M. ulcerans?

Back 59

2 weeks to 3 years with an average of 2-3 months.

Front 60

Relicates extracellularly in the dermis and subcutanous tissue with production of the mycolactone toxin (tissue necrosis and immunosupression)

Back 60

M. ulcerans

Front 61

The stage of infection with M. ulcerans in which disease manifests as firm, non-tender nodule, has an incubation period and replicates extracellularly and produces toxin:

Back 61

Pre-ulcerative stage

Front 62

The stage of infection with M. ulcerans in which the nodules erode forming a painless, continually spreading ulcerative lesion. Inflammatory cells are scarce in the active lesion.

Back 62

The ulcerative stage

Front 63

How is M. ulcerans treated?

Back 63

With sugery to remove infected tissue, antibiotic therapy, and heat packs (b/c it doesn't grow well in heat)

Front 64

This form of mycobacterium cannot be grown on laboratory media:

Back 64

M. leprae

Front 65

M. leprae grows best at what temperature?

Back 65

25-33, does not grow well at 37 C.

Front 66

This bacteria is an obligate intracellular pathogen that multiplies slowly, is seen in mononuclear phagocytes, esp. histiocytes and in the Schwann cells of the nerves:

Back 66

M. leprae

Front 67

What is the primary host of M. leprae and how is it transmitted?

Back 67

Its primary host is humans and is transmitted person to person through respiratory droplets.

Front 68

What type of people does M. leprae infect?

Back 68

Most people are resistant, but children are more susceptible than adults and anyone with a defect in cell mediated immunity

Front 69

What does M. leprae cause and how does it spread in the body?

Back 69

It causes leprosy. After respiratory exposure it invades the bloodstream but doesn't causes sepsis. It then migrates to the skin because it prefers cooler areas.

Front 70

Seen in histiocytes and Schwann cells and grows as an obligate intracellular pathogen. Has a particularly strong prediliction for nerves.

Back 70

M. Leprae

Front 71

This form of leprocy has a benign, non-progressive course, with asymmetric loss of nerve function (temperature sensitivity), macular skin lesions with few bacteria in the lesions and CMI intact:

Back 71

Tuberculoid leprosy

Front 72

This infection has a rapid progressive course with nodular skin lesions, slow, symmetric nerve involvement (with loss of sense of touch), abundant bacteria in the skin lesions, continuous bacteremia, and CMI markedly depressed:

Back 72

Lepromatous leprosy

Front 73

How is leprosy diagnosed and treated?

Back 73

Diagnosed with DNA probes with PCR and is treated with combined therapy of dapsone/rifampin and clofazimine if lepromatous. There is no vaccine