Intracellular Bac Microbiology

Front 1

what are the char of Mycobacterium?

Back 1

Non-motile, non-spore-forming, aerobic, fungus-like, G+ rod.

Front 2

describe the cell struc of Mycobacterium?

Back 2

Complex cell wall structure
High lipid content (60%), wax-like, hydrophobic
Slow growth: 3-8 weeks to detect growth
Resistant to disinfectants and common antibiotics
Mycolic acid: drug target (isoniazid)
Cord factor (glycolipid): mycolic acid + trehalose
LPS-like structure: lipoarabinomannan (LAM)
Acid-fastness: cannot be decolorized with acid solutions

Front 3

what does M. avium-intracellulare cause?

Back 3

systemic disease in AIDS patients
cervical lymphadenopathy in children

Front 4

what does M. scrofulaceum cause?

Back 4

cervical lymphadenopathy in
children (scrofula)

Front 5

what does M. kansasii cause?

Back 5

TB-like disease

Front 6

what does M. marinum cause?

Back 6

swimming pool granuloma

Front 7

how prevalent is M. tuberculosis?

Back 7

Leading cause of morbidity and mortality worldwide
One-third of the world population is infected and 3 million death each year
The disease incidence is magnified by the concurrent epidemic of HIV infection
In the US, <15,000 in 2003, most in foreign-borne persons

Front 8

who are the risk groups for M. tuberculosis in US?

Back 8

homeless person, prisoners, HIV patients, health care workers

Front 9

what's the reservoir for M. tuberculosis?

Back 9

: human,

Front 10

what's transmission of M. tuberculosis?

Back 10

inhalation of infectious aerosols

Front 11

what are the 4 possible outcomes of M. tuberculosis inhalation?

Back 11

A. Immediate clearance of the organism
B. Chronic or latent infection
C. Rapidly progressive disease (primary disease)
D. Active disease many years after the infection (reactivation disease):

Front 12

which outcome is the predominant form of M. tuberculosis in most countries?

Back 12

Active disease many years after the infection (reactivation disease):

Front 13

what are the statistics of developing active disease of M. tuberculosis?

Back 13

-5 to 10% of infected develop active disease in their lifetime
- 10% of patients with AIDS develop active disease within one year

Front 14

how does M. tuberculosis try to colonize human? if they succeed?

Back 14

Infect the lung and penetrate to the alveoli
If the innate defense system of the host fails to eliminate this infection, the bacilli proliferate inside alveolar macrophages.

Front 15

what's the key to M. tuberculosis' virulence?

Back 15

ability to survive within unstimulated macrophages

Front 16

how does M. tuberculosis survive in mac?

Back 16

cord factor prevents fusion of phagosome with lysosomes

Front 17

what type of infection can M. tuberculosis cause if able to survive in mac?

Back 17

Chronic, lifelong infection

Front 18

what do macs do in response to being infected?

Back 18

The infected macrophages produce cytokines and chemokines (triggered by LAM) that attract other phagocytic cells, which eventually form a nodular granulomatous structure called the tubercle.

Front 19

what's the result if M. tuberculosis bac replication isn't controlled?

Back 19

bacilli enter the local draining lymph nodes: lymphadenopathy

Front 20

what form of tb do you have if bac have caused lymphadenopathy?

Back 20

primary TB

Front 21

what's the Ghon complex?

Back 21

The lesion produced by the expansion of the tubercle into the lung parenchyma and lymph node involvement
-Lung and lymph node involvement together make Ghon complex

Front 22

how long can M. tuberculosis bac proliferate?

Back 22

until an effective cell-mediated immune (CMI) response develops, usually two to six weeks after infection.

Front 23

are antibodies made against M. tuberculosis?

Back 23

yes

Front 24

what's the most effective immunity against M. tuberculosis?

Back 24

effective immunity is CMIR

Front 25

what's caseation necrosis?

Back 25

Failure by the host to mount an effective CMI response and tissue repair leads to progressive destruction of the lung (tb)

Front 26

what happens in disseminated miliary tb?

Back 26

lesions resembling millet seeds (Progressive Primary TB

Front 27

how does M. tuberculosis become infectious to others?

Back 27

Bacilli can also spread into the lung airways: infectious to others

Front 28

what's the mortality rate of M. tuberculosis?

Back 28

80% of such persons will die.
Others will develop chronic disease or recover spontaneously

Front 29

describe the chronic disease of M. tuberculosis:

Back 29

repeated episodes of spontaneous healing and tissue breakdown

Front 30

what's reactivation TB?

Back 30

Results when the persistent bacteria in a host suddenly proliferate (progressive secondary TB)

Front 31

what immunosuppressive cond reactivate TB?

Back 31

HIV infection and AIDS
End-stage renal disease
Diabetes mellitus
Malignant lymphoma
Corticosteroid use
Diminution in CMI associated with old age

Front 32

WHAT ARE the tb symptoms?

Back 32

Gradual onset
Inexplicable weight loss, constant fatigue, night sweats, cough productive of mucopurulent sputum, shortness of breath, chest pain
May cough up blood (cavity disease)

Front 33

how do you diagnose tb?

Back 33

Chest x-ray
Collect sputum sample
Tuberculin test (Mantoux test)

Front 34

how do you handle sputum sample to diagnose tb?

Back 34

Stain for acid-fast bacilli (AFB)
Culture and identify

Front 35

how do you handle tuberculin test to diagnose tb?

Back 35

Skin test for CMIR to M. tuberculosis
Inject PPD (purified protein derivatives) intradermally
Positive means that the patient has been infected at some time (may not be current infection)
False positives with recent BCG vaccine or infection w/ other Mycobacteria

Front 36

what is a positive tb test w/ induration of >5mm?

Back 36

HIV-positive persons
Recent contacts of TB case
Immunosuppressed patients

Front 37

what's a positive tb test w/ an induration >10mm?

Back 37

Recent arrivals (<5 yr) from high-prevalence countries
Children <4 yr of age
Prisons and jails nursing homes and other health care facilities
Mycobacteriology laboratory personnel

Front 38

what's a positive tb test w/ an induration >15mm?

Back 38

Persons with no risk factors for TB
Southeast regions

Front 39

do you report tb to anyone?

Back 39

health department

Front 40

what's tx for someone w/ tb?

Back 40

Multiple drug therapy:
Isoniazid [INH] (inhibits mycolic acid syn.)
Ethambutol [EMB] (inhibits arabinogalactan syn.)
Rifampin [RIF, RMP] (inhibits RNA syn.)
Pyrazinamide [PZA] (?)

Front 41

what's tx for someone exposed to tb but no active disease?

Back 41

Isoniazid (INH) for three months

Front 42

If exposed to TB and Mantoux test or culture positive (active disease), how do you treat?

Back 42

Initial: INH+RIF+PZA+EMB, 4 drug 2 months
Continuation: INH + RIF, 4 months

Front 43

what is mdr tb resistant to?

Back 43

resistant to isoniazid and rifampicin

Front 44

how do you prevent tb in countries where tb is uncommon?

Back 44

screen everyone with Mantoux test, and treat those who become PPD-positive

Front 45

how do you prevent tb in countries where tb is common?

Back 45

Immunize with attenuated (live) BCG vaccine (Bacille Calmette-Guerin): an attenuated strain of M. bovis (enhance CMIR)

-Also protects against leprosy

Front 46

how common is M. leprae?

Back 46

~30,000,000 cases world-wide, most common in Asia (especially India) and Africa
105 cases in US in 2004

Front 47

what does M. leprae grow in?

Back 47

humans, experimental animals, armadillos

Front 48

how do you get leprosy?

Back 48

body secretions from leprosy patients

Front 49

is M. leprae intracellular or extracellular?

Back 49

strict intracellular

Front 50

what are the general symptoms of M. leprae cause?

Back 50

Infect dermal macrophages and the Schwann cells
Chronic disease of the skin, peripheral nerves, and mucosa of upper respiratory tract

Front 51

what are the symptoms of patients w/ vigorous CMI?

Back 51

tuberculoid leprosy (paucibacillary Hansen’s disease)
hypopigmented skin macules
damage to sensory, autonomic, and motor nerves

Front 52

what happens to patients who can't elicit a strong CMI response to leprosy?

Back 52

lepromatous leprosy (multibacillary Hansen’s disease)
disfiguring skin leisions, nodules
extensive tissue distruction

Front 53

what's the treatment for paucibacillary leprosy?

Back 53

rifampin + dapsone for 6 months

Front 54

what's the treatment for multibacillary leprosy?

Back 54

rifampin + dapsone + clofazamine for 2 years

Front 55

can proper treatment reverse leprosy?

Back 55

yes

Front 56

what's the reservoir for : M. avium or M. intracellulare?

Back 56

soil
water
undercooked poultry

Front 57

how common are M. avium or M. intracellulare infections?

Back 57

One of the most common bacterial infection in AIDS patients with low CD4 count (CD4 < 100)
Disseminated infection with high bacterial loads in liver. Spleen, bone marrow, etc
-Most common mycobacterial disease in the US

Front 58

what are symptoms of M. avium or M. intracellulare infections?

Back 58

non-specific, including fever, night sweats, abdominal pain, diarrhea, and weight loss (which often precedes the onset of fever).
Can cause localized disease: focal lymphadenitis

Front 59

how do you diagnose M. avium or M. intracellulare infections?

Back 59

Isolation of the organism in culture of the blood or lymph node

Front 60

do you treat M. avium or M. intracellulare infections?

Back 60

MAC disease is associated with a shortened survival in AIDS. Therapy for MAC is indicated in HIV infection

Front 61

what's the treatment for M. avium or M. intracellulare infections?

Back 61

Clarithromycin and azithromycin

Front 62

who does M. bovis infect?

Back 62

Infects humans and cattle

Front 63

what's the reservoir for M. bovis?

Back 63

Cattle

Front 64

how is Mycobacteium bovis transmitted?

Back 64

unpasteurized milk

Front 65

what's M. bovis infection like?

Back 65

Infection like TB

Front 66

how do you prevent M. bovis?

Back 66

BCG vac. (live, attenuated)

Front 67

are actinomyces acid fast?

Back 67

no

Front 68

describe Nocardia asteroides?

Back 68

G+, aerobic filamentous bacteria that fragment; weakly acid fast

Front 69

where can you find Nocardia asteroides?

Back 69

in soil rich with organic matter

Front 70

how do you get an infection w/ Nocardia asteroides?

Back 70

Acquired by inhalation (pulmonary) or traumatic introduction (cutaneous)

Front 71

who is a Nocardia asteroides infection most common in?

Back 71

-patients with chronic pulmonary disease
-immunocompromised patients

Front 72

what are the primary sites of a Nocardia asteroides infec?

Back 72

lungs are the primary sites of nocardial infection: bronchopulmonary disease

Front 73

what are the symptoms of Nocardiosis?

Back 73

Disseminates to the CNS (brain abscesses),
(> 40% of disseminated brain abscesses)

Primary or secondary cutaneous infections

There are no pathognomonic signs or symptoms for nocardiosis
it should be suspected in any patient who presents with brain, soft tissue or cutaneous lesions, and a concurrent or recent pulmonary process

Front 74

how do you diagnose a Nocardiosis infec?

Back 74

Gram's stain, Acid-fast staining, Culture

Front 75

what's the treatment for a Nocardiosis infec?

Back 75

sulfonamide

Front 76

what are the characteristics of Listeria monocytogenes?

Back 76

Small
Gram positive rod
facultative anaerobe
motile
Facultative intracellular parasite

Front 77

where can you find Listeria monocytogenes?

Back 77

Primary sources: soil and decaying vegetable matter. Also found in the feces of mammals, birds, etc

Front 78

how is L. monocytogenes transmitted?

Back 78

Foodborne disease: contaminated milk, soft cheese, undercooked meat (franks, cold cuts), raw vegetables

Front 79

what conditions can L. monocytogenes grow in?

Back 79

Can grow at 4-45oC and in high salt: food contamination with prolonged refrigeration

Front 80

how common is L. monocytogenes?

Back 80

Estimated > 2500 cases/yr in the US
Highest mortality rate (20-30%) among all foodborne diseases

Front 81

what can L. monocytogenes do to survive in host?

Back 81

Grows in macrophages & epithelial cells
Infects the GI tract, penetrate the intestinal epithelium from enterocytes or M cells in Peyer’s pathces
Replicate and move within macrophages

Front 82

how do L. monocytogenes survive in macs?

Back 82

Escape phagolysosome
Exotoxin: listeriolysin O
Phospholipase C

Front 83

how does L. monocytogenes move in body?

Back 83

Spread between cells (and escape immune detection): ActA induces actin polymerization
Act allows polymerization at fast speed at tips of listeria
Secretes molecule that makes actin depolarize
Polymerize and depolymerize very quickly

Front 84

what are type of disease can L. monocytogenes cause?

Back 84

Liver-spleen-disseminated disease

Front 85

what are symptoms of L. monocytogenes in healthy adult?

Back 85

influenza-like illness with or without gastroenteritis

Front 86

what are symptoms of L. monocytogenes in infant infec?

Back 86

early onset disease
late onset disease

Front 87

describe early onset disease in L. monocytogenes:

Back 87

(“granulomatosis infantiseptica”)
acquired transplacentally in utero
occurs within a few hours with high mortality rate
disseminated abscesses and granulomas in multiple organs

Front 88

describe late onset disease in L. monocytogenes

Back 88

occurs within 2 weeks
infection during birth or from environment
presents with meningitis

Front 89

what are symptoms of L. monocytogenes infec in Immunocompromised patients and pregnant women?

Back 89

meningitis
primary bacteremia

Front 90

how do you diagnose L. monocytogenes?

Back 90

Based on clinical setting:
neonatal sepsis or meningitis
meningitis in immunocompromised (HIV, transplants, etc.)
meningitis in elderly
fever during pregnancy (3rd trimester)
Culture enrichment at 4oC

Front 91

how do you treat L. monocytogenes?

Back 91

ampicillin

Front 92

how do you prevent L. monocytogenes?

Back 92

avoid processed meats if in high risk group

Front 93

what are the char of Legionella pneumophila?

Back 93

G- aerobe but stain poorly; nutritionally fastidious (requires Fe & Cys)

Front 94

where can you find L. pneumophilia?

Back 94

-lives in amoebae often associated with biofilm
-Found in cooling towers, water distribution systems, home water systems (including hot water heaters).

Front 95

how is L. pneumophilia transmitted?

Back 95

inhaling infectious aerosols
No documented person-to-person transmission

Front 96

how common is L. pneumophilia?

Back 96

2,093 cases in 2004, most in high risk patients
Causes 2-6% of all cases of community-acquired pneumonia

Front 97

where does L. pneumophilia proliferate in body?

Back 97

Replicate in macrophage: prevention of phagolysomone fusion

Front 98

how can your body beat down L. pneumophilia?

Back 98

CMI!

Front 99

what are the consequences of L. pneumophilia infection?

Back 99

pontiac fever
legionnaire's disease

Front 100

describe Pontiac fever:

Back 100

acute, self-limiting febrile disease without pneumonia
fever, headache, chills, myalgia, malaise developed over 12 hrs and persisted for 2-5 days

Front 101

what are the symptoms of Legionnaire's disease?

Back 101

after an incubation of 2-10d there is an abrupt onset of fever, chills, headache, chest pain and dry cough
Bronchopneumonia: inflammation-abscesses in lung tissue
multiple organs become involved: gastrointestinal tract (diarrhea), liver, CNS, and kidneys
fatality rate ~15-20% (respiratory failure)

Front 102

how common and severe are Pontiac attack and Legionnaire's disease?

Back 102

Pontiac fever- 95% of attack
Legionnaire's- low rate, severe

Front 103

how do you diagnose L. pneumophilia?

Back 103

culture (gold standard, but most of clinical labs can’t do it)
immunofluorescent probes for Legionella in sputum
Urinary Antigen Test (the most common method; for serogroup 1-6)

Front 104

what's the treatment of L. pneumophilia?

Back 104

macrolide (clarithromycin, azithromycin) or
fluoroquinolone (ciprofloxcin, levofloxcin)