Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
104 Cards in this Set
- Front
- Back
what are the char of Mycobacterium?
|
Non-motile, non-spore-forming, aerobic, fungus-like, G+ rod.
|
|
describe the cell struc of Mycobacterium?
|
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 |
|
what does M. avium-intracellulare cause?
|
systemic disease in AIDS patients
cervical lymphadenopathy in children |
|
what does M. scrofulaceum cause?
|
cervical lymphadenopathy in
children (scrofula) |
|
what does M. kansasii cause?
|
TB-like disease
|
|
what does M. marinum cause?
|
swimming pool granuloma
|
|
how prevalent is M. tuberculosis?
|
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 |
|
who are the risk groups for M. tuberculosis in US?
|
homeless person, prisoners, HIV patients, health care workers
|
|
what's the reservoir for M. tuberculosis?
|
: human,
|
|
what's transmission of M. tuberculosis?
|
inhalation of infectious aerosols
|
|
what are the 4 possible outcomes of M. tuberculosis inhalation?
|
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): |
|
which outcome is the predominant form of M. tuberculosis in most countries?
|
Active disease many years after the infection (reactivation disease):
|
|
what are the statistics of developing active disease of M. tuberculosis?
|
-5 to 10% of infected develop active disease in their lifetime
- 10% of patients with AIDS develop active disease within one year |
|
how does M. tuberculosis try to colonize human? if they succeed?
|
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. |
|
what's the key to M. tuberculosis' virulence?
|
ability to survive within unstimulated macrophages
|
|
how does M. tuberculosis survive in mac?
|
cord factor prevents fusion of phagosome with lysosomes
|
|
what type of infection can M. tuberculosis cause if able to survive in mac?
|
Chronic, lifelong infection
|
|
what do macs do in response to being infected?
|
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.
|
|
what's the result if M. tuberculosis bac replication isn't controlled?
|
bacilli enter the local draining lymph nodes: lymphadenopathy
|
|
what form of tb do you have if bac have caused lymphadenopathy?
|
primary TB
|
|
what's the Ghon complex?
|
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 |
|
how long can M. tuberculosis bac proliferate?
|
until an effective cell-mediated immune (CMI) response develops, usually two to six weeks after infection.
|
|
are antibodies made against M. tuberculosis?
|
yes
|
|
what's the most effective immunity against M. tuberculosis?
|
effective immunity is CMIR
|
|
what's caseation necrosis?
|
Failure by the host to mount an effective CMI response and tissue repair leads to progressive destruction of the lung (tb)
|
|
what happens in disseminated miliary tb?
|
lesions resembling millet seeds (Progressive Primary TB
|
|
how does M. tuberculosis become infectious to others?
|
Bacilli can also spread into the lung airways: infectious to others
|
|
what's the mortality rate of M. tuberculosis?
|
80% of such persons will die.
Others will develop chronic disease or recover spontaneously |
|
describe the chronic disease of M. tuberculosis:
|
repeated episodes of spontaneous healing and tissue breakdown
|
|
what's reactivation TB?
|
Results when the persistent bacteria in a host suddenly proliferate (progressive secondary TB)
|
|
what immunosuppressive cond reactivate TB?
|
HIV infection and AIDS
End-stage renal disease Diabetes mellitus Malignant lymphoma Corticosteroid use Diminution in CMI associated with old age |
|
WHAT ARE the tb symptoms?
|
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) |
|
how do you diagnose tb?
|
Chest x-ray
Collect sputum sample Tuberculin test (Mantoux test) |
|
how do you handle sputum sample to diagnose tb?
|
Stain for acid-fast bacilli (AFB)
Culture and identify |
|
how do you handle tuberculin test to diagnose tb?
|
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 |
|
what is a positive tb test w/ induration of >5mm?
|
HIV-positive persons
Recent contacts of TB case Immunosuppressed patients |
|
what's a positive tb test w/ an induration >10mm?
|
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 |
|
what's a positive tb test w/ an induration >15mm?
|
Persons with no risk factors for TB
Southeast regions |
|
do you report tb to anyone?
|
health department
|
|
what's tx for someone w/ tb?
|
Multiple drug therapy:
Isoniazid [INH] (inhibits mycolic acid syn.) Ethambutol [EMB] (inhibits arabinogalactan syn.) Rifampin [RIF, RMP] (inhibits RNA syn.) Pyrazinamide [PZA] (?) |
|
what's tx for someone exposed to tb but no active disease?
|
Isoniazid (INH) for three months
|
|
If exposed to TB and Mantoux test or culture positive (active disease), how do you treat?
|
Initial: INH+RIF+PZA+EMB, 4 drug 2 months
Continuation: INH + RIF, 4 months |
|
what is mdr tb resistant to?
|
resistant to isoniazid and rifampicin
|
|
how do you prevent tb in countries where tb is uncommon?
|
screen everyone with Mantoux test, and treat those who become PPD-positive
|
|
how do you prevent tb in countries where tb is common?
|
Immunize with attenuated (live) BCG vaccine (Bacille Calmette-Guerin): an attenuated strain of M. bovis (enhance CMIR)
-Also protects against leprosy |
|
how common is M. leprae?
|
~30,000,000 cases world-wide, most common in Asia (especially India) and Africa
105 cases in US in 2004 |
|
what does M. leprae grow in?
|
humans, experimental animals, armadillos
|
|
how do you get leprosy?
|
body secretions from leprosy patients
|
|
is M. leprae intracellular or extracellular?
|
strict intracellular
|
|
what are the general symptoms of M. leprae cause?
|
Infect dermal macrophages and the Schwann cells
Chronic disease of the skin, peripheral nerves, and mucosa of upper respiratory tract |
|
what are the symptoms of patients w/ vigorous CMI?
|
tuberculoid leprosy (paucibacillary Hansen’s disease)
hypopigmented skin macules damage to sensory, autonomic, and motor nerves |
|
what happens to patients who can't elicit a strong CMI response to leprosy?
|
lepromatous leprosy (multibacillary Hansen’s disease)
disfiguring skin leisions, nodules extensive tissue distruction |
|
what's the treatment for paucibacillary leprosy?
|
rifampin + dapsone for 6 months
|
|
what's the treatment for multibacillary leprosy?
|
rifampin + dapsone + clofazamine for 2 years
|
|
can proper treatment reverse leprosy?
|
yes
|
|
what's the reservoir for : M. avium or M. intracellulare?
|
soil
water undercooked poultry |
|
how common are M. avium or M. intracellulare infections?
|
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 |
|
what are symptoms of M. avium or M. intracellulare infections?
|
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 |
|
how do you diagnose M. avium or M. intracellulare infections?
|
Isolation of the organism in culture of the blood or lymph node
|
|
do you treat M. avium or M. intracellulare infections?
|
MAC disease is associated with a shortened survival in AIDS. Therapy for MAC is indicated in HIV infection
|
|
what's the treatment for M. avium or M. intracellulare infections?
|
Clarithromycin and azithromycin
|
|
who does M. bovis infect?
|
Infects humans and cattle
|
|
what's the reservoir for M. bovis?
|
Cattle
|
|
how is Mycobacteium bovis transmitted?
|
unpasteurized milk
|
|
what's M. bovis infection like?
|
Infection like TB
|
|
how do you prevent M. bovis?
|
BCG vac. (live, attenuated)
|
|
are actinomyces acid fast?
|
no
|
|
describe Nocardia asteroides?
|
G+, aerobic filamentous bacteria that fragment; weakly acid fast
|
|
where can you find Nocardia asteroides?
|
in soil rich with organic matter
|
|
how do you get an infection w/ Nocardia asteroides?
|
Acquired by inhalation (pulmonary) or traumatic introduction (cutaneous)
|
|
who is a Nocardia asteroides infection most common in?
|
-patients with chronic pulmonary disease
-immunocompromised patients |
|
what are the primary sites of a Nocardia asteroides infec?
|
lungs are the primary sites of nocardial infection: bronchopulmonary disease
|
|
what are the symptoms of Nocardiosis?
|
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 |
|
how do you diagnose a Nocardiosis infec?
|
Gram's stain, Acid-fast staining, Culture
|
|
what's the treatment for a Nocardiosis infec?
|
sulfonamide
|
|
what are the characteristics of Listeria monocytogenes?
|
Small
Gram positive rod facultative anaerobe motile Facultative intracellular parasite |
|
where can you find Listeria monocytogenes?
|
Primary sources: soil and decaying vegetable matter. Also found in the feces of mammals, birds, etc
|
|
how is L. monocytogenes transmitted?
|
Foodborne disease: contaminated milk, soft cheese, undercooked meat (franks, cold cuts), raw vegetables
|
|
what conditions can L. monocytogenes grow in?
|
Can grow at 4-45oC and in high salt: food contamination with prolonged refrigeration
|
|
how common is L. monocytogenes?
|
Estimated > 2500 cases/yr in the US
Highest mortality rate (20-30%) among all foodborne diseases |
|
what can L. monocytogenes do to survive in host?
|
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 |
|
how do L. monocytogenes survive in macs?
|
Escape phagolysosome
Exotoxin: listeriolysin O Phospholipase C |
|
how does L. monocytogenes move in body?
|
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 |
|
what are type of disease can L. monocytogenes cause?
|
Liver-spleen-disseminated disease
|
|
what are symptoms of L. monocytogenes in healthy adult?
|
influenza-like illness with or without gastroenteritis
|
|
what are symptoms of L. monocytogenes in infant infec?
|
early onset disease
late onset disease |
|
describe early onset disease in L. monocytogenes:
|
(“granulomatosis infantiseptica”)
acquired transplacentally in utero occurs within a few hours with high mortality rate disseminated abscesses and granulomas in multiple organs |
|
describe late onset disease in L. monocytogenes
|
occurs within 2 weeks
infection during birth or from environment presents with meningitis |
|
what are symptoms of L. monocytogenes infec in Immunocompromised patients and pregnant women?
|
meningitis
primary bacteremia |
|
how do you diagnose L. monocytogenes?
|
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 |
|
how do you treat L. monocytogenes?
|
ampicillin
|
|
how do you prevent L. monocytogenes?
|
avoid processed meats if in high risk group
|
|
what are the char of Legionella pneumophila?
|
G- aerobe but stain poorly; nutritionally fastidious (requires Fe & Cys)
|
|
where can you find L. pneumophilia?
|
-lives in amoebae often associated with biofilm
-Found in cooling towers, water distribution systems, home water systems (including hot water heaters). |
|
how is L. pneumophilia transmitted?
|
inhaling infectious aerosols
No documented person-to-person transmission |
|
how common is L. pneumophilia?
|
2,093 cases in 2004, most in high risk patients
Causes 2-6% of all cases of community-acquired pneumonia |
|
where does L. pneumophilia proliferate in body?
|
Replicate in macrophage: prevention of phagolysomone fusion
|
|
how can your body beat down L. pneumophilia?
|
CMI!
|
|
what are the consequences of L. pneumophilia infection?
|
pontiac fever
legionnaire's disease |
|
describe Pontiac fever:
|
acute, self-limiting febrile disease without pneumonia
fever, headache, chills, myalgia, malaise developed over 12 hrs and persisted for 2-5 days |
|
what are the symptoms of Legionnaire's disease?
|
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) |
|
how common and severe are Pontiac attack and Legionnaire's disease?
|
Pontiac fever- 95% of attack
Legionnaire's- low rate, severe |
|
how do you diagnose L. pneumophilia?
|
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) |
|
what's the treatment of L. pneumophilia?
|
macrolide (clarithromycin, azithromycin) or
fluoroquinolone (ciprofloxcin, levofloxcin) |