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Flashcards in Mycobacteria Deck (61):

Mycobacterium are neither gram positive or gram negative; __________ are used instead/

-Acid fast stains


3 groups of mycobacteria

1. M. tuberculosis complex
2. nontuberculosis mycobacteria
3. M. leprae


Physiology and structure of mycobacteria

-slow rate of replication
-lipid-rich outer layer of mycolic acids
-resistant to desiccation
-acid-fast stains, not gram stains
-nonspore forming, non-motile bacilli
-obligate aerobes


3 several important properties due to myobacteria's outer layer of mycolic acids

-resistance to gram staining
-resistance against dessication which is important in airborne transmission
-myocolic acid biosynthesis is target for INH drug


Mycobacteria are facultative _______ pathogens



M. tuberculosis niche and mechanism for survival

-replication within macrophages
-stays within vesicle and prevents its fusion with lysosomes


Because M. tuberculosis is spread by an airborne route, it usually first encounters ________ and then is carried to a __________.

-alveolar macrophage
-regional lymph node


At the level of histopathology, the immune response to mycobacterial infections is dominated by __________.

-inflammatory aggregates of macrophages and T cells
-may contain multinucleated giant cells


Caseous necrosis often develops at the centers of _______ granulomas.



What type of immune response is required to combat tuberculosis?

-cell-mediated rather than humoral response, as expected in an intracellular pathogen
-Th1 response is most effective


While M. tuberculosis replicated well in resting macrophages, it can be killed by _______.

-activated macrophages


Why do HIV patients suffer from a high rate of tuberculosis?

-they lack their CD4+ T cell responses which are crucial in the cell mediated response necessary to combat TB


CD4+ T cells which recognize M. TB and become activated produce ________. What does this do?

-this in turn activates macrophages to produce TNF-alpha and to kill bacteria within their phagosomes


TB is one of the leading infectious causes of death worldwide. About ______ of the world's population are infected. Most of these infections are asymptomatic and fall into the category of LTBI. These people however have about a _______ lifetime risk of developing active TB.

-1/3 (2 billion)


T/F: TB is a relatively new disease of humanity.

-false; been with humans from the beginning


TB was also known as _____ in Europe.



Rates of TB continued to fall until the mid 1980s when the _______ spurred a rise in the incidence again.

-AIDS epidemic


Blocks/defects in what 3 things increase susceptibility to mycobacteria

-CD4+ T cell responses
-TNF blockage
-IFN-gamma receptor defects


Current problems with TB

-still many latent infections
-increasing drug resistance
-global levels of disease remain high, partly due to HIV


Risk factors for TB

-homelessness, urban poverty, malnutrition, crowding, alcoholism
-increases in inmates, healthcare workers, and immigrants from regions with high endemic TB


Transmission of TB

-airborne transmission by aerosol droplet nuclei
-can remain suspended in air for hours


Protection from TB requires what kind of mask?

-N95 respiratory mask


T/F: Having HIV doesnt increase risk of getting TB

-true, just makes it worse


Clinical diseas of primary TB infection

-aerosol deposition of bacilli into alveoli
-replication in macrophages and migration to regional LN
-control of infection with development of cellular immunity
-often no evidence of primary infection beyond position TST
-Lymphohematogenous seeding of lungs and extrapulmonary sites


Latent TB infection (LTBI)

-controlled primary infection without clinical disease
-no evidence of active TB on chest x-ray
-chest x-ray may show calcification at pulmonary site of initial infection (Ghon focus) or in mediastinal nodes (Ranke complex)


Reactivation of TB

-may occur after initial control of infection by immune system
-risk of reactivation if issue developed in cell-mediated immunity


In pulmonary TB, reactivation is most common where?

-apex of lung


Histologic Characteristics of pulmonary TB

-caseous necrosis and formation of cavities
-rupture of cavities into bronchi and spread to other areas of lung


Symptoms of Pulmonary TB

-local symptoms: cough and sputum production, shortness of breath
-Prominent systemic symptoms: fever, chills, night sweats, fatigue, weight loss
-highly contagious


3 other forms of TB outside of pulmonary TB

-primary progressive TB pneumonia
-Miliary TB
-extrapulmonary TB


Primary progressive TB pneumonia

-local disease following initial infection


Miliary TB

-progressive, disseminated hematogenous tuberculosis
-when M. tb overwhelms the immune system


Extrapulmonary TB

-direct spread along mucosal surfaces: GI tb, laryngeal TB
-direct extension form lungs to pleural space
-lymphohematogenous spread


What can extrapulmonary TB via lymphohematogenous spread cause?

-lymphadenitis (scrofula)
-renal TB
-Skeletal TB "pott's disease"


Lab diagnosis of TB

-Tuberculin skin test (TST or Mantoux test): intracutaneous injection of purified protein derivative (PPD)
-interferon-gamma release assays


Limits to Tuberculin skin test

-false positive TST reactions: other mycobacterium in environment, recent BCG vaccination
-false negative TST reactions: weakened cellular immune response, malnutrition or chronic disease, AIDS patients
-criteria for interpretation of TST reflect patient risk factors


T/F: it is the redness of a TST, not the induration that is diagnostic of TB

-false; it is the induration
-15 mm in everyone, lower if in higher risk population


How does a IGRA work?

-stimulates patient T cells with 2 peptides secreted by M. tb
-tests production of INF-gamma by patient T cells
-not affected by vaccination with BCG because uses 2 peptides not included in that vaccine


Culture and staining of M. tb

-smear and culture of sputum: culture may take 2-3 weeks or more to grow, DNA probes often used to rapidly ID isolate
-Acid-fast staining
-Fluorochrome stains


Molecular detection of TB

-PCR assays
-Xpert MTB/RIF assay: automated, rapid detection of Mtb, heminested real-time PCR of rpoB, detection of rifampin resistance


First line drugs for active TB

-Isoniazid (INH)
**Add Streptomycin for TB meningitis


Isoniazid (INH)

-inhibits mycolic acid synthesis
-strong, early bactericidal activity againt replication M. tb
-toxicity issues


Toxicity and Isoniazid

-peripheral neuropathy: competitively inhibits activity of pyridoxine as cofactor, so give P supplement for patients with nutritional deficiencies and chronic diseases


Rifampin and side effects

-inhibits RNA polymerase
-Side effects: orange body fluids, hepatitis, interactions with other drugs


Pyrazinamide function and toxicity

-targets 30S ribosomal protein RpsA
-inhibits trans-translation and recycling of stall ribosomes
-may act against semi-dormant organisms
-toxicity: hepatitis and polyarthralgia



-inhibits synthesis of cell wall arabinogalactan
-toxicity: retrobulbar neuritis: decreased red-green color discrimination or decreased visual acuity


Treatment of active TB

-use at least 3, usually 4, first line drugs
-treat for 6 months at least: 2 months on all 4, followed by 4 months of INH and RIF
-directly observe therapy to monitor adherence


How does one monitor TB while on medication?

-obtain sputum at least monthly
-90-95% should be negative sputum by 3 months-
-considered not contagious if 3 consecutive AFB smears are negative


Treatment of LTBI

-9 months of INH or 6 months of rifampin
-hepatic toxicity from INH increases over age 35


What type of vaccine is BCG vaccine?

-live, attenuated
-limited efficacy
-can cause disease in immunocompromised


What are the NTM?

-mycobacteria except M. tuberculosis and M. leprae
-divided into slow and rapid growers
-also classified by pigment production


Epidemiology of NTM

-frequently found in the environment


Clinical diseases from NTM

-Pulmonary diseases: chronic cough, fatigue, weight loss, NO fever
-Disseminated MAC: in HIV patients with Cd4+ <50, fever, weight loss, anemia, diarrhea, hepatosplenomegaly, no respiratory symptoms
-hypersensitivity pneumonitis: hot tub lung
-cervical lymphadenitis: in young children, usually from MAC, swollen but limited signs of inflammation
-Skin and soft tissue infections: rapid growers


Testing and laboratory diagnosis of NTM

-usually need culture of organism
-may be found as non-pathogens in cultures from non-sterile sites


Treatment of NTM

-multiple drug regimens
-prolonged courses of treatment
-antibiotic prophylaxis for HIV patients to prevent disseminated MAC


Leprosy is also called ________.

-Hansen's disease


T/F: Leprosy is easy to culture in vitro

-false; still cannot be
-infects wild armadillos and can be cultured in mouse footpads


How is leprosy spread?

-contact with nasal secretions or droplet spread
-perhaps biting insects?


Clinical manifestations of leprosy

-grows as lower temperatures found within skin and extremities
-peripheral sensory nerve damage
-infiltrative skin lesions
-2 categories of disease: multibacillary or paucibacillary


How is Leprosy diagnosed?

-history, exam, and biopsy
-NO CULTURE bc it cannot be grown in vitro


Treatment of leprosy

-multidrug regimens
-rifampin, dapsone, clofazimine
-5 years of treatment