24 - Mycobacterium Species Flashcards
Mycobacterium
- “Fungus bacterium”, named due to mould-like pellicle that floats on liquid (hydrophobic)
- Rod shaped, non motile bacterial cells
- Slow growing, strict aerobes
Characteristics of Mycobacterium
- Not classically gram positive or negative
- Unique, lipid rich cell wall (resists typical stains, thin layer of peptidoglycan, contains mycolic acids)
- Acid fast
How are pathogenic species grouped
- Growth rate (rapid vs slow)
- Disease (TB or not RB)
- Or by both
M. tuberculosis complex (MTBC)
- Slow growth rate
- Cord test positive
- All species capable of causing TB
- e.g. M. tuberculosis, africanum, bovis
Non TB Mycobacteria (NTM)
- All species that doesn’t cause TB or leprosy
- Slow or rapid growth rate
- Cord test negative
Tuberculous mycobacterial disease
- Mainly lung infection
- Weakness, weight loss, fever, cough
- Manifests slowly
- Airborne transmission
- Risk of transmission determined by
TB/HIV co infection
- TB progresses more rapidly with untreated HIV (Greater risk of reactivation, faster disease progression)
- Delayed diagnosis
- Further immune dysfunction
What is risk of transmission of TB determined by
- Infectious status of patient
- Proximity and frequency of contact
- Environmental factors
- Possible host factors in the exposed person
Initial infection of TB
- Droplet nuclei inhaled (can contain 1-3 bacilli, and remain airborne for minutes to hours)
- After inhalation, droplet nuclei can reach the alveolar membrane
Innate immune phase of TB
- Most Bacilli are contained or destroyed
- Some survive phagocytosis by blocking lysosome fusion with phagosome (replicate in macrophages, released when macrophages die)
- Major cell types: macrophages, neutrophils, dendritic & natural killer cells
- Bacilli grow until threshold number of organisms is reached
- No immediate host response as no toxin produced
Adaptive immune phase in TB
- Bacteria released from macrophages travel to lymph nodes and present to lymphocytes
- Stimulates cell mediated immunity
Cell mediated immune response in TB
- Recruitment and activation of T lymphocytes
- Release of lymphokines, monokines and cytokines by T cells
Release of lymphokines, monokines and cytokines by T cells
- Promotes recruitment of cells to infection site
- Activates macrophages to kill bacilli
- Triggers formation of early granuloma - Macrophages fuse to form multi nucleated giant cells or differentiate into foamy cells and surround the granuloma
latent TB
- Most bacilli die and granulomas heal
- Becomes latent TB (non-infectious)
First effective drug in TB
Streptomycin
Factors increasing incidence of TB
- Immigration from countries where TB is common
- Emergence of HIV
- Increased poverty
- Development of multi drug resistant strains
- Reduced funding for TB control
Cocktail of drugs used in treatment
Isoniazid, Rifampin, Ethambutol, Pyrazinamide
Causes of Multi Drug Resistant TB
- Administration of improper treatment regimens
- Poor supply of drugs
- Poor quality of drugs
- Poor patient compliance
- Poor follow up
- Lack of surveillance of drug resistance patterns
Mechanism of multi drug resistance
- Occurs via spontaneous chromosomal mutations
- Mutation confers advantage (selective pressue)
Current TB vaccine
- Bacille Calmette Guerin (BCG)
- Live, attenuated strain of M. bovis
Mycobacterium leprae
- Disease of nerves in persons with immune dysfunction
- Selectively affects the cooler parts of body (e.g. skin, URT, testes)
- Nerve damage causes anaesthesia, leads to unnoticed injury
- Spread by dropleys
Tuberculoid form of leprosy
Limited, non infectious, proper immune response
Lepromatous form of leprosy
Widespread infection, many lesions,
immunocompromised
Lab diagnosis of leprosy
- Non-culturable, obligate intracellular
- Diagnosed by microscopy: biopsy or split skin smears
Mycobacterium ulcerans
- Causes Buruli ulcer
- Third most common mycobacterial disease after TB and leprosy
- Environmental reservoir (stagnant water)
