Mycobacteria

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MYCOBACTERIA

General characteristics
slender rods ,non motile and do not form spores
are strictly aerobic
Most species grow slowly
lipid-rich cell walls that are resistant to penetration by chemical dyes, such as
those used in the Gram stain
They stain poorly but, once stained, cannot be easily decolorized so they called
acid-fast.
Their cell walls contain unique mycolic acids .
Their cell walls make them impermeable to chemical disinfectants, and resistance
to acids or alkalis.
also resistant to drying, but not to heat or ultraviolet irradiation
Bacteria classified in the genus Mycobacterium on the basis of
 Acid- fastness
 Presence of mycolic acid
 A high G+C
MYCOBACTERIUM TUBERCULOSIS
• Are intracellular pathogens and able to establish lifelong infection
• Slow growing
• Humans are the only reservoir
• Obligate aerobe & non – sporulated
• Withstand week disinfectants and drying
• Acid-fast bacteria due to high concentration of lipids/mycolic fatty
acids in the cell wall
Virulence Mechanisms and Virulence Factors of M.tb
M.tb does not possess the toxins, capsules and fimbriae
However, a number of structural and physiological
properties of the bacterium are contributed to bacterial virulence
and the pathology tuberculosis
 Cell wall of M.tb is thick consisting of plasma membrane surrounded by a complex wall
structure harboring virulence factors such as:
• Peptidoglycan
• Arabinogalactans
• Mycolic fatty acid (long chain fatty acids)
• Glycolipids
• Lipoarabinomanans (down regulate the oxidative cytotoxic mechanism)
Clinical significance:
 Primary tuberculosis occurs in a person who has had no
previous contact with the organism.
• 10% of those with an arrested primary infection develop
clinical tuberculosis at some later time in their lives.
 Primary tuberculosis is usually acquired via the respiratory
tract; therefore, the initial lesion occurs in a small bronchiole
or alveolus in the mid lung periphery.
 Primary tuberculosis follows one of two courses:

1. If the lesion arrests, the tubercle undergo fibrosis and calcification,

2. alternatively, if the lesion breaks down, the caseous material is


discharged, and a cavity is created that can facilitate spread of the
infection.
• The organisms are dispersed by the lymph and the bloodstream, and
can be seeded in the lungs, regional lymph nodes, or various distant
tissues, such as liver, spleen, kidneys, bone, or meninges.
• In progressive disease, the resulting tubercles may expand, leading to destruction
of tissue and clinical illness; for example,
 chronic pneumonitis,
 tuberculous osteomyelitis, or
 tuberculous meningitis
 In the extreme instance, active tubercles develop throughout the body, and a
serious condition known as miliary (disseminated) tuberculosis results.

N.B: The disease can undergo haematogenous & lymphatic dissimination


 Reactivation of tuberculosis: Reactivation is apparently
caused by an impairment in immune status, often associated
with malnutrition, alcoholism, advanced age, or severe stress.
 Immunosuppressive medication or diseases such as
diabetes and, particularly, AIDS, are common
preconditions.
Clinical Presentation
 Weight loss
 Productive cough (For more than a month)
 Chest pain
 High fever
 Night sweating
 Haemoptysis
Laboratory identification:

Specimens: Sputum, CSF, Biopsy or FNA

1. Ziehl Neelson staining / AFS

2. Mycobacterial culture
 Middle brook 7H10 & 7H11 media
 Lowenstein - Jensen egg based media
 Middlebrook 7 H9 & 7H12

3. Molecular Techniques
Treatment
 First line anti-TB drugs: Isoniazid (INH), Rifampin,
Ethambutol, Pyrazinamide, Streptomycin
 N.B: B/n 1 in 106 & 1 in 108 tubercle bacilli are
spontaneous mutants resistant to first line drugs ----
MDRTB
 Second line anti-TB drugs: Kanamycine, Capreomycin
Cycloserine, Ethionamide, Ciprofloxacin
 Because strains of the organism resistant to a particular agent
emerge during treatment, multiple drug therapy is employed to
delay or prevent emergence.
 Drug resistance: Mutants resistant to each of these agents have
been isolated even prior to drug treatment.
 Multidrug-resistant M tuberculosis (MDR-TB) (resistant to both
isoniazid and rifampin) is a major and increasing problem in
tuberculosis treatment and control.
 Such strains are prevalent in certain geographic areas (hospitals
and prisons).
Prevention & control
 Early case detection & treatment
 Decreasing of over crowding
 Pasteurization of milk --- ↓ M. bovis infection
 Health education
 Immunization
 A vaccine against tuberculosis has been available since early in the twentieth century.

 It is produced from Bacille Calmette-Gurin (BCG), an attenuated strain of M. bovis.

 When injected intradermally, it can confer tuberculin hypersensitivity and an

enhanced ability to activate macrophages that kill the pathogen.


 is about eighty percent protective against serious forms of tuberculosis, such as

meningitis in children, and has been used in mass immunization campaigns.


Mycobacterium leprae

 it has not been cultivated on nonliving bacteriologic media


 It causes leprosy
 Typical acid-fast bacilli
 The bacilli are often found within the endothelial cells of
blood vessels or in mononuclear cells.
Epidemiology
Leprosy (Hansen disease) is a worldwide much larger problem
M. leprae is transmitted from human to human through:
• prolonged contact;

• more commonly through nasal droplets from a patient with


lepromatous disease.
The incubation period is probably 2–10 years.
Without prophylaxis, about 10% of exposed children may acquire the
disease.
Leprosy is a chronic granulomatous condition of peripheral nerves and
mucocutaneous tissues, particularly the nasal mucosa.
 In tuberculoid leprosy,
 the lesions occur as large maculae (spots) in cooler body tissues such as skin
(especially the nose, outer ears, and testicles), and in superficial nerve
endings.
 Neuritis leads to patches of anesthesia in the skin.
 Non contageous (small number of organisms present)
 Cases have minimal disease and positive skin test
 Known as paucibacillary Hansen’s disease
 Lepromatous leprosy,
 nodular dermal and mucosal lesions develop.
 Nerve inflammation and neuro paralysis follow,
 eventually resulting in mutilations.
 Large numbers of organisms are present in the lesions
 Spreads systematically with involvement of RES
 Known as multibacillary Hansen’s disease
Clinical finding
 Lesions involving:
 Skin (causing disfigurement)
 Superficial nerves
 Nose, pharynx, eyes and testicles
 Lymphadenopathy
 Incubation period-2 -10 years
Laboratory identification:

Specimen:
 Scrapings from skin/nasal mucosa
 Biopsy from earlobe
 Ziehl Neelson staining technique
 Culture
 has not been successfully maintained in artificial culture, but can be grown in the footpads of
mice and in the armadillo.
 Histology
 Molecular techniques
Treatment
 Dapsone & rifampin
 Suppress the growth of M. leprae

N.B: Without prophylaxis, about 10% of exposed children


acquire the disease
 Prevention and control
 Identification & treatment of cases
 Provision of chemopropylaxis------ risk groups
 BCG vaccination -------endemic areas
 Health education

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