Bacteriology 11: Mycobacteria, Nocardia, Actinomyces Flashcards

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1
Q

What staining method do we use for mycobacteria?

A

Acid-fast method. Does not stain well by gram method

Mycobacteria have a unique cell wall structure rich in mycolic acids, making them acid-fast. This means they resist decolorization by acids during staining procedures.

They are structurally classified as thin rods

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2
Q

Mycobacteria cell wall

A

Their cell walls contain high levels of mycolic acid and lipids, making them waxy and hydrophobic. This causes them to have slow growth for visible colonies.

Contain mycolic acid which has a waxy consistency and is hydrophobic
-allows cell to adhere to each other = causes aggregation
-protect against detergents, drugs and desiccation
-acts as a barrier to nutrient uptake, making it difficult for essential nutrients to enter the bacterial cell. This slows down their metabolism and replication.

Also contains Lipoarabamannan (LAM) which is structurally/functionally similar to LPS in gram (-)

Cell-envelope structure inside to out
Cytoplasm
Cytoplasmic cell membrane
Peptidoglycan
Arabinogalactan
Mycolic acids
-lipoarabinomannan (extend from cytoplasmic membrane to the outside)

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3
Q

Why does Tuberculosis love the lungs?

A

TB is caused by Mycobacterium tuberculosis primarily targets the lungs because the lungs provide an ideal environment for the bacteria to thrive. They are OBLIGATE AEROBES

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4
Q

The cord factor

A

The cord factor is a glycolipid molecule found in the cell walls of Mycobacterium tuberculosis and other pathogenic mycobacteria.
It plays a critical role in the virulence and pathogenesis of TB.

The cord factor contributes to the bacteria’s ability to evade the immune system and cause disease.
The cord factor is also responsible for the characteristic “serpentine cord-like” growth of the bacteria in culture, where the bacteria grow in tight, rope-like formations. grow in filaments

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5
Q

During what stage does granuloma formation for TB occur and Why would TB cause granuloma formation?

A

Granuloma formation allows TB to hide from host.

-contain infection
-latency

While granulomas help prevent the spread of the bacteria (contain the infection) they also provide a niche for the bacteria to persist in a dormant state, contributing to latent TB. The breakdown of granulomas can lead to reactivation TB and the progression of the disease.

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6
Q

What causes the reactivación of TB

A

Reactivation: In some cases, especially when the immune system weakens, the granuloma can break down, leading to the reactivation of TB and the spread of bacteria.

f the granuloma breaks down, the bacteria can be released into the lung tissue or the bloodstream, leading to reactivation TB or disseminated TB. This breakdown is more likely in people with weakened immune systems, such as those with HIV, diabetes, age, malnutrition, alcoholism.

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7
Q

Is the granuloma formed by the host or by Mycobacterium Tuberculosis?

A

The granuloma is formed by the host’s immune system.

When M. tuberculosis enters the lungs and infects macrophages, the bacteria evade destruction within these immune cells.
The immune cells aggregate around the infected macrophages, forming a well-defined structure. This structure is the granuloma.

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8
Q

TB diagnosis

A

acid fact stain = b/c TB = mycobacteria
We can grow TB in cultures but the growth is very slow due to the mycobacteria cell wall containing mycolic acid and high lipid concentration. There we must do a Tuberculin/Mantoux Test

-PPD is injected beneath the skin (towards the dermis) and “read” 48-72 hours later intradermal inoculation

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9
Q

Active TB diagnosis

A

chest x-ray
IGRA (interferon-gamma release assays) = confirmation
More sensitive than PPD

The PPD will show you have TB but it wont be able to differentiate b/w latent and active
Chest X-Ray:
Purpose: Helps visualize lung abnormalities and is a key diagnostic tool.
Findings:
Active TB: May show lung infiltrates, cavitary lesions, or lymphadenopathy.
Latent TB: Typically shows normal chest X-ray findings unless there is progression to active disease.

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10
Q

TB prevention and where and for whom is it used for

A

Vaccine
-BCG (Bacille cal meter-Guerin)
-live strain of Mycobactrium Bovis
-not used in the U.S

Used in developing countries to protect children against disseminated forms of TB

does not protect against pulmonary TB

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11
Q

TB treatment

A

Combo of antibiotics for extended periods (months) to ensure the complete eradication of the bacteria and prevent the development of drug resistance.

The treatment regimen varies depending on whether the TB infection is latent or active.
ANTI-TB AGENTS: isoniazid, Rifampin, Pyrazinamide and ethambutol

MDR-TB: resistant to isoniazid and rifampin
XDR-TB: literally everything

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12
Q

TB treatment

A

Combo of antibiotics for extended periods (months) to ensure the complete eradication of the bacteria and prevent the development of drug resistance.

The treatment regimen varies depending on whether the TB infection is latent or active.
The PPD will show you have TB but it wont be able to differentiate b/w latent and active. Must do Chest X-RAY to visualize lung abnormalities and is a key diagnostic tool.

ANTI-TB AGENTS: isoniazid, Rifampin, Pyrazinamide and ethambutol

MDR-TB: resistant to isoniazid and rifampin
XDR-TB: literally everything

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13
Q

Mycobacterium Avium complex (MAC)

A

Mycobacterium avium complex (MAC) refers to a group of closely related mycobacterial species, primarily Mycobacterium avium and Mycobacterium intracellulare, that cause infections, particularly in immunocompromised individuals causing pulmonary infection
MAC is an opportunistic pathogen

The cells are heavily infected

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14
Q

Nocardia
-gram +/-
-shape
-w/ or w/o O2
-distinct feature
-the human pathogens associated with this genus

A

-gram (+)
-bacilli = rod and they’re branched formation
-obligate aerobe and saprophytic
-cell wall contains mycolic acid (also seen in mycobacteria)
-N.asteroides and N.brasiliensis

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15
Q

Nocardia
-found in
-transmission
-pathogenesis

A

-found in soil worldwide
-inhalation of aerosolized bacteria (pulmonary)
inoculation injection from prick/skin trauma (cutaneous)
eye trauma
-Nocardia tens to remain localized in healthy patients vs. spread to many parts of the body in those w/ weak immune systems = Nocardiosis

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16
Q

Nocardiosis

A

Dissemination of Nocardia
-acute, chronic or relapsing

Most cases present as
-pulmonary infection (bronchopneumonia) = cough, fever, difficulty breathing
-nodule and cavities in the lung w/ acute inflammation
-dissemination to the brain can occur

17
Q

Nocardia clinical manifestations

A

-cellulitis
-keratitis
-brain abscess

18
Q

Nocardia diagnosis

A

Gram stain
OR
Culture from purulent skin lesions/sputum = acid fast stain

19
Q

Nocardia treatment

A

Tests for antibiotic sensitivity

-Trimethoprim-sulfamethoxazole is the drug of choice
=bactrim = TMP/SMX (always given together)
=folic acid metabolism synthesis antibiotics
=PABA —> DHF —> THF

20
Q

Actinomyces
-gram +/-
-shape
-w/ or w/o O2
-distinct feature

A

-gram (+)
-filamentous rods + increase branching and elongation compared to branching of Nocardia
-obligate anaerobe
-produce sulfur granules in pus and tissues

21
Q

Actinomyces epidemiology in the mouth

A

Are part of the normal flora and are a major component of dental plaque, particularly at the gingival crevice.

Ass. w/ root surface caries and their numbers increase during gingivitis.

22
Q

Actinomyces epidemiology overall

A

Despite being a normal inhabitant of mucosal surfaces (mouth, female genital tract, GI tract), Actinomyces can become pathogenic (opportunistic pathogen), causing a chronic, slowly progressive infection called actinomycosis when mucosal barriers are disrupted.

They are highly adapted to live on mucosal surfaces, but do not cause disease unless they get into deeper tissues with lower O2 levels since they are obligate anaerobes.

When mucosal barriers are breached, they can cause actinomycosis, a chronic infection characterized by abscesses, tissue fibrosis, and sinus tract formation. Cervicofacial actinomycosis is the most common form, often associated with dental infections (tooth extraction, periodontal disease) or trauma to mouth/jaw.

23
Q

Actinomyces Israelli

A

Early colonizer in plaque biofilms with many interactions

24
Q

Actinomyces Naeslundii

A

early colonizer in plaque biofilms w/ many interactions

25
Q

Most common form of Actinomycosis

A

Cervicofacial Actinomycosis (most common form):
Usually associated with dental infections, tooth extractions or trauma to mouth/jaw.
Angle of the jaw is generally involved.

Presents as a slowly progressive jaw or neck swelling with abscesses, and sinuses draining pus. The pus may contain sulfur granules, which are small, yellow particles made up of bacterial colonies.

26
Q

Chronic pelvic inflammatory disease is caused by what and due to colonization of what bacteria ?

A

intrauterine devices
Actinomycosis Israelii (early colonizer) has been found in cervical smears of women using Intrauterine contraceptive devices (IUD)

Actinomyces is a genus of Gram-positive, filamentous bacteria that are part of the normal flora of the mouth, GI tract, and female genital tract. When mucosal barriers are breached, they can cause actinomycosis, a chronic infection characterized by abscesses, tissue fibrosis, and sinus tract formation

27
Q

Eubacterium
-gram +/-
-shape
-w/ or w/o O2?
-distinct feature

A

-gram variable
-Rods - filaments
-obligate anaerobes
-Asaccharolytic = organisms are those that do not utilize carbohydrates as a primary source of energy.

28
Q

Eubacterium Role in the oral cavity

A

Isolated from plaque biofilms and calculus
-caries, periodontal disease, dentoalveolar abscesses
Comprise over 50% of the anaerobes of periodontal pocket

29
Q

Eubacterium Yurii

A

Involved in “corn-cob” formation in dental plaque

this strain is the one that is shown in the only picture of Eubacterium