Podcast
Questions and Answers
Which of the following mechanisms allows Mycobacterium leprae to evade the host's immune response within macrophages?
Which of the following mechanisms allows Mycobacterium leprae to evade the host's immune response within macrophages?
- Triggering apoptosis in infected macrophages, limiting the spread of the bacterium to surrounding tissues.
- Inhibiting the acidification of the phagosome, preventing the activation of lysosomal enzymes. (correct)
- Stimulating the production of reactive oxygen species to overwhelm the macrophage's defense mechanisms.
- Activating the complement pathway to promote opsonization and subsequent clearance by other immune cells.
In lepromatous leprosy, the humoral immune response driven by Th2 cells is considered ineffective against Mycobacterium leprae primarily because:
In lepromatous leprosy, the humoral immune response driven by Th2 cells is considered ineffective against Mycobacterium leprae primarily because:
- Th2 cytokines suppress the activity of cytotoxic T cells, which are crucial for eliminating intracellular pathogens.
- The bacteria reside within cells, making them inaccessible to circulating antibodies. (correct)
- The excessive antibody production leads to immune complex formation, causing widespread inflammation and tissue damage.
- Antibodies produced by B cells are unable to penetrate the thick, waxy cell wall of _M. leprae_.
A patient presents with hypopigmented skin patches and localized loss of sensation. A skin biopsy reveals granulomas but very few acid-fast bacilli. Which of the following immunological profiles is most consistent with these findings?
A patient presents with hypopigmented skin patches and localized loss of sensation. A skin biopsy reveals granulomas but very few acid-fast bacilli. Which of the following immunological profiles is most consistent with these findings?
- Increased regulatory T cell (Treg) activity, suppressing both Th1 and Th2 responses and promoting bacterial persistence.
- Predominance of Th2 cytokines (IL-4, IL-5, IL-10) and high antibody titers against _M. leprae_.
- Dominant Th1 response with elevated levels of IL-2 and IFN-γ, leading to macrophage activation and granuloma formation. (correct)
- Suppressed cell-mediated immunity with impaired macrophage activation and reduced IFN-γ production.
Why is multidrug therapy (MDT) essential in the treatment of leprosy?
Why is multidrug therapy (MDT) essential in the treatment of leprosy?
The predilection of Mycobacterium leprae for infecting peripheral nerves is directly linked to its affinity for:
The predilection of Mycobacterium leprae for infecting peripheral nerves is directly linked to its affinity for:
A researcher aims to study the growth characteristics of Mycobacterium leprae in vitro. Which of the following approaches is most likely to yield successful cultivation of the bacteria?
A researcher aims to study the growth characteristics of Mycobacterium leprae in vitro. Which of the following approaches is most likely to yield successful cultivation of the bacteria?
A patient with lepromatous leprosy exhibits facial nerve paralysis, leading to lagophthalmos. What is the primary concern associated with this condition?
A patient with lepromatous leprosy exhibits facial nerve paralysis, leading to lagophthalmos. What is the primary concern associated with this condition?
The unique staining property of Mycobacterium leprae as an acid-fast bacillus (AFB) is attributed to which of the following cell wall components?
The unique staining property of Mycobacterium leprae as an acid-fast bacillus (AFB) is attributed to which of the following cell wall components?
In the context of leprosy diagnosis, a positive lepromin skin test typically indicates:
In the context of leprosy diagnosis, a positive lepromin skin test typically indicates:
What is the underlying pathological mechanism that leads to the collapse of the nose observed in some cases of lepromatous leprosy?
What is the underlying pathological mechanism that leads to the collapse of the nose observed in some cases of lepromatous leprosy?
Flashcards
Mycobacterium Leprae
Mycobacterium Leprae
Rod-shaped bacterium that causes leprosy (Hansen’s disease); an obligate intracellular organism that grows slowly at cool temperatures.
Pathogenesis of M. Leprae
Pathogenesis of M. Leprae
M. leprae enters through broken skin/lungs, targeting cooler areas like skin, peripheral nerves, and upper respiratory tract mucosa; infects Schwann cells, causing demyelination and nerve injury.
Immune Response to Leprosy
Immune Response to Leprosy
Involves a cell-mediated response via Th1 and Th2 cells; Th1 cells activate cytotoxic T cells and macrophages, while Th2 cells promote B-cell activation and antibody production.
Risk Factors for Leprosy
Risk Factors for Leprosy
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Clinical Features: Lepromatous
Clinical Features: Lepromatous
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Skin Biopsy for Leprosy
Skin Biopsy for Leprosy
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PCR for Leprosy
PCR for Leprosy
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Lepromin Skin Test
Lepromin Skin Test
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Treatment of Leprosy
Treatment of Leprosy
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Clinical Features: Tuberculoid
Clinical Features: Tuberculoid
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Study Notes
- Mycobacterium leprae is a rod-shaped, obligate intracellular bacterium, meaning it can only survive inside cells.
- It causes leprosy, also known as Hansen’s disease.
- Optimal growth occurs at cool temperatures (27–33°C), with slow proliferation; it is also an obligate aerobe.
Pathogenesis of Mycobacterium Leprae
- M. leprae enters through broken skin or the lungs, targeting cooler body areas like skin, peripheral nerves, and upper respiratory tract mucosa.
- It infects Schwann cells of peripheral nerves, which are responsible for myelin sheath formation around axons.
- M. leprae binds to laminin-2 on Schwann cells through phenolic glycolipid 1 (PGL-1), leading to demyelination and nerve injury.
- It evades destruction inside macrophages by inhibiting phagolysosomal fusion, allowing intracellular replication.
Immune Response
- Leprosy initiates a cell-mediated immune response via T-helper cells (Th1 and Th2).
- Th1 cells produce interleukin-2 (IL-2) and interferon gamma (IFN-γ), activating cytotoxic T cells, macrophages, and natural killer cells.
- Th2 cells release IL-4, IL-5, and IL-10, stimulating B-cell activation and antibody production.
Risk Factors
- Close contact with infected individuals or armadillos, which serve as animal reservoirs of the bacteria, increases risk.
- Older age and immunosuppressive conditions like diabetes, malignancy, or HIV infection are also risk factors.
Clinical Features of Leprosy
- Lepromatous form presents as numerous, raised, poorly demarcated skin lesions, often on the extremities.
- Symptoms of the Lepromatous form include diminished or absent sensation in affected areas and paresthesias (tingling or numbness) in hands or feet.
- Facial changes such as lion-like features, skin thickening, and eyebrow/eyelash loss is a sign of the Lepromatous form.
- In the Lepromatous form, extremity destruction includes collapse of the nose and loss of fingers/toes and ocular involvement such as uveitis.
- Facial nerve paralysis in the Lepromatous form leads to lagophthalmos (inability to close eyelids), potentially causing corneal ulcers.
- Lepromatous form induces a Th2 cell response resulting in a humoral (antibody-based) immune response which is ineffective against intracellular pathogens.
- Extensive skin involvement and symmetric nerve damage is due to the Lepromatous form, also known as multibacillary leprosy, which entails large bacterial numbers in lesions.
- Tuberculoid form presents as hypopigmented or reddish, well-demarcated skin patches.
- Symptoms of the Tuberculoid form, include mild nerve involvement, large peripheral nerve tenderness, hand weakness (claw fingers), and foot drop.
- Tuberculoid leprosy induces a Th1 cell response and a cell-mediated immune response.
- Tuberculoid form results in limited skin lesions and asymmetric nerve involvement, also called paucibacillary leprosy because of the low numbers of bacteria in lesions.
Diagnosis of Leprosy
- Diagnosis involves examining active skin lesion biopsies for acid-fast bacilli.
- Lepromatous form shows foam cells (lipid-laden macrophages) with many bacilli.
- Tuberculoid form displays few acid-fast bacilli and granulomas (immune cell collections).
- Polymerase chain reaction (PCR) detects M. leprae DNA.
- A positive Lepromin skin test (induration after 48 hours) suggests tuberculoid leprosy, a negative result suggests lepromatous leprosy.
- M. leprae is an acid-fast bacillus (AFB) due to its high mycolic acid content, which makes its cell wall waxy.
- M. leprae is hydrophobic and impermeable to routine stains like Gram stain, thus special stains like Ziehl-Neelsen are needed for visualization.
- The bacterium cannot be cultivated in vitro and must be inoculated in nine-banded armadillos due to their lower body temperature.
Treatment
- Multidrug therapy is crucial to prevent resistance.
- Lepromatous form is treated with dapsone, rifampin, and clofazimine for 12 months.
- Tuberculoid form is treated with dapsone and rifampin for 6 months.
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