Infectious neuropathies: leprosy, diphtheria, zoster
- Lesion
Some microbes live in nerves (leprosy), some poison myelin (diphtheria), and some hide in nerve ganglia and come back (shingles).
What it is
Infections damage peripheral nerves in several ways. Mycobacterium leprae invades Schwann cells of cool superficial nerves; the host's immune response decides the form, from few-lesion tuberculoid leprosy with granulomas that destroy nerves, to lepromatous leprosy with nerves full of bacilli. Leprosy still occurs in Colombia and is a leading infectious cause of neuropathy worldwide. Diphtheria toxin causes demyelination, beginning with palatal and eye muscles. Varicella-zoster virus remains latent in sensory ganglia and reactivates as shingles. HIV causes distal painful polyneuropathy and other forms; Lyme disease causes facial palsy and radiculoneuritis; CMV causes polyradiculopathy in advanced AIDS.
Structure
- Tuberculoid leprosy: epithelioid granulomas within and around nerves, destroying them; acid-fast bacilli hard to find.
- Lepromatous leprosy: sheets of foamy macrophages (lepra cells) and Schwann cells packed with acid-fast bacilli (Fite stain); nerves thicken and fibrose.
- Diphtheria: segmental demyelination without much inflammation, starting near the dorsal root ganglia.
- Zoster: haemorrhagic inflammation of the sensory ganglion, Cowdry A inclusions, neuronal loss and later fibrosis.
Step by step
- M. leprae enters Schwann cells by binding laminin-2 and dystroglycan of the basal lamina.
- The bacilli multiply slowly in cool nerves of the skin and limbs.
- A strong Th1 response forms granulomas that clear bacilli but destroy nerve (tuberculoid).
- A weak cellular response lets bacilli fill macrophages and nerves (lepromatous); immune reactions can flare later.
- Loss of sensation leads to painless injuries, ulcers, infections and resorption of fingers and toes.
Leprosy at the two poles
| Feature | Tuberculoid | Lepromatous |
|---|---|---|
| Immune response | Strong Th1 (IFN-γ, IL-2) | Weak cellular, Th2-type |
| Skin lesions | Few, well-defined, anaesthetic | Many, nodular, symmetric; leonine face |
| Bacilli | Few | Very many |
| Nerve pathology | Granulomas destroy nerves early | Bacilli-filled Schwann cells and macrophages |
| Lepromin skin test | Positive | Negative |
Clinical notes
- Leprosy is curable with multidrug therapy, and early treatment prevents deformity; Colombia still reports new cases each year.
- Diphtheria is prevented by vaccination; the neuropathy appears weeks after the throat infection.
- Antiviral treatment of zoster in the first days lowers pain; vaccination reduces the risk of zoster and postherpetic neuralgia.
Test yourself
Think of the answer, then tap the question to see it.
Which cell does Mycobacterium leprae invade in nerves?
The Schwann cell.
How do tuberculoid and lepromatous leprosy differ in immunity?
Tuberculoid has a strong Th1 response with granulomas and few bacilli; lepromatous has weak cellular immunity and many bacilli.
How does diphtheria toxin cause neuropathy?
It blocks protein synthesis in Schwann cells, producing demyelination.
Where does varicella-zoster virus stay latent?
In sensory ganglia (dorsal root and cranial nerve ganglia).
Elsewhere in DurgiPedia
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Leprosy (World Health Organization, 2025); Diphtheria (World Health Organization, 2025); Herpes Zoster (StatPearls (NCBI Bookshelf), 2025).
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Representative model, for educational purposes only.