Spirochaetes
⭐ Definition and common properties ★★★
Spirochetes are long, slender, helical, soft and actively motile prokaryotes.
Common properties
- Long and slender, helical in shape
- Reproduce by binary fission
- Sensitive to penicillin
- Structure: an outer membrane (sheath) · AXIAL FILAMENTS (endoflagella) · a protoplasmic cylinder
| Family | Genus | Species and disease |
|---|---|---|
| Spirochaetaceae | Treponema | T. pallidum subsp. pallidum (TP) → SYPHILIS |
| Borrelia | B. burgdorferi → Lyme disease B. recurrentis → relapsing fever | |
| Leptospiraceae | Leptospira | L. interrogans → leptospirosis |
The definition alone is one mark; the remaining three come from the properties.
Structure — an outer membrane (sheath), axial filaments (endoflagella) lying between the sheath and the protoplasmic cylinder, and the protoplasmic cylinder itself. The endoflagella are what make them actively motile with a corkscrew movement.
Position — they are true bacteria: they divide by binary fission and are sensitive to penicillin. Their softness and flexibility, not any deficiency, is what sets them apart from ordinary bacilli.
The three medically important genera — Treponema (syphilis), Borrelia (Lyme disease, relapsing fever) and Leptospira (leptospirosis).
An ordinary motile bacterium — E. coli, Salmonella — pushes itself along with flagella that stick out into the surrounding fluid. A spirochaete's flagella are wrapped around the protoplasmic cylinder, underneath the outer sheath. That is what endoflagella or axial filaments means.
Rotating them does not beat the fluid; it makes the whole helical cell corkscrew. And a corkscrew works where a propeller does not — in viscous media and through tissue.
Two consequences you can see clinically. T. pallidum penetrates intact mucous membranes; Leptospira penetrates intact mucosa and small skin abrasions. Neither needs a wound or a vector.
And in the laboratory: because the organism is too slender to see by ordinary light microscopy but is actively motile, it is diagnosed by dark-field microscopy of living, unstained material — you find it by its movement.
- Define a spirochete. → A long, slender, helical, soft and actively motile prokaryote
- Name its three structural components. → Outer membrane (sheath), axial filaments (endoflagella), protoplasmic cylinder
- Name the three genera and their diseases. → Treponema — syphilis · Borrelia — Lyme disease and relapsing fever · Leptospira — leptospirosis
- Are they penicillin-sensitive? → Yes
Treponema pallidum — biological properties ★★★
| Property | Detail |
|---|---|
| Morphology | 6–15 µm long, 0.1–0.2 µm in diameter; coiled evenly with 1 µm spacing; actively motile |
| Staining | Silver staining — the Fontana silver impregnation stain — brown colour. Active movement is seen under dark-field light microscopy without staining |
| Culture | NOT successfully cultured in vitro |
| Resistance | Very weak — easily inactivated by heat (42 °C), cold (4 °C), desiccation and disinfectants. Sensitive to penicillin and tetracycline |
Virulence factors and pathogenesis
| Factor | Action |
|---|---|
| Outer membrane proteins | Adherence |
| Hyaluronidase | Promotes invasion |
| Coating with host fibronectin | Protects against phagocytosis |
| The host immune response | Results in tissue destruction — the granulomatous lesions of tertiary syphilis |
Infection with T. pallidum is limited to humans, and is acquired by direct sexual contact and, less commonly, transplacentally (congenital disease) or through occupational exposure. The source of infection is patients with primary and secondary lesions.
- Describe T. pallidum. → 6–15 µm long, 0.1–0.2 µm wide, evenly coiled at 1 µm spacing, actively motile
- How is it visualised? → Fontana silver impregnation stain (brown), or by its active movement under dark-field microscopy without staining
- Can it be cultured? → No — not successfully in vitro
- Name its four virulence factors. → Outer membrane proteins (adherence) · hyaluronidase (invasion) · host fibronectin coating (antiphagocytic) · the host immune response causing tissue destruction
- How is syphilis acquired? → Direct sexual contact; less commonly transplacentally or by occupational exposure. Infection is limited to humans
⭐ Acquired (venereal) syphilis ★★★
Primary syphilis
| Detail | |
|---|---|
| Incubation | 10–90 days |
| Development | TP multiply → erythema, induration → hard chancre |
| Symptoms | A painless “HARD CHANCRE” — a slightly elevated, round, superficial ulcer with a firm base · swollen regional lymph glands · highly contagious, less destructive |
| Course | After 2–6 weeks the skin lesion heals WITHOUT treatment, and TP enter the lymphatics and disseminate |
Secondary syphilis — after an asymptomatic period of 2–24 weeks
| Detail | |
|---|---|
| Process | TP multiply in many different tissues |
| Symptoms | A pale red rash throughout the body — skin, mucosa, organs, eyes · slight fever, generalised lymphadenopathy, malaise |
| Contagiousness | The lesions are HIGHLY CONTAGIOUS; they last 2–6 weeks |
Latent infection
No symptoms, but antibody positive. Lasts 3–10 years. One-third to one-half of cases progress to tertiary syphilis. The deck's key-points slide puts it precisely: latent disease is characterised by the absence of symptoms but with a positive serologic test result.
Tertiary syphilis
| Detail | |
|---|---|
| Characteristic lesion | Granulomatous lesions — GUMMAS |
| Behaviour | Highly DESTRUCTIVE, less CONTAGIOUS |
| Sites | Skin, eyes, bones, CNS and cardiovascular system — almost any tissue |
| Cause | A hyperimmune reaction to TP |
| Manifestations | CNS: neurosyphilis → paralysis · eye: blindness · heart: aneurysm (aortic damage) |
| Fatalities | 80% cardiovascular involvement · 20% neurologic involvement |
Read the three stages side by side and one pattern runs through them, and it is the answer to the deck's own examination question.
Primary — highly contagious, less destructive. A single painless ulcer teeming with organisms.
Secondary — lesions highly contagious. Organisms everywhere; little permanent damage.
Tertiary — highly destructive, less contagious. Gummas that wreck the aorta and the brain, but containing almost no organisms.
The seesaw is explained by one sentence in §2: the host immune response results in tissue destruction. Early on the organism multiplies freely, so the patient is infectious and undamaged. Later the immune system has learned to attack it, so the organisms are few — and the hyperimmune reaction against those few is what destroys tissue. The gumma is a granuloma, exactly as in tuberculosis.
So the deck's question — in which stage is a person considered not infectious? — has the answer E. Tertiary.
Two traps in this history. The chancre is painless, so it is ignored; and it heals without treatment, so the patient believes it is over. The disease continues silently for a decade. Penicillin is the drug of choice at every stage, and this is why screening matters.
- Describe primary syphilis. → Incubation 10–90 days; a painless hard chancre — a raised round superficial ulcer with a firm base — with swollen regional nodes; highly contagious, less destructive; heals in 2–6 weeks without treatment as TP disseminate via the lymphatics
- Describe secondary syphilis. → After 2–24 asymptomatic weeks: pale red rash over skin, mucosa, organs and eyes; slight fever, generalised lymphadenopathy, malaise; lesions highly contagious for 2–6 weeks
- Describe latent infection. → No symptoms but antibody positive; lasts 3–10 years; one-third to one-half progress to tertiary
- Describe tertiary syphilis. → Granulomatous gummas, highly destructive and less contagious, from a hyperimmune reaction; neurosyphilis and paralysis, blindness, aortic aneurysm; 80% of deaths cardiovascular, 20% neurologic
- In which stage is the patient not infectious? → Tertiary
- What is the drug of choice? → Penicillin, at all stages
Congenital syphilis ★★★
In pregnant women with early syphilis, about 50% of fetuses are aborted or stillborn; the rest present diverse syphilitic symptoms.
| Stage | Features |
|---|---|
| Early congenital syphilis — during the first 2 years of life | Rhinitis (runny nose) · vesicular rash and bullae · osteochondritis (bone destruction, e.g. of femur and tibia) · cardiovascular syphilis |
| Late congenital syphilis — after 2 years of age | Interstitial keratitis · tooth deformation — notched incisors and moon molars · eighth-nerve deafness · neurosyphilis and cardiovascular lesions · bone deformation — saddle nose and sabre shin |
The classical trio of late congenital syphilis: interstitial keratitis · notched (Hutchinson's) incisors · eighth-nerve deafness.
Prevention and treatment: safe sexual practice; treat patients to eliminate the source of infection; penicillin.
Transplacentally to the fetus is exactly the definition Unit 4 §4 flagged: vertical transmission, a 2019 Section I item, meaning mother-to-offspring spread whether transplacental, at delivery, or by breast milk.
T. pallidum is one of the standard examples, alongside HBV, HIV, rubella and CMV. It is also why antenatal syphilis screening exists in every country's programme: the mother may be entirely asymptomatic in the latent stage, and half the pregnancies end in abortion or stillbirth.
Note the pattern in the two rows above. Early congenital syphilis is active infection — rhinitis full of organisms, a rash, inflamed growing bone. Late congenital syphilis is the scar — deformed teeth that formed badly, a collapsed nasal septum, a bowed tibia, a deaf nerve. The same contagious-then-destructive sequence as acquired disease, played out over a childhood.
- What happens to the fetus in maternal early syphilis? → About 50% are aborted or stillborn; the rest have congenital syphilis
- Name the features of early congenital syphilis. → Rhinitis, vesicular rash and bullae, osteochondritis, cardiovascular syphilis — in the first two years
- Name the features of late congenital syphilis. → Interstitial keratitis, notched incisors and moon molars, eighth-nerve deafness, neurosyphilis, cardiovascular lesions, bone deformation (saddle nose, sabre shin)
- What is Hutchinson's triad? → Interstitial keratitis, notched incisors, eighth-nerve deafness
Leptospira interrogans ★★★
| Property | Detail |
|---|---|
| Morphology | 0.1 µm in diameter, 6–20 µm long; tightly coiled with very fine spirals (0.1–0.2 µm wide); HOOKED ENDS |
| Serotypes | 273 |
| Resistance | Survives several weeks to months in water or moist soil. Sensitive to heat (killed at 56 °C in 10 min), desiccation, disinfectants and penicillin |
Leptospirosis — a zoonosis with worldwide distribution
| Detail | |
|---|---|
| Source | Rats and pigs — the organism multiplies in the KIDNEY and is shed in the URINE. Leptospira are maintained in nature by chronic renal infection of carrier animals, specifically rodents |
| Route of transmission | Direct contact with contaminated water or moist soil, or infected animal urine — Leptospira can penetrate INTACT mucous membranes or skin through small cuts and abrasions · GI tract by ingesting contaminated food or water · vertical transmission through the placenta to the fetus |
| Clinical course | Intact mucosa or broken skin → blood (bacteraemia) → all tissues: liver, kidney, CNS. Incubation 7–14 days |
| Initial symptoms | An influenza-like illness — fever, chills, severe headache, myalgia, malaise, nausea and vomiting — persisting about 7 days |
| Progression | To severe systemic illness: meningitis, haemorrhage, hepatic and renal dysfunction |
The most serious form of leptospirosis: jaundice, renal dysfunction and haemorrhage, with a high mortality. Death is due to renal failure.
Treatment requires penicillin, amoxicillin, ampicillin or doxycycline. Prevention rests on reducing the risk of exposure to soil and water contaminated with rodent urine.
In the animal, Leptospira sets up a chronic renal infection and is shed in the urine — which is how it survives in nature without killing its host, and why the reservoir is permanent.
In the human, the same organ preference produces renal dysfunction, and death in Weil's disease is due to renal failure.
Between them lies the epidemiology: rodent urine contaminates water and moist soil, where the organism survives for weeks to months, and it penetrates intact mucosa — no bite, no vector, no wound needed. That is why leptospirosis is a disease of flooding, rice paddies, sewers and recreational water, and why prevention is exposure reduction rather than vaccination.
Contrast the two spirochaetes of this unit. T. pallidum: human-only, sexually transmitted, uncultivable, chronic over decades. L. interrogans: a zoonosis from water, acute over days, killing through the kidney. Same shape, opposite lives.
- Describe Leptospira. → 0.1 µm wide, 6–20 µm long, tightly coiled with fine spirals and HOOKED ENDS; 273 serotypes
- Where is the reservoir maintained? → In chronic renal infection of carrier animals, especially rodents — shed in the urine
- How is it transmitted? → Contact with contaminated water or moist soil or animal urine, penetrating intact mucosa or small skin abrasions; ingestion; and vertically through the placenta
- Describe the clinical course. → Entry → blood → liver, kidney, CNS; incubation 7–14 days; influenza-like illness for about 7 days, then severe systemic illness with meningitis, haemorrhage, hepatic and renal dysfunction
- What is Weil's disease? → Infectious jaundice — the most serious form, with jaundice, renal dysfunction and haemorrhage, high mortality, death from renal failure
- How is it treated and prevented? → Penicillin, amoxicillin, ampicillin or doxycycline; reduce exposure to soil and water contaminated with rodent urine
Revision
The deck's summary slide
Definition: spirochete · common properties of spirochetes · major pathogens — TP causing syphilis and L. interrogans causing leptospirosis. The deck's question — “in which stage of syphilis can a person be considered not infectious?” — has the answer E. Tertiary.
The whole unit on one screen
| Question | Answer |
|---|---|
| ⭐ Definition? | Long, slender, helical, soft, actively motile prokaryotes |
| Structure? | Outer sheath · axial filaments (endoflagella) · protoplasmic cylinder |
| Three genera? | Treponema (syphilis) · Borrelia (Lyme, relapsing fever) · Leptospira (leptospirosis) |
| TP culture? | Cannot be cultured in vitro |
| TP staining? | Fontana silver (brown) or dark-field unstained |
| Primary syphilis? | Painless hard chancre, 10–90 d, heals untreated in 2–6 wk |
| Secondary? | After 2–24 wk — pale red rash all over, highly contagious |
| Latent? | No symptoms, antibody positive, 3–10 yr; ⅓–½ progress |
| Tertiary? | Gummas — destructive, not contagious; 80% deaths cardiovascular |
| Congenital? | Hutchinson's triad — keratitis, notched incisors, deafness |
| Leptospira? | Hooked ends; rodent urine in water/soil; Weil's disease, death from renal failure |
| Treatment? | Penicillin for both |
- Define spirochete for 4 marks. → Long, slender, helical, soft, actively motile prokaryotes, with an outer sheath, axial filaments (endoflagella) and a protoplasmic cylinder; they divide by binary fission and are penicillin-sensitive
- Give the four stages of acquired syphilis. → Primary (painless hard chancre, contagious, self-healing) · secondary (generalised pale red rash, highly contagious) · latent (asymptomatic, antibody positive, 3–10 years) · tertiary (destructive gummas, CNS and cardiovascular, not contagious)
- Why is tertiary syphilis destructive but not infectious? → It is a hyperimmune granulomatous reaction to few organisms, not active multiplication
- What is Hutchinson's triad? → Interstitial keratitis, notched incisors, eighth-nerve deafness — late congenital syphilis
- Describe leptospirosis. → A zoonosis from rodent urine in water or moist soil, penetrating intact mucosa; influenza-like illness progressing to meningitis, haemorrhage and hepatic and renal dysfunction; Weil's disease is the severe jaundiced form, killing by renal failure