Dracunculus Medinensis: Synonyms

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Dracunculus medinensis

SYNONYMS
Gordius medinensis Linnaeus, 1758;
Filaria medinensis L.; Fuellebornius medinensis Leiper,
1926.
Disease and common names
Dracunculiasis or dracunculosis, dracontiasis;
guinea or medina worm, le dragonneu,filaire de Medine.
Geographical distribution
Dracunculus is now found only in the
Countries of West and Central Africa justsouth of the
Sahara (Benin, Burkina Faso, Central African Republic, C ˆ
ote d’Ivoire,Ghana, Mali, Mauritania, Niger, Nigeria,
Sudan, Togo and Uganda). There are also very small foci in
Cameroon and Ethiopia and possibly still in Chad, Kenya
and Senegal. Infection has been officially eliminated from
the formerly endemic areas in
India (1999) and Pakistan (1994) in the last few years and
the disease has probably now vanished from Saudi Arabia
andYemen.
Location in host
Adult females emerge from the subcutaneous tissues,
usually of the foot or lower limbs but sometimes from
any part of the body.
Morphology
The mature female measures 500–800 mm 1.0–2.0 mm.
The mouth has a triangular oval opening surrounded by a
quadrangular cuticularized plate, with an internal circle of
four double papillae.
The vulva opens halfway down the body but is non-
functional in the mature worm.
The uterus has an anterior and a posterior branch and is
filled with 1–3 million embryos; it fills the entire body cavity
(pseudocoel), the gut being entirely flattened.
Males recovered from experimental infections in animals
measure 15–40 mm 0.4 mm (Fig. 114). The tail has 4 (3–6)
Morphology 2

Adult female and smaller male of D.medinensis.


Morphology 3
 pairs of preanal and 4–6 pairs of postanal papillae; the
subequal spicules are 490–750 μm long, with a
gubernaculum measuring about 117 μm.
Life Cycle
Adult females in subcutaneous tissues of the legs and
arms.
Blister forms over nematode. Breaks when exposed to
water.
Nematode uterus ruptures and discharges first stage
juveniles into the water (ovoviviparous).
Juveniles ingested by copepod (intermediate host, 2
molts within copepod).
Copepod swallowed by human.
Juveniles migrate via lymph system.
Develop to adults in subcutaneous tissues.
First-stage larvae of Dracunculus medinensis in water (phase contrast) after being
expelled by adult female (actual size 0.66 mm).
Dracunculus medinesis
(Dracunculiasis)
Group 8
Clinical
Manifestations/Symptoms
There are usually none while the female worms are
moving freely through the connective tissues,until
blister forms and toxic fluids result in:-

 a rash accompanied by severe itching


 nausea
 vomiting
 diarrhea
 dizziness.
Clinical Manifestations cont..
In many patients (30–80%), urticaria, sometimes
accompanied by fever, giddiness, gastrointestinal
symptoms, dyspnoea and infraorbital oedema, appears
the day before the blister forms but vanishes in a few
hours.
Clinical Manifestations cont..
Secondary bacterial infections of opening are
possible.

There may be later symptoms--fibrosis of the skin,


muscles, tendons and joints ( may interfere with
locomotion or use of limbs).

Dracunculiasis can
migrate to the foot
Clinical Complications
Redness and swelling (Cellulitis)
Boils (Abscesses)
Generalized Infection (Sepsis)
Joint Infections (Septic Arthritis)
Lock Jaw (Tetanus)
Pathogenesis
The blister fluid consists of a bacteriologically sterile fluid
containing lymphocytes, neutrophils, eosinophils and larvae.

The female worm bursts in the tissues before emergence,


releasing many thousands of larvae upon contact with water
(temperature sensitive)

This results in an intense tissue reaction, with myositis and


formation of an abscess containing up to 0.5 l of pus, which
can lead to chronic ulcerations, bubo or epididymo-orchitis in
males.
Pathogenesis cont..
Adult females sometimes enter joints and liberate
larvae into the synovial fluid, causing oedema,
congestion and plasma-cell infiltration of the synovial
membrane.

Once larvae have been released from the emerging


female worm, there is a strong adhesive reaction at the
cuticle along the whole length of the worm.
Pathogenesis cont..
In the early stages, the tissue reaction consists of
inflammatory cells and is followed by a foreign- body
giant-cell reaction.

This makes extraction of the worm difficult and


increases the chances of secondary bacterial infection
along the track of the worm, with cellulitis.
Diagnosis
Clinical and parasitological
• Local itching, urticaria and a burning pain at the site
of a small blister are usually the first signs of
infection,sometimes a palpable and sometimes
moving worm.

• The blister bursts in about 4 days and active larvae,


can be recognized under a low-powered microscope.
Diagnosis cont..
Immunological.
• ELISA, dot ELISA and SDS-PAGE/Western blotting

The fluorescent antibody test using deep-frozen


first-stage larvae.
Treatment
 Surgery
• Surgical removal of mature female worms before
emergence is sometimes possible using a small incision.

 Chemotherapy
• Thiabendazole,niridazole, metronidazole, mebendazole
and albendazole have been reported as hastening the
expulsion of worms and may act as anti-inflammatory
agents.
Prevention and Control
Mode of transmission
Filter or boil water, or treat with chlorine to kill intermediate
host

Reservoir
Avoid bathing or wading or drinking contaminated water -
reservoir

Susceptible Host
Remove worms by extraction or with surgery
Drug Therapy
Prevention and Control
Mode of Transmission/Reservoir/Point of Entry/Point of
Exit/Susceptible Host
Health education interventions by local health workers
Sudanese boys using pipe filters to prevent guinea worm
disease

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