What is gnathostomiasis?
Gnathostomiasis is a zoonosis (an infection passed on from animals) caused by larvae of a nematode (unsegmented roundworm). The most common cause is Gnathostoma spinigerum. Other species include G. hispidum.
Cutaneous gnathostomiasis is known by various names across the world including:
- Yangtze River oedema
- Shanghai rheumatism
- Tuao chid
- Panniculitis nodular migratory filica.
Who gets gnathostomiasis?
Gnathostomiasis is endemic in countries where food is eaten raw or is undercooked. The affected regions include South East Asia, Japan, Latin America, China, India, and Africa. The first Australian case was confirmed in 2011 in Western Australia.
Gnathostomiasis is rare. However, the diagnosis should be considered in people with cutaneous lesions and eosinophilia that have recently travelled in endemic countries.
What causes gnathostomiasis?
Gnathostomiasis is caused by ingesting larvae in improperly cooked foods such as fish, chicken, snakes and frogs. Typically, sushi does not pose a risk of gnathostomiasis, as more expensive saltwater fish do not carry the larvae.
In humans, intermittent symptoms appear when the late third-stage larvae migrate through the tissues. The larvae cannot reach sexual maturity in a human host.
What are the clinical features of gnathostomiasis?
Generalised symptoms may develop within 24–48 hours after consuming the larvae. Such symptoms include:
- Fever and malaise
- Urticaria
- Gastrointestinal symptoms: diarrhoea, nausea, vomiting, anorexia and epigastric/right upper quadrant abdominal pain (epigastric or pain)
- These symptoms may last for 2–3 weeks, as the larva migrates through the wall of the stomach, intestines or liver.
Cutaneous gnathostomiasis
Cutaneous gnathostomiasis presents as linear non-pitting oedema.
- It may be erythematous, pruritic or painful.
- Usually, it is solitary. However, multiple lesions have been reported.
- The most common sites are the trunk or upper limbs.
- The larvae leave tracking marks (known as larva migrans profunda) and subcutaneous haemorrhages.
Lesions are seen on the face are associated with spread to the central nervous system or eyes.
Visceral gnathostomiasis
The visceral disease is due to migration of gnathostomiasis larvae within the body
Pulmonary symptoms
- Cough
- Pleuritic chest pain
- Haemoptysis
- Pneumothorax
- Lobar consolidation or collapse
Gastrointestinal symptoms
- Sharp pains
- Can be mistaken for appendicitis or intestinal obstruction
Genitourinary symptoms
- Uncommon
- Haematuria
- Passage of larvae in urine
- Haematospermia
- Vaginal bleeding
Ocular symptoms
- Uveitis
- Iritis
- Glaucoma
- Retinal scarring
- Retinal detachment
Auricular symptoms
- Mastoiditis
- Sensorineural hearing loss
The central nervous system (CNS)
- Potentially life-threatening
- Subarachnoid haemorrhage
- Coma
- Brain stem involvement: respiratory failure
- Eosinophilic meningitis
CNS disease can present as progressively worsening disease over several days. Symptoms include:
- Incontinence
- Loss of sensation
- Headaches
- Radicular pain in the limbs
- Weakness or partial paralysis of limbs.
How is gnathostomiasis diagnosed?
Gnathostomiasis is diagnosed by serology in blood or cerebrospinal fluid (CSF) when CNS is involved.
It may be suspected in the presence of significant blood or CSF eosinophilia (up to 50% of total white cell count). Note that eosinophilia disappears in chronic disease when larvae enter subcutaneous tissues.
Magnetic resonance imaging (MRI) shows diffuse spinal cord enlargement and areas of increased signal intensity.
A skin biopsy may show characteristic features. See also gnathostomiasis pathology.
What is the treatment for gnathostomiasis?
Gnathostomiasis larvae in the skin are removed surgically.
Medical treatment may include ivermectin or albendazole.
What is the outcome for gnathostomiasis?
If cutaneous or visceral gnathostomiasis is left untreated, the larvae may continue to cause intermittent symptoms until they die, which can be up to 12 years. The patient is considered clear of disease if asymptomatic for 12 months after treatment, eosinophilia has resolved, and ELISA levels have decreased.
Relapse can occur up to 7 months after treatment, necessitating retreatment and close follow-up. There is a high mortality rate for patients with CNS involvement.