Nematodes and zoonotic nematodes Flashcards
Why would humans get infected with zoonotic nematodes?
Often we are accidental hosts.
Some can develop fully in humans whereas some arrest development.
How many trichonella species infect humans?
7 spp. E.g. trichonella spiralis
What is the distribution of trichonella spiralis and why is it a problem? What is it a disease of?
From the arctic to the tropics, is Mr Worldwide.
Is a major economic problem in porcine animal production.
Is a disease of meat eaters! Infects carnivorous and omnivorous animal tissue.
Describe the infection cycle of trichonella spiralis.
Is ingested –> emerges in the duodenum –> burrows into the intestinal mucosa where they mate –> the females then give birth to L1 larvae –> L1 penetrate through intestinal wall –> enter into blood and lymphatic circulation -> invade muscle cells and transform into a nurse cell (produce a nest inside of which is a coiled intracellular L1 with surrounding collagen).
Describe the infection cycle of trichonella spiralis.
Is ingested –> emerges in the duodenum –> burrows into the intestinal mucosa –>
What is the domestic cycle for t spiralis? What is the main source of human infection?
domestic cycle in rats and pigs. Pigs are the main source of human infection (eating pork).
What is the domestic cycle for t spiralis? What is the main source of human infection?
domestic cycle in rats and pigs. Pigs are the main source of human infection.
How long do larvae remain infective for within decaying meat?
Months!
What is something interesting to note about the temporal epidemiology of t spiralis cases?
Often cases are clustered and are associated with a particular feast or festival where large numbers of people would be eating infected pork.
How can horses also be a source of infection for t spiralis?
If infected rats get ground up in horse fodder and fed to the horses.
What is the arctic cycle of t spiralis and who does this present a problem for?
Arctic cycle in polar bears, arctic foxes and walruses. This is a problem for Inuits who eat raw meat which may be contaminated.
(There was a 50% prevalence in Alaskan Inuits in the 80s).
What animals are involved in the African cycle of t spiralis?
Bush pigs, warthogs and lions etc.
What determines the severity of infection with t spiralis?
The number of infective larvae strongly correlates with the infection severity, and produces a spectrum of pathology.
What is the host response as T spiralis larvae migrate out to muscle tissue?
An acute inflammatory response is produced. Swelling of the tongue and eyelids is often seen.
What are the symptoms often associated with a heavy infection of T spiralis?
Myocarditis, pneumonitis, diarrhoea.
If the larvae migrate through the CNS, neurotrichonellosis can occur as well as sublingual bleeding, rashes and fatality.
What is the chronic stage of T spiralis?
The cyst formation stage in tissues.
How would we diagnose T spiralis?
Look at the dietary history (e.g. could be linked with community epidemics), use serology or a biopsy.
How do we treat t spiralis? When should treatment be administered?
Early treatment is essential as it is hard to treat once encystment in muscles occurs. Treat with antihelminthics within the first few weeks, if not use long term corticosteroids for control if this window is missed.
-Albendazole or mebendazole
How do we control trichonella spiralis?
- Cook food above 55 degrees or freeze below -fifteen degrees for 20 days (species dependent).
- Meat inspection in abattoirs
- Don’t feed pork to pigs.
Where are the majority of cases of capillaria phillipinensis?
China, Phillipines, Thailand.
What is the main definitive host for capillaria philipinensis?
Marine birds.
What is the transmission cycle between the definitive host and humans for C philipinensis?
Eggs from marine birds are eaten by fish and human acquire infection by eating raw or undercooked fish.
Describe the pathogenesis produced by C phillipinensis.
Adults reside in the mucosa and produce a severe inflammatory response.
This parasite can cause internal autoinfection which can lead to a huge parasitic burden.
Malabsorption and protein loss are part of the pathogenesis.
How do we diagnose c philipinensis?
Look in the stool for eggs. They look similar to trichirus but are smaller and not as lemon shaped.
How do we treat c philipinensis?
Prolonged benznidazole treatment. Only the adults are susceptible and the juveniles are not affected which means the longer treatment takes into account the maturation of the juveniles.
What are the two types of pathology that toxocara species can produce?
Visceral larval migrans and ocular larval migrans.
What are the two main species of toxocara?
Canis and cati (from dogs and cats respectively).
Which age group is affected most by Toxocara?
Peaks in children.
What is the lifecycle of toxocara?
Adults are in the intestines of puppies and cats and eggs are excreted in the faeces –> the larvae arrest at L2 if in the adult dog but puppies can become infected if the female is pregnant –> humans can swallow eggs where they develop into L2 larvae which then migrate –> migration and death of the larvae causes an inflammatory response.
What ist he most common serial pathology found with toxocara.
Occular larval migrans. Granuloma forms in the retina where the larvae are trapped.
How do we diagnose toxocara?
Not egg detection as eggs are not shed so we cannot see them.
WE look at exposure history (exposure to young dogs or contaminated soil) and look at typical clinical signs as well as doing blood tests.
How do we treat toxocara?
Albendazole and corticosteroids.
What is the paediatric presentation of toxocara?
Unexplained febrile illness, eosinophilia.
How do we control Toxocara?
- Wash dogs (remove eggs from fur)
- Hand washing after play
- Deworm puppies
- Raw chicken liver consumption avoidance
What is the latin name for the rat lungworm?
Angiostrongylus catonensis
What does angiostrongylus catonensis cause in humans?
Eosinophilic meningitis.
What is the geographical epidemiology of angiostrongylus catonensis?
South Asia and Pacific region, also Africa and the Caribbean.
What is the lifecycle of angiostrongylus cantonensis?
The life cycle is complex and involves a rodent definitive host and an appropriate mollusk intermediate host, usually land snails or slugs (Fig. 6). Adult worms mature in rat brains, enter the central circulation, and mate in the pulmonary arteries producing eggs. The eggs become first-stage larvae that penetrate pulmonary vessels to access the respiratory tree, where they are coughed up, swallowed, and excreted in feces. These second-stage larvae must be consumed by land snails or slugs in order to mature into infective third-stage larvae, be eaten by rodents, and maintain the parasite’s life cycle. Man becomes a dead-end host by consuming raw intermediate mollusk hosts, or food items contaminated by their slime, or by consuming raw, crustacean (shrimp, crabs, fish, frogs) transport, or paratenic, hosts that consumed infected mollusks. In man and paratenic hosts, the neurotropic larvae migrate to the central nervous system (CNS) (neural larva migrans) seeking to mature into young adults as in rat brains, but eventually die causing EM.
How is angiostrongylus cantonensis acquired?
By eating slugs/snails, contaminated salad, anything contaminated with snug/snail slime.
Is angiostrongylus cantonensis fatal?
Can be benign OR fatal depending on if a strong granuloma is produced which may cause focal necrosis in the brain or anterior chamber of the eye.
How is angiostrongylus cantonensis diagnised and treated?
Antihelminthics are NOT given as this could produce an even stronger inflammation which could be fatal if it causes focal necrosis in the brain or eye.
Where is anisakid acquired from?
Raw fish
What are the two types of anisakid? What do they infect?
Simplex and dicipiens. Infect marine mammals. They live in the gut and viscera of fish (not gutting directly after catching can cause the parasites to spread into the tissue of the fish.
What is the lifecycle of anisakis?
Adult stages of anisakid nematodes reside in the stomach of marine mammals, where they are embedded in the mucosa in clusters. Unembryonated eggs produced by adult females are passed in the feces of marine mammals image . The eggs become embryonated in water, undergoing two developmental molts, and hatch from the eggs as free-swimming ensheathed third-stage (L3) larvae. These free-swimming larvae are then ingested by crustaceans. The ingested larvae grow within the crustacean hemocoel, and become infective to fish and cephalopod paratenic hosts. After preying upon infected crustaceans, the digested L3 larvae migrate from the paratenic host intestine into the abdominal cavity, and eventually to the tissues of the mesenteries and skeletal muscle. Through predation, tissue-stage L3 larvae can be transmitted among paratenic hosts. Fish and squid maintain L3 larvae that are infective to humans and marine mammals.
When fish or squid containing third-stage larvae are ingested by definitive host marine mammals, the larvae molt twice and develop into adult worms. After ingestion by humans, the anisakid larvae penetrate the gastric and intestinal mucosa, causing the symptoms of anisakiasis.
What is the pathogenesis seen in anisakis infection?
Epigastric/ abdominal pain, vomiting.
Infection is self-limiting as larvae die and the infection resolves.
However, as it is so immunogenic, secondary exposure can provoke extreme anaphylaxis in previously sensitised people.
How do we diagnose anisakis?
Ask about previous exposure to raw fish.
Often mistaken for peptic ulcers and appendicitis.
How do we control for anisakis?
Freeze fish at -20 for 24 hours. Cook fish.
How do we treat anisakis?
Hard, some reports of effective treatment with albendazole.
Describe the geographical epidemiology of gnathostoma spinigerum.
SE Asia and Central and South America.
What is the lifecycle of gnathostoma spinigerum?
In definitive hosts (cats, dogs and pigs), adult worms of most Gnathostoma spp reside in a tumor-like mass in the gastric wall; adult worms of some species are found in the esophagus or kidney. Adults mate and produce unembryonated eggs, which pass through a small opening in the tumor-like mass and ultimately into the feces. Eggs become embryonated in water, and eggs release sheathed first-stage larvae (L1). Freshwater copepods, which serve as first intermediate hosts, ingest the free-swimming L1, and the larvae molt twice to become early third-stage larvae (EL3). Following ingestion of the copepod by a suitable second intermediate host, the EL3 migrate into the tissues of the host and develop further into advanced L3 larvae (AL3). When the second intermediate host is ingested by a definitive host, the AL3 develop into adult parasites in the gastric wall. Alternatively, the second intermediate host may be ingested by a paratenic host, in which the AL3 do not develop further but remain infective. Humans become infected by eating raw or undercooked meat of second intermediate or paratenic hosts containing AL3. In the human host, AL3 migrate in various tissues and may develop into immature adults but never achieve reproductive maturity; they may range in size from 2 mm to about 2 cm depending on the species and the extent of development. Whether humans can become infected by drinking water that contains infected copepods is not clear
How long do the larvae of gnathostoma spinigerum live?
Long lived! About 10 years.
What are the clinical symptoms of gnathostoma spinigerum?
The clinical symptoms depend on the migration of the larvae, whether it is visceral or subcutaneous.
We see migratory oedema (Migration in the subcutaneous tissues (under the skin) causes intermittent, migratory, painful, pruritic swellings (cutaneous larva migrans). Patches of oedema appear after the above symptoms clear).
OR can cause eosinophilic meningitis.
How do we diagnose gnathostoma spinigerum?
Use serology, clinical history (e.g. eosinophilia, migratory lumps, diet).
How do we treat gnathostoma spinigerum.
Prolonged benznidazole and ivermectin (also perhaps albendazole)- it may never be cured!
How do we control for gnathostoma spinigerum?
Cook freshwater fish (about 5 minutes at 75 degrees).
What are the two phyla of helminths and what are the two classes within one of these phyla?
Platyhelminths and nematodes (phyla) and cestodes and trematodes (class).
Trematodes being flukes and cestodes being tapeworms.
What are the general features of helminths?
- Large and complex
- Most are extracellular
- Acquited by larval/egg ingestion or skin penetration.
- Usually, grow and moult in the host
- Many are zoonotic
What are the two lifecycles of helminths?
Direct and indirect, requiring one host or two or more hosts respectively.
What is the definitive and intermediate host?
Definitive- harbours the sexually mature stage.
Intermediate- harbours the larval/non-sexual stages.
What does the burden of helminth infection depend on and why?
Dependent on the level of exposure as most of the worms do NOT replicate inside the host (however some may have autoinfective cycles). (Cumulative infection).
Which demographics are generally more affected by worms?
Children- they are more exposed and they suffer more from the pathology (often having anaemia, malnutrition etc).
Also, women. We have other factors that put pressure on the iron reserve such as lactation, menstruation etc.
What are nematodes?
Roundworms
What are cestodes?
Tapeworms (flatworms)
What are trematodes?
Flukes (flatworms)
Describe the morphology of nematodes
- Cuticle on the outside (environmental resistance)
- Mouth and anus (two ends)
- Complete digestive system
- Longitudinal muscles (to thrash sideways)
- Dioecious (separate males and females)
- Male smaller than female
How many moults do nematodes undergo?
Four moults (Egg–> L4–> adult).
What do females of filarial nematodes give birth to?
Live larvae! Eggs hatch inside the female.
Broadly, what are the three groups of nematodes? What are their requirements for being transmitted?
- Soil-transmitted- need soil microbes for egg embryonation
- Filarial- require a mosquito or insect
- Zoonotic- humans are often accidental and dead-end hosts
Which is, arguably, the most important human nematode?
Hookworm (ancyclostoma duodenalis).
Which intestinal nematode is NOT soil-transmitted?
Enterobius vermicularis (pinworm).
What is the general direct lifecycle of intestinal nematodes?
Eggs in faeces –> hatch into larvae in soil –> oral ingestion or percutaneous penetration.
What are the two main modes of actions of antihelminthics and give examples?
- Microtubule polymerisation blockers. Blocks glucose uptake and hence starvation of worms. Benznidazole.
- Neurotransmitters that block neuromuscular junctions. Cause worm paralysis. Ivermectin, pyrantel and piperazine.
What is the geographical and socioeconomic distribution of enterobius vermicularis (pinworm)?
Tropical to temperate. Broad geographical range! People from rich to poor are affected.
What is the lifecycle of enterobius vermicularis?
Simple and direct lifecycle.
Eggs are orally ingested and hatch into male and female worms (dioecious) which develop in the intestine –> worm moves to the anus and deposits fertilised eggs on skin with a glue –> glue generates itches which results in the transfer of the eggs onto hands –> dispersal is propagated.
Where do adults of enterobius vermicularis life?
In the appendix and caecum (pouch connected to junctions of the small and large intestine).
What is the defining feature we can look for to diagnose enterobius vermicularis?
Lateral alae which make it look like a pointy lemon!
What are common symptoms of enterobius vermicularis?
- Pruritis ani
- Loss of appetite
- Disturbed sleep
How do we diagnose enterobius vermicularis? Why do we do this?
Tape test. Do this because eggs are not shed in stool.
HOw is enterobius vermicularis treated? What is the problem with treatment?
Single-dose of mebendazole. Should be retreated 3 weeks later. The environment is easily contaminated (e.g. even the CURTAINS can have eggs on) so therefore it is easy to treat but hard to control.
What is the geographical and age epidemiology of trichuris trichuria?
Tropical and sometimes temperatate. Africa, Central America, SE Asia have the highest prevalence. Children the most affected.
WHere do trichuris trichuria reside?
Caecum, and colon. Their back ends hang out into the lumen to mate.
What is the lifecycle of trichuris trichuria?
SImple and direct.
Eggs are swallowed and hatch –> larvae develop into adults (taking about 8 weeks) in the caecum or colon –> females release eggs which are shed in stool –> they embryonate in the soil (takes about 2-4 weeks in hotter countries and up to 6 months in temperate climates)–> eggs are ingested through contaminated food and burrow through epithelium to form a schistosome surrounded by a syncitium.
How do we control for trichuris trichuria?
- Sanitation is key.
- Human habits such as using night soil aid propagation so we need reformed behaviour.
- Stop geophagia (eating soil in times of famine). Or pregnant women eating clay.
What are the clinical presentations of trichuris trichuria?
- Haemmorhaging (may cause anaemia in severe cases) from burrowing into mucosal epithelium
- Inflammatory response
-Heavy infections may cause “dysentery”, bacterial infection from the damaged epithelium, and rectal prolapse (from chronic oedema of mucosa).
How do we diagnose trichuris trichuria
Eggs in stool.
- Direct smear- is insensitive but may be useful for heaby infection
- Formyl ether concentrate
- Kato katz thick smear
- Serology (may not distinguish between past and present infection).
- PCR is not done in the field as it is hard to get DNA from eggs.
How would one carry out a Kato Katz smear?
Use a template and fill the hole with stool to give a pellet. Soak then slide in glycerol and use the set amount of stool to count the eggs. This gives a quantitative measure of eggs per gram. (This is a low tech field method).
What is the flotal method?
Adding salt water makes the eggs float from the faeces.
Mix sample with formylin and spin and resuspend in salt solution. Then we can count the eggs.
May not be so useful in the field as requires a centrifuge.
WHich is the only helminth we do serology diagnosis for?
Strongyloides.
Which helminths can and can’t we do antigen detection tests for?
CAN for schisto and LF. CANNOT for soil transmitted helminths.
What are the morphological characteristics of the trichuris trichuria egg?
Lemon/ tea tray shape.
50-55µm.
Yellow brown stained by bile.
How do we treat trichuris trichuria?
Benznidazole. Small doses over several days.
One large dose is not as effective and has only a 10% cure rate.
Oxantel is also used but is not as effective as is poorly absorbed and has high concentrations in the large bowel.
What does the WHO recommend for trichuris trichuria?
-regular school-based chemotherapy as heavy infections can impair physical and cognitive development in children.
What is the lifecycle of ascaris lumbricoides?
Swallow egg which hatches in intestine –> penetration of intestinal wall and migration to the liver through the circulation where it finally ends up in the lungs –> penetrates trachea and is swallowed back to the intestien.
How many ascaris lumbricoides eggs can be produced every day?
200,000
How resistant are ascaris lumbricoides eggs?
Once embryonated, they are very resistant and may persist in the environment for up to 8 years.
What is the lifespan of ascaris lumbricoides in a human?
About a year.
How long does it take ascaris lumbricoides from egg to adult worm?
About 8 weeks.
What is Loeffler’s syndrome?
Accumulation of eosinophils in the lungs in response to a parasitic infection.
May produce a dry cough, fever and blood stained sputum.
What are the three stages of infection by ascaris lumbricoides? What are the clinical symptoms for each stage?
- Lung stage- causes a strong eosinophilic reaction causing a dry cough, fever and blood-stained sputum (Loeffler’s syndrome).
- Intestinal stage. Abdominal discomfort, acute pain, diarrhoea and malabsorption. in RARE cases, we get intestinal blockage from the formation of a bolus (of worms).
- Ectopic infection. Migration of worms:
- Intestine associated (e.g. appendix, parenteral ducts, bile ducts, liver abscess, anus, peritoneal cavity)
- Larynx
- Urethra, vagina
- Nose, mouth, tear ducts, brain
- Heart and lungs
What may promote ectopic ascaris lumbricoides?
Anaesthesia is a common trigger. Fever and antihelminthic treatment also trigger a panic response!
How do we diagnose ascaris lumbricoides?
- Adults in stool and sometimes vomit
- Eggs in stool (fertile corticated, fertile decorticated or infertile).
How do we treat ascaris lumbricoides. How do the drugs take effect?
Benznidazole in combination with piperazine. These cause flaccid paralysis which prevents the risk of obstruction.
Improvement of sanitation for long term efficacy.
What does the WHO recommend for ascaris lumbricoides?
School based chemotherpay in areas with >20% prevalence.
What are the two main hookworms?
Necator americanus and Ancyclostoma duodenalis.
What is the common/main pathology associated with hookworm?
Hookworm anaemia as they suck blood from the intestinal wall.
What is the distribution globally of hookworms limited by?
Humidity/ moisture, and temperature. Therefore mainly in warm, moist climates.
How do hookworms such as Necator americanus and Ancyclostoma duodenalis infect humans?
Skin penetration, not oral infection.
What are the geographical epidemiologies fr Necator americanus and Ancyclostoma duodenalis.
Necator- S America, Africa, SE Asia (used to be a big problem in the souther US states).
Ancyclostoma- SE asia, some Africa, S America.
Why are hookworms termed worms of laziness?
Made people tired as they became anaemic.
Describe the morphology of hookworms.
- About 1cm long
- Yellow/pink
- Male has a copulatory bursa to grab the female.
- Dorsal facing buccal capsule (Necator has two cutting blades and Ancyclostoma has two cutting sets of teeth).
Describe the hookworm lifecycle.
Skin penetration through the skin by infective larvae –> enter the circulation and end up in the lungs –> penetrate alveoli and go through the trachea to be swallowed –> intestine–> excreted in stool –> rapidly hatch in soil to L1 which feeds on soil bacteria –> L2, L3. Takes about 10 days to get to L3 which is the infective larval stage.
How big are the hookworm eggs?
About 60µm, at this stage we cannot distinguish species.
Describe the differences in hookworm and strongyloides?
Hookworm- long buccal cavity
Strongyloides- short buccal cavity.
What do infective hookworm L3 larvae look like?
Retained sheath of L2, pointed tail, very active in soil and move to the tips of vegetation to be picked up.
How do hookworms penetrate?
Either through unbroken skin e.g. feet, or orally by penetrating the mucosa of mouth (in unwashed vegetables etc). Use helminth elastase to penetrate the skin by degrading elastin in the skin to form a path through.
When does egg laying occur in the infective cycle of hookworm?
About 58 weeks post-infection.
What is the clinical presentation of hookworm infection?
- Rash (depenent on no of infective larvae)–> “ground itch”.
- Cutaneous larval migrans
- Loeffler’s syndrome in heavy infections
- Mental and physical stunting in children
- Possible cardiac insufficiency.
WHy may hookworm be fatal in children?
They move around a lot in the intestine i.e. have multiple attachment sites. Due to use of anticoagulants, these wounds can bleed for a long time and can cause about 100ml of blood loss per day which could be fatal in children.
What do hookworms feed on? What may be a clinical result of this?
(Globin in) blood.
Reduced levels of serum albumin (from blood eating) causes dysregulation of oncotic pressure, resulting in oedema.
How do we diagnose hookworm?
- Eosinophilia in the acute phase
- Look for 60µm eggs in stool
Which two other eggs look very similarto hookworm eggs but are rarely found in humans?
Trichostrongylus
Ternidens diminutus
(These two eggs look the same but are bigger).
How do we treat hookworm?
Benznidazole. Anaemia treated with iron therapy.
School-based chemotherapy in areas of >20% prevalence.
How could we prevent hookworm?
Wearing shoes etc. Ensuring no defaecation on plantations.
Where is strongyloides stercoralis common?
Warm climates. Distribution overlaps with hookworm.
What is unusual about strongyloides in the human intestine?
There are only females and they reproduce pathogenetically.
Also, eggs hatch in the host to L1 so no eggs are shed in the stool.
What is the direct lifecycle of strongyloides?
L1 rhabatiform larvae in soil moult within 1-4 days to L3. Infection occurs through skin penetration. Heart-lung migration cycle (swallowed –> gut). Parthogenetic reproduction in female.
What is rhabditid larvae?
specifically designating an oesophagus having two swellings or bulbs, as in rhabditids and in a non-parasitic larval stage of certain other nematodes; having such an oesophagus
What is the indirect lifecycle of stronglyloides?
L1 become free-living soil nematodes which are male AND female. Males and females mate. Males are only free-living. Females can penetrate and produce eggs which moult fro L1-3.
What is the morphology of strongyloides? (L1 and 3).
L1
- 250-300µm long
- Pointed tail
- Short buccal cavity
L3
- 550µm
- Notched/blunt tail
- Lacks sheath
How can Strongyloides L1 larvae cause autoinfection (two ways)?
Moult to M3 which then penetrates mucosa which then do heart lung migration back to the intestine.
(Internal autoinfection).
Migrate to anal region and undergo perianal penetration, followed by heart lung cycle back to intestine.
(External autoinfection)
Why can Strongyloides have long lasting infections, even after an individual leaves an endemic area?
Cycles of autoinfection to maintain long systemic infection.
What is disseminated strongyloides? What is it triggered by?
An association with immunosuppression. Particularly triggered by corticosteroids.
Why is it hard to diagnose strongyloides?
Eggs not shed in faeces. Often antihelminthics are given even if no clinical symptoms, especially if going for a transplant where corticosteroids will be used.
What are the predisposing conditions to Strongyloides infection?
- HTLV1 (Human T Lymphotropic virus, suppresses TH2 lymphocytes)
- Corticosteroid use (immunosuppression)
Why is HIV NOT a predisposing factor for strongyloides?
Affects TH1 lymphocytes with not as much effect on TH2 lymphocytes so it is thought that the TH2 response is enough to control the infection.
What is the pathogenesis associated with strongyloides?
- Dermatitis following skin penetraton
- Rash and tracts as autoinfective L3 larvae migrate through the skin and lungs
- Loeffler’s syndrome
- Acute phase abdominal pain
- Diarrhoea
- Oesinophilia
- Chronic infection may be asymptomatic or produce collitis.
What is the pathogenesis associated with disseminated strongyloides?
- Strong lung reactions.
- Pulmonary distress and haemorrhage
- Damage to submucosa
- Destruction of the intestine (villus atrophy, ulceration, secondary infection with bacteria)
How is strongyloides diagnosed?
- Difficult parasitologically as eggs are intermittent in stool- must do serial smears. At LEAST 3 stool samples.
- For disseminated disease may use a direct smear but for lower infections, we can use concentrating methods. Look for worms in urine and sputum for DS.
- Can use charcoal culture to promote free living culture of worms.
- Oedemal aspirates
-Immunodiagnosis using elisa for L3 specific antigens (95% sensitive and specific)
How is strongyloides treated?
First treated with ivermectin then secondarily with albendazole.
(regular long term retreatment in immunosuppressed patients)
What does persistence of strongyloides infection depend on?
- Adequate soure of reinfection
- Defaecation habits e,g, night soil
- Environmental factors(shade, warmth, moisture)
- Opportunity for infective stages to be taken up
How do we control for strongyloides?
Health education, clean water, compose faeces for min 1 year, footwear, chemotherapy (mass, selective or targeted).
