Strongyloides

Family- StrongyloididaeGenus- 1. Strongyloides2. Parastongyloides3. Leipernema

Strongyloides• Also known as thread worms• Nearly 52 species• Infect birds, reptiles, amphibians, livestock and other primates• Important zoonotic spp. are1. S. stecoralis2. S. fueleborni3. S. ransomi ( Experimentally human can be infected)• Some important parasites of animals area) S. ransomib) S. westeric) S. papilosus

History…..

• Previously known as Cochin China Diarrhoea (First discovered in 1876 in French soldiers who had been in Cochin China)

• Discovered by French Naval Physician Louis Norman (1876)

• Bravey (1877) named it separately Anguillula stercoralis (Free living rhabditiform) & A. intestinalis (Intestinal filarifom)

• Grassi & Parona (1878)- Homogonic cycle• Peroncito (1881) – Heterogonic cycle

S. stercoralis

•1.0 mm length•50μ diameter•Filariform

Adult female

•Free-living adult males measure up to 750 µm long; free-living females measure up to 1.0 mm long.•Mucosa of duodenum, jejunum of man, other primates and dog•Parthenogenetic repoduction in parasitic phase

Rhabditiform oesophagus

Short Buccal Canal Rhabditiform

oesophagusGenital primodium

L1 Larva

180-380 µm longFree living stageExcreted through faeces

Notched Tail

L3 stage

600 µm longTail is notchedFilariform OesophagusInfective stage (Enters host through direct skin penetration)

Life cycle

Homogonic cycle• Adverse environmental condition1) Acidic soil2) Temperature (<200 C or >370 C) Egg L1Excreted through

facesGIT L3 (Infective stage)

L3 enters through direct skin penetrationMigrate through blood vessels to lungsRupture alveoli and blood vesselsReach tracheaSwallowed back to intestine where they mature

Heterogonic cycle

• Alternate type of L.C. (Free living + Parasitic)• amplifier mechanism• Under suitable condition

• Egg

Environmental cue is detected by 2 Amphidian Neuron at the mid stage of L1 and accordingly development occurs

L1

Free living adult (Rhabditifom) Egg

L3(Filariform & Infective)

Super infection1. Hyper infection2. Auto infection

Hyper Infection

Auto infection

• Filarifom larva excreted though faeces• Penetrate skin though perianal or perineal

region2 factors regulates super infection1. Host resistance2. Self regulatory mechanism (Crowding effect

due to declining level of Ecdysteroids after certain level of population)

Epidemiology

• Poor countries• Tropical• Warm and humid

climatePrevalence is up to 85%

• Hot and semi arid areaPrevalence is less than

3%

Disease in HumanDepends upon immunity of human In immune individual remain as Hypobiotic formUntil immune breakdown occurs (Mostly after

receiving coticosteroids)Clinical signs according to site of localization of

parasite (Cutaneous/ Pulmonary/ Gastro intestinal form)

Cutaneous Symptoms

• Erythematous pustule at the site of entry

• Leads to intense pruritus and urticariae (more severe in previously sensitized individual)

• Linear/ serpiginous urticarial inflammatiom (Larva currens)

• Peripheral eosinophillia

Lava CurrensDistinguished from cutaneous larva migrans by its rapid migration, perianal involvement and wide band of urticaria and chronicity of infection

Pulmonary Symptoms1. Bronchopneumonia2. Breaking of capillary results in haemorrhage3. Peripheral eosinophillia Associated witha) Age <5 yearsb) Steroid therapyc) Use of anti histaminesd) Chronic debilitating disease

Intestinal symptoms• More dominant form• Atrophy of villi and hyperplasia of crypts (Thickening of

intestinal wall)• Cattharal gastroenteritis• Diarrhoea, epigastric pain, dyspnoea>50% cases don’t show any signsManifests more severe infection due to hyper infection

when immune breakdown occurs

Disseminated form• In immuno compromised individuals (particularly on

steroid therapy)• Due to hyper infection• Any system can be affected (mostly respiratory

system)• Sometimes purulent meningitis• Helps in dissemination intestinal bacteriaSteroid therapy- immunity breakdown + ecdysteoid

like substance in host tissue & intestinal wall.increase moulting from L1 to L3

In animals…..

• Only observed in puppies• >6 months resistant to autoinfection• May be sub-clinical• In clinical cases- Loss of appetite, purulent

conjunctivitis, bronchopneumonia• At site of entry puritus, erythema, alopecia• GI symptoms- Diarrhoea symptoms, abdominal pain,

vomiting• In severe cases dehydration, emaciation, anemia and

bloody diarhoea is seen

Source of infection1. Human reservoir host2. Skin penetration is more common3. In dogs also through oral, transmammary, uterine

route transmission occurs

Diagnosis…• Detection of L1 stage1. Faecal smear2. Baermann’s Technique3. Agar plate culture4. High salt conc. method Test on 3 different day• ELISA Cross reactivity with other nematodes (Improved by

adsorption of test sera with Onchoserca gutturosa extract)

Low sensitivity (Impoved by Biotinylated conjugate or Avidin peoxidase conjugate)

• Indirect Immunofluroscence

Baermann’s Technique

• L3 stage can be detected in parentral tissue/body fluid (in disseminated infection), sputum and tracheal wash

• Parastongylus trichosuri (parasite of Australian marsupials) is used as lab model for Strongyloides

Strongyloid on blood agar

Treatment• Difficult in disseminated form (more number of L3 )• Drugs active against adult

1. Albendazole- 100mg/kg (Dog) PO, BID, 3 days2. Thiabendazole- 50mg/kg (Dog), 50-100mg/kg (Human)

PO, OD, 3 days3. Fenbendazole- 50mg/kg (Dog) & 25mg/kg (Human) PO,

OD, 3 days4. Ivermectin- 0.2mg/kg (both), single dose

Follow up weekly upto 2-3 wks to ensure that no migrating larva survived

Prevention1. Sanitary disposal of faeces2. Treatment of clinical and sub-clinical cases3. Using protective shoes4. Washing hand before eating5. Before steroid therapy patient s’d be treated for

strongyloidiasis and complete removal

S. fuelleborni• More common in cental african humid jungle e.g.- Cameroon, Ethiopia, Central African Republic, New

Guinea• Also found in other places Zambia, Democratic Republican

of Congo, African Savannah• In human it causes abdominal pain and diarrhoea• In primates it causes benign infection to intense

haemorrhagic diarrhoea• In faeces eggs are detected for diagnosis