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ASCARIS LUMBRICOIDES.

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Presentation on theme: "ASCARIS LUMBRICOIDES."— Presentation transcript:

1 ASCARIS LUMBRICOIDES

2 CASE HISTORY 6 year old daughter of a seasonal farm worker
Presents with malnourishment, abdominal swelling, cough, wheeze and fever. CXR reveals a lobar pneumonia X-Ray plain abdomen revealed suspicion of worms Admitted for initial antibiotic therapy After 2 days of antibiotic, worm was found in her bed

3 Stool examination reveals…
No mucous No pus cells No RBCs BUT….

4 ASCARIS LUMBRICOIDES (The ROUND WORM)

5 Introduction Common Roundworm that is parasitic in the intestines of humans Most common helminthic human infection Largest nematode to infect the human intestine An estimated 807-1,221 million people in the world are infected (according to CDC) Ascaris, hookworm, and whipworm are known as soil-transmitted helminths 

6 SUPERFAMILY ASCARIDOIDEA
Two species – one in humans and other in pigs Ascaris lumbricoides – humans Rural >> urban Children > adults

7 Geographical Distribution
Worldwide High prevalence in underdeveloped countries that have poor sanitation (parts of Asia, South America and Africa) Occurs during rainy months, tropical and subtropical countries

8 HABITAT ADULT WORM- lumen of small intestine mainly the jejunum Maintains its position by its muscle tone

9 morphology Egg: three kinds of the eggs
fertilized eggs, unfertilized eggs and decorticated eggs. 5 aspects: size, color, shape, shell and content.

10 1. Fertilized eggs: broad round to oval in shape, brown to golden brown (always bile stained) in color, an average size × µm. The shell- thick, smooth, translucent with an outer mammillated albuminous coat stained brown by bile. The content is a fertilized unsegmented ovum. There is a crescent shaped clear space at the each end inside the shell.

11 2.Unfertilized egg: Longer and slender 80 x 55μm Thin shelled- ranges from irregular mammilations to a relatively smooth layer completely lacking the rugosities. content – small atrophied ovum with mass of disorganised, highly refractable granules of various sizes. Does not float in saturated salt solution

12 3. Decorticated eggs: Both fertilized and unfertilized eggs sometimes may lack their outer albuminous coats and are colorless.

13 can survive for prolonged periods as long as warm, shade, moist conditions are available
can live up to 10 years Resistant to low temperatures, desiccation and chemicals resistant to usual methods of chemical water purification removed by filtration and are killed by boiling. Eggs embryonate but do not hatch until ingested by man developing larvae are destroyed by sunlight, high temperature and desiccation.

14 ADULT WORM Light brown or pink to white in color
tapered ends- anterior being thinner than the posterior Mouth opens at anterior end; possesses 3 finely toothed lips Female (25-40cm) longer and stouter than the male (15-25 cm) Ovaries are extensive; contain upto 27 million eggs at a time

15

16 HOST- Definitive host : Man Intermediate Host : -none- INFECTING AGENT- embryonated egg

17 Modes of transmission ingestion of water or food (raw vegetables or fruit in particular) contaminated with embryonated A.lumbricoides eggs. Children playing in contaminated soil may acquire the parasite from their hands Occasionally inhalation of contaminated dust

18 LIFE CYCLE

19

20 1. Fertilized unsegmented eggs passed in feces
2. Development in soil – rhabditiform larva develops within eggs by 10 – 40 days Now, these embryonated eggs are infective & humans ingesting such eggs along with raw vegetables/water are infected 3. Infection by ingestion and liberation of larva -rhabditiform larva (0.25mm) hatches out of eggs

21 Life cycle contd ….. 4. Larva penetrate gut wall, and through portal circulation  liver  inferior vena cava  right heart  reach pulmonary circulation Larvae grow bigger (2mm) and moult twice  break through pulmonary capillaries into the alveoli 5. Re-entry into stomach and small intestine- They now crawl up the bronchi  trachea  larynx  swallowed back into pharynx  oesphagus  stomach  reach small intestine

22 Life cycle contd ….. 6. Sexual maturity and egg liberation- In the small intestine, the larvae develop into adult worms Male fertilizes female and gravid female starts laying eggs Eggs pass out in feces -> Cycle complete

23 Massive infection – some larvae can reach the general circulation to be filtered out into various organs and tissues- kidneys, brain, spinal cord and others do not reach maturity and get destroyed

24 HOST IMMUNE RESPONSE Innate Immune Response
Macrophage, neutrophils and most importantly eosinophils The worms coated with IgG or IgE increase the release of eosinophil granules on the worm’s surface Adaptive Immune Response Th2 immune response with high IL-4 production, high levels of IgE, eosinophilia and mastocytosis Prior infection does not confer protection

25 pathogenicity Larvae in the lungs-
Destroy the capillaries haemorrhage Migration of inflammatory cells  Ascaris pneumonitis / Loeffler’s syndrome) Lung tissue destroyed  secondary bacterial infections. larvae in general circulation- Filtered out to various organs  unusual clinical symptoms Brain, spinal cord, kidneys and heart.

26 Clinical features of Ascariasis
Symptoms are due to  The migrating larva – Larva in the lungs : condition known as Ascaris pneumonia (Loeffler’s syndrome) characterized by low grade fever, cough, urticarial rashes, eosinophilia & blood tinged sputum which may contain larvae

27 Clinical features cont ….
b) Larvae in general circulation: Some times larvae pass through pulmonary circulation into systemic circulation and they get filtered into various organs Symptoms depend upon site of localization & no. of larvae involved CNS – Epileptic fits; Eye – Chorioretinitis Kidney – Nephrotic syndrome

28 Clinical features cont ….
2. Symptoms due to the adult worm  Spoliative action :– compete with the host for nutrition lead to a state of malnutrition & night blindness (Vit. A deficiency)  usually seen in hyper infected children Anti-enzymes – anti-tryptic and anti-peptic

29 b) Toxic action :- Body fluid is toxic and gives rise to symptoms  Typhoid like fever Urticaria; Facial edema; Conjunctivitis & Irritation of the respiratory tract

30 A huge worm load in the intestines will lead to –
c) Mechanical obstruction - A huge worm load in the intestines will lead to – Intestinal obstruction Intussusception

31 Migration of adult worms from their normal habitat to other body sites
Ectopic Ascariasis - Migration of adult worms from their normal habitat to other body sites reach stomach  be vomited out From esophagus  escape from nose or mouth respiratory tract may cause suffocation biliary tract obstructive jaundice Appendix appendicitis  Perforation  peritonitis

32 complications Intestinal obstruction, intussusception and volvulus
Obstruction of intra and extra hepatic bile ducts Peritonitis due to intestinal perforation Chronic pancreatitis Acute and chronic appendicitis Pneumonitis, Bronchitis and Asthma

33 Lab diagnosis Direct evidences- A. Demonstration of adult worms 
In feces or vomit - worms are passed out spontaneously or after an antihelminthic X ray after barium meal – string like shadows Ultrasound abdomen- Hepatobiliary /pancreatic ascariasis Single/ bundle of worms Pseudo-tumor like appearance

34

35 Lab diagnosis 2. Demonstration of eggs in stool 
Saline wet mount of stool sample will show fertilized & unfertilized eggs Female worm lays 200,000 eggs/day Concentration methods are usually not required

36 Indirect evidences – Blood examination – Eosinophilia in early stages Skin allergic test – “Scratch test” - uses powdered Ascaris Ag ; unreliable Serological tests – useful in Extra intestinal Ascariasis

37 Treatment Albendazole - single oral dose of 400mg
Mebendazole- 100mg orally twice daily for 3 days Pyrantel pamoate – single dose 10mg/kg Piperazine citrate

38 Mebendazole & Albendazole  not recommended in pregnancy & heavy infestations as they may trigger ectopic ascariasis Pyrantel pamoate & Piperazine citrate  recommended in pregnancy & heavy infestations

39 Prevention Good hygiene ; hand washing
Proper disposal of human excreta Treatment of parasitized individuals Avoid contaminated food and water especially in areas of poor sanitation Wash, peel or cook all raw vegetables and fruits

40 control Periodic mass treatment of children with single doses of Albendazole or Mebendazole – helps reduce transmission in community Environmental sanitation Limit/stop using human faeces as fertilizer Health education

41 ANSWER THESE QUESTIONS
Write an essay on life cycle ,pathogenesis laboratory diagnosis of Ascariasis ? Write difference between fertilized and unfertilized egg of A.lumbricoides Draw labelled diagram of Ascaris eggs

42 Thank u


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