Intestinal Nematodes

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INTESTINAL NEMATODES

Phylum Nematoda 

unsegmented, elongated and cylindrical



sexes are separate ; females larger than males



posterior end of male usually curved

Life cycles: 



include

1) the egg stage 2) 4 larval stages 3) adult stage Adult female may be: A. Oviparous – eggs are oviposited and embryo develops outside the maternal body (A. lumbridoides) B.Viviparous – female gives birth to larvae (C. Philippinensis) C.Parthenogenetic – can produce viable eggs without being fertlized by the male worms (S. stercoralis)

CLASSIFICATION

Phylum Nematoda 

Class Aphasmidia (lacking phasmids or caudal receptors)



Class Phasmidia ( with phasmids or caudal papillae)

Class Phasmidia ( with phasmids) Species which parasitize the small intestines     

1. 2. 3. 4. 5.

Ascaris lumbricoides Necator americanus Ancylostoma duodenale Strongyloides stercoralis Capillaria philippinensis

Species which parasitizes the large intestines  

1. Enterobius vermicularis 2. Trichuris trichiura

Ascaris Lumbricoides 

The most common intestinal roundworm of man



Occurs most frequently in tropical and subtropical regions of Asia, Central and South America and Africa



Estimated to infect 1.2 billion individuals (1/5 of the world’s population)

Ascaris lumbricoides 

Thrives in areas with lack of sanitation and poverty and ignorance



Most common source of infection – soil contaminated foods esp. in raw vegetables



2 separate populations and reservations 1. adult Ascaris – parasitizing man 2. Ascaris eggs - environment

Ascaris lumbricoides (Morphology) 

Adult – creamy white or pinkish yellow A. Female – tapered at both ends; large; - measures 20 t0 35 cm by 5 mm ; may grow up to 45 cm long - reproductive potential : 240,000 eggs/day B. Male – curved posteriorly - measures 15 to 25 cm by 3 mm

Ascaris lumbricoides (Morphology) 





Fertilized eggs: mostly oval or spherical, golden brown : capable of further development in soil from single cell to embryonated eggs Shell contains: 1. inner non-permeable lipoidal vitelline membrane 2. thick transparent middle layer or glycogen layer 3. outermost coarsely mammilated albuminoid layer Absent mamillated layer  decorticated

Ascaris lumbricoides (Morphology) 

Unfertilized eggs

1st two layers absent; shell is thinner - generally larger, narrower, more elongate - inside are highly refractile granules of varying sizes - can never undergo development in soil -

Ascaris lumbricoides (Life cycle)

Ascaris lumbricoides (Pathology & Clinical Manifestations) 

Migratory larvae  hemorrhages and destruction of the lung parenchyma as the larvae breaks break through the capillaries - asthmatic type of respiration - cough with rales and chest pain - Ascaris pneumonitis - Loeffler’s syndrome ( allergic eosinophilic infiltration of the lungs)



Larva  bloodstream  lodge in brain, spinal cord, the eyeball, kidneys 

Ascaris lumbricoides (Pathology & Clinical Manifestations  -

Adult worms in small intestines: Decreased fat and nitrogen absorption Lactose intolerance Decreased growth rates in children Diarrhea, vague abdominal pain, loss of appetite



Vomited Ascaris  pass larynx  suffocation



May enter Eustachian tube  otitis media

Ascaris lumbricoides (Pathology & Clinical Manifestations) 

Due to erratic behavior  May become entangled  intestinal obstruction  Appendix  acute appendicitis  Bile duct  biliary ascariasis  Liver  multiple abscesses  Perforate the bowel  peritonitis  Gallstones (Ascaris eggs)

Ascaris lumbricoides (Diagnosis) 1. 2.

Direct Fecal Smear (DFS) – 2 mg of stool used Kato-Katz technique – 40-60mg of stool ADVANTAGES: a)quantitative: can count the number of eggs found in a measured stool sample b) can determine egg reduction rate after treatment c)determine intensity of infection

Negative stool exam: i. When patients are actually free from infection j. During early larval migration via blood stream k. When worms are still sexually immature l. When only male worms are found in intestines

Ascaris lumbricoides (Treatment) 

Broad Spectrum antihelminthics neuromuscular blocking effect on parasites → paralysis of worms 1. albendazole- 400 mg single dose 2. mebendazole – 500 mg single dose 3. pyrantel pamoate – 10 mg/kg single dose



Community based chemotherapy – interval of 4 months or 3 times a year for 3 years



Among schoolchildren – treatment at least twice a year at an interval of 4-6

Ascaris lumbricoides (Control)  



Mass treatment Selective treatment – treating only those found positive for eggs on stool * Targeted group – treating children alone

Ascaris lumbricoides (Prevention) 

 



Sanitary disposal of human excreta Personal hygiene Avoiding use of human feces for fertilizer Thorough cooking of food

The Hookworms 1. 2. 3. 4.

Necator americanus* Ancylostoma duodenale* Ancylostoma braziliense Ancylostoma caninum

* soil-helminths that infect man

HOOKWORMS (Morphology) Adult

Rhabditiform larva ( 1st stage) Filariform larva (3rd

Necator americanus

Ancylostoma duodenale

Small,cylindrical,fusiform, graywhite -females>males - Posterior end of the male has broad,membranous caudal bursa with rib-like rays -Ventral pair of semilunar cutting plates Resemble those of - hook-like head

-

Conspicuous and parallel throughout their lengths; conspicuous transverse striations present on the sheath in the tail

Inconscpicuous buccal spears and transverse striations on the sheath in the tail region

Strongyloides; somewhat larger, more attenuated posteriorly, and have a longer buccal cavity;

Larger - single-paired male & female reproductive organs -head continues in the same direction as the curvature of the body - 2 pairs of curved ventral teeth

- Same -

Ancylostoma duodenale

Copulatory bursa

Necator americanus

COPULATORY BURSA

Hookworm rhabditiform larva

Hookworm filariform larva

Hookworm egg 

Eggs: 

 

ovoidal, thin-shelled, colorless 4-8 cell stage in constipated stool – embryo may develop inside shell

• Differentiation of Necator and Ancylostoma – difficult and impractical

Hookworms: Life Cycle

The Hookworms : Pathology and Clinical Manifestations I. CAUSED BY LARVAL STAGE 1. Ground Itch / Coolie Itch - Intense localized itching, edema, erythema and papulovesicular eruption - Lasts up to 2 weeks - Site of entrance of filariform larvae  dermatitis

The Hookworms : Pathology and Clinical Manifestations 2. Creeping eruption or Cutaneous Larva Migrans - Due to exposure of the skin to filariform larvae of A. braziliense/caninum;

A.

- occasional – N. americanus and duodenale

- Serpiginous tunnel in stratum germinativum of skin - Larvae move at a rate of several mm to few cm per day - Pruritus  pyogenic infection

The Hookworms : Pathology and Clinical Manifestations 3. Pulmonary lesions - Petecchial hemorrhages - Eosinophilic and leucocytic infiltration

The Hookworms : Pathology and Clinical Manifestations II. CAUSED BY ADULT WORM  Hookworm anemia 

Due to continuous mechanical suction of blood from intestinal mucosa    

Microcytic, hypochromic anemia Loss of RBC in gut 0.03-0.05 ml blood/ day (N. americanus) 0.16-0.34 ml blood/day (A. duodenale)

The Hookworms : Pathology and Clinical Manifestations 

Hypoalbuminemia 

Combined loss of blood and lymph

HOOKWORMS (Diagnosis) 

Ground itch and creeping eruption - character of lesion - history of contact with soil



recovery of eggs on stool ( DFS, Kato, Formalin Ether concentration)

HOOKWORMS (Epidemiology)    

Hookworm infections: 96% - N. americanus 2% - Ancyclostoma 2% - mixed



Sandy loam type of soil with plenty of rain  favorable for infection



Chief sources of infection: Unsanitary disposal of feces Use of human feces as fertilizer

 

HOOKWORMS (Treatment) 

Treat all infections Severe anemia – increase Hgb to 7-8 g/dL before dealing with worm infection



Severe hypoalbuminemia – deworm quickly





Broad spectrum anti-helmintics: 1. albendazole 2. mebendazole 3. pyrantel 4. oxantel/pyrantel



Ferrous sulfate – 200 mg TID p.o for 3 months

HOOKWORMS (Control Measures)  





Proper disposal of feces Proper treatment of human excreta used as fertilizer Personal hygiene – use of shoes/slipper Avoiding ingestion of raw vegetables not washed properly

Strongyloides stercoralis 

Disease : Strongyloides, Cochin-China diarrhea, Threaworm



Epidemiology : infections runs parallel with hookworm infection



Infective stage – filariform larvae – skin penetration

Life Cycle of Strongyloides Adult parasite, Eggs Rhabditiform Female, in small → in → larva hatches Intestine of man mucosa from egg ↑ Esophagus 1. Autoinfection 2.Direct Cycle 3.Indirect ↑ in intestine (like hookworm) Swallowed ↑ Passed in feces into soil Pharynx Becomes ↑ filariform larva Free living adult (M & F) Trachea Penetrates intestinal ↑ mucosa Eggs Breaks out Into alveoli Larva in colon Rhabditiform larva ↑ Lungs Filariform larva on

Strongyloides (Rhabditiform larva) -

-

-

free-living Smaller than the filariform larva Female: muscular doublebulbed esophagus and the intestine is a straight cylindrical tube Male: smaller than female; ventraly curved tail, 2 copulatory spicules, gubernaculum with no caudal alae

Strongyloides (Filariform larva) -

-

-

-

parasitic; semitransparent, with fine striated cuticle Slender tapering anterior end and short conical pointed tail Buccal cavity has 4 distinct lips Uteri contain a single file of 8-12 thinshelled transparent, segmented ova

Strongyloides stercoralis (Pathology & Manifestations) 



Filariform larva – entry skin penetration “petechial hemorrhage, congestion & edema, pruritus - lungs >>>pneumonitis (cough), pleural effusion Filariform & Adult – intestines >>>GIT disturbances Stool – water mucous diarrhea depends on   



A. Intessity of infection B. Duration C. Host-tissue rxn = encapsulated the worms

Blood picture – leukocytosis (WBC 25,000) Eosinophilia ( 40%)

Strongyloides stercoralis (Diagnosis) 

Finding the rhabditiform larvae – feces or duodenal aspirate direct or concentration methods



Eggs can only be obtained by drastic purge /NGT duodenal aspirates

Strongyloides stercoralis (Treatment) 

1. Albendazole– drug of choice - 400 mg x 3 days - eradicates 80% of infections



2.

Thiabendazole - 50mg/kg into 2 divided doses daily X 2 days after meals

Strongyloides stercoralis (epidemiology) -

-

Found throughout the world More of a fecally-transmitted worm that a soil-tansmitted helminth because it is infective shortly after passage with the feces Low local prevalence More frequently found among male children 7-14 years old than among females and adults

Strongyloides stercoralis (Prevention) 

Proper waste disposal



Protection of the skin from contact with contaminated soil



Early detection & Treatment of cases

Capillaria philippinensis (Epidemiology)  







Capillariasis first recorded in Northern Luzon Also reported in Thailand, Iran, Japan, Egypt, Korea, Taiwan and India Migratory fish-eating birds are considered natural hosts In the Philippines, this has been documented in the Northern Luzon provinces,Zambales, Southern Leyte, Compostela Valley and Zamboanga del Norte Mode of transmission: eating uncooked small freshwater/brackish water fish; Northern people like to eat “bagsit” and other fish found in lagoons

Capillaria philippinensis (Parasite Biology) 

MALE

- 1.5-3.9mm - spicule 230-300um long and has unspined sheath - thin filamentous anterior end and a slightly thicker and shorter posterior end - esophagus has rows of secretory cells - anus is subterminal



FEMALE - 2.3-5.3mm

- thin filamentous anterior end and a slightly thicker and shorter posterior end - esophagus has rows of secretory cells - anus is subterminal - vulva seen at the junction of anterior and middle thirds

Capillaria philippinensis (Parasite Biology) 

EGG - peanut-shaped with striated shells and flattened bipolar plugs - 36-45um by 20um - embryonate in the soil or water

Capillaria philippinensis (Life Cycle)

Capillaria philippinensis (Clinical Manifestations) 

Symptoms: abdominal pains, gurgling stomach (borborygmus), and diarrhea; weight loss, malaise, anorexia, vomiting, and edema



Laboratory findings: severe protein-losing enteropathy, malabsorption of fats and sugars, decreased excretion of xylose, low electrolyte levels (esp. potassium), and high levels of immunoglobulin E

Capillaria philippinensis (Diagnosis) 

 

Direct fecal smear – finding the egg Stool concentration method Duodenal aspiration

Capillaria philippinensis (Treatment) 

 

Electrolyte replacement and high protein diet – in severe cases Antidiarrheal agents Antihelminthics - albendazole 400 mg once daily x 10 days

- mebendazole 200mg twice daily x 20 days * Albendazole preferred as it destroys larvae more readily than mebendazole

Enterobius vermicularis 

Enterobiasis – human pinworm - characterized by perianal itching

Enterobius vermicularis (Morphology) 

Adults: small, whitish or brownish in color anterior end – pair of lateral cuticular expansion (LATERAL WINGS or CEPHALIC ALAE)

MALE

posterior esophageal bulb male - 2-5 mm ; tail curves ventrad; single copulatory spicule female – 8-13 mm ; long pointed tail FEMALE

 



 





Eggs: measure 50-60 um by 20- 30 um elongated, ovoid, flattened on the ventral side similar to letter “D” egg shell – two layers (outer thick hyaline albuminous shell and Inner embryonic lipoidal membrane) larva – folded once within the shell (creating a line visible along the egg’s long axis)

Enterobius vermicularis Life Cycle

Life Cycle: 

 





 

eggs deposited by a single female vary from 4,672 to 16,888 (mean 11,105/day) female usually dies after oviposition male dies after copluation eggs become fully mature/embryonate within 6 hours eggs are resistant to putrefaction and disinfectants succumb to dehydration in dry air within a day may remain viable up to several days under cool and moist conditions

Enterobius vermicularis (Pathology and Manifestations) 1/3 asymptomatic  3 forms: I. Pathology at the site of attachment of the worm  Minute ulcerations or abscesses in cecal mucosa II. Pathology due to egg deposition in the perineal area - intense itching or pruritus in the perianal region - scratching  scarified - pruritus ani  hemorrhage, eczema, bacterial infection of the anal and perianal regions and perineum III.Pathology caused by migrating adults - migrating worms lay eggs in genital organs  vulvovaginitis - worms enter fallopian tube  salpingitis 

Enterobius vermicularis (Diagnosis)    

 

History and physical exam Perianal cellulose tape swab – D shaped ova - best time is soon after patient awaken and before bathing 5% only are demonstrable in feces worms may be seen migrating out of the child’s anus at night

Enterobius vermicularis (Epidemiology) 1. Infection may occur through: a.Hand to mouth transmission – most common transmission b. Inhalation of airborne eggs in dust c.Retroinfection through the anus - eggs hatch in the perianal region and larvae migrate back into large intestine 2. Only nematode that cannot be controlled through sanitary disposal of human feces because eggs are deposited in the perianal region.

Enterobius vermicularis (Epidemiology) 1.

4.

5.

6.

Local prevalence - 29% among schoolchildren from exlcusive private schools - 56% among those from public schools Local prevalence higher in females compared to males Have been collected from fingertips and fingernails of schoolchildren Adult female worms migrate to the perianal area even during daytime but more migration occurs at night time.

Enterobius vermicularis (Treatment) Pyrantel pamoate – drug of choice - 10 mg/kg with a second dose 2-4 weeks later 2. Albendazole – 400 mg as single dose 1.

3. Mebendazole – 500 mg tab as single dose

Enterobius vermicularis (Prevention & Control) 



  

all members of household who are positive should be treated at least 7 consecutive post-treatment perianal smears using scotch-tape swab method shld be negative - declare negative infection personal hygiene cut fingernails short bed linens and clothing of infected persons – sterilized by boiling

Trichuris trichiura   





Whipworm Soil-transmitted Frequently occurs together with Ascaris Children from 5 – 15 years old are more frequently infected In the Philippines, prevalence is from 80-84%

Trichuris trichiura 

Factors affecting transmission: a. Indiscriminate defecation of children around yards b. Poor health education c. Poor personal, family and community hygiene.

Trichuris trichiura (Parasite Biology) 

Male worm - 30 – 45mm

- shorter than female - coiled posterior end with a single spicule and retractile sheath - attenuated anterior 3/5 traversed by a narrow esophagus; posterior 2/5 contains the intestine and a single set of reproductive organs



Female worm - 35-50 mm - bluntly rounded posterior - attenuated anterior 3/5 traversed by a narrow esophagus; posterior 2/5 contains the intestine and a single set of reproductive organs - lays 3,000-10,000 eggs/day

Trichuris trichiura (Parasite Biology) 

EGG - 50-54um by 23 um - lemon shaped with pluglike translucent polar prominences - yellowish outer and a transparent inner shell - embryonic development takes place in the environment when eggs are deposited in clayish soil

Trichuris trichiura (Parasite Biology)  





Inhabit the large intestine Entire whip-like portion embedded into the intestinal wall of the cecum Eggs become embryonated within 2-3 weeks No heart-lung migration

Trichuris trichiura (Life Cycle)

Trichuris trichiura (Clinical Manifestations) 

  





Worms embedded in the mucosa can cause petechial hemorrhages Rectal prolapse Appendicitis >20,000 eggs/gm of feces: severe diarrhea or dysenteric syndrome Light infections: asymptomatic In heavy parasitism: bloodstreaked stools, abdominal pain, anemia, weight loss

Trichuris trichiura (Laboratory Diagnosis) 

In heavy infections, clinical symptoms may be relied upon to make a diagnosis



In light infections: 1. direct fecal smear 2. Kato thick smear method

Trichuris trichiura (Treatment) 

Mebendazole 500 mg single dose in light infections; 2-3 days therapy in moderate and heavy infections – drug of choice



Albendazole 400 mg single dose – alternative drug

Trichuris trichiura (Prevention and Control) 



Mass treatment if infection rate is > 50% Preventive measures a. Treatment of infected individuals b. Sanitary disposal of human feces by constructing toilets c. Washing of hands with soap and water before and after meals d. Health education on sanitation and personal hygiene e. Thorough washing and scalding of uncooked vegetables especially in those areas where night soil is used as fertilizer

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