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NEMATODES
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MARK M. CALBAN, MD, MPM
CSU
Colle e of Medicine & Sur er
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ASCARIS LUMBRICOIDES Male
Cross Section
1. Cuticle and Hypodermis
2. Longitudinal MuscleLayer
3. Vas Deferens
4. Testis
5. Lateral Line w/
Excretory Canal6. Intestine
7. Pseudocoelom
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ASCARIS LUMBRICOIDES Female
Cross Section
1. Cuticle and
Hypodermis
2. LongitudinalMuscle Layer
3. Ovary
4. Oviduct
5. Uterus
6. Intestine
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ASCARIS LUMBRICOIDES Lips
The THREE (3)lips & sensory
papillae are seen at
the anterior end.The margin of each
lip is lined withminute teeth whichare NOT visible atthis magnification.
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What is the lifespan of the adult
ascaris worm?
A. 1 year
B. 2 years
C. 5 yearsD. 10 years
E. NONE OF THE ABOVE
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The female ascaris worms lays approx
how many eggs/day?
A. 100,000
B. 200, 000
C. 300,000D. 400,000
E. NONE OF THE ABOVE
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PATHOLOGY
Reactions of tissues to invading larvae.
Irritation of the intestine by the mechanical and toxic actionof the adult.
Complications arising from the parasites extra intestinalmigration.
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PATHOLOGY
Tissue phase: With heavy or repeated
infection, pneumonia,
cough, low-grade fever,
30% to 50% eosinophilia
(Lfflers syndrome) resultfrom migration of larvae
through the lungs (1 to 2
weeks after ingestion of
eggs).
Allergic asthmatic reactionmay occur with reinfection.
Intestinal phase: Intestinal or appendixobstruction results frommigrating adults in heavyinfections.
a. Vomiting and abdominal pain resultfrom adult migration.
b. Protein malnutrition can occur inchildren with heavy infections and poordiets.
c. Some patients are asymptomatic.
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PATHOLOGY LARVA:
Ascaris Pneumonitis/Loefflers Syndrome
Difficulty of breathing,cough, fever, lunginfiltration.
May become ERRATIC
ADULT: Diarrhea
Malnutrition
Villous AtrophyWorm bolus/obstruction
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Pathogenesis & Clinical Findings
The major damageoccurs during larval migrationrather
than from the presence of the adult worm in the intestine.
The principal site of tissue reaction are the lungs, where
inflammation with an eosinophilic exudate occurs inresponse to larval antigens (Loefflers Syndrome)
Because the adults derive their nourishment from ingested
food, a heavy worm burdenmay contribute to
malnutrition, especially in children in developingcountries.
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PATHOLOGY
Complications fromintestinal obstructionarecaused by tangling of thelarge worms or migrationof adults to other sites, such
as the appendix, bile duct,or liver(detectable byradiograph).
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Intestinal Ascariasis
Protruberant Abdomen
Intermittent Colicky
Cramps
Loss of Appetite
Jejunal Mucosa broadening and
shortening of villi,
elongation of crypts,
decrease in villus crypts
ratio, round cellinfiltration of lamina
propria
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Laboratory Diagnosis
DIRECT FECAL SMEAR
2mg of Feces + 1 gtt NSSLPO/MPO KATO TECHNIQUES
20-60mg feces
qualitative tech, MASSexamination KATO KATZ TECHNIQUE
QuantitativeEgg counts/gram fecesdetermine egg reduction aftertreatmentDetermine intensity of ascarisinfection.
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TREATMENT
Albendazole- Drug of Choice; 400mg SD
Mebendazole - 500mg SD
Pyrantel Pamoate - 10mg/kg
Ivermectin - 200ug/kg SD
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PREVENTION
HANDWASHINGProper disposal of human wastes
Health Education
Mass Chemotherapy done periodically
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Trichuris trichiura
(Whipworm/)
Disease Caused: Trichiuriasis
Cousin of Ascaris
Trichocephalus trichiura
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Trichiuris trichiura
Common Name: Whipworm
Holomyarian Type of Somatic Muscle Arrangement.
Final Host: Man
Habitat: Large Intestine
Diagnostic Stage: Ova
Infective Stage: Embryonated Ova; MOT: Ingestion
Portal of Entry: Mouth
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49Anterior 2/3 attenuated & Thin
Posterior 1/3 fleshy & robust
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Bipolar Plug
Foot Ball Shape
Lemon-Shaped
Barrel-Shaped
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MAJOR PATHOLOGY AND SYMPTOMS
The surface of the colon may be matted
with worms. Patients will have:
a. Bloody or mucoid diarrhea
b. Weight loss and weaknessc. Abdominal pain and tenderness(colitis may be seriously debilitating)d. Increased peristalsis and rectal
prolapse, especially in children
Chronic infections in children
Growth stuntingStool is loose with mucus (and obviousblood) in heavy infection.
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Enterrorhagia,RECTALPROLAPSE
(increased
peristalsis that
occurs in an effort
to expel the
worms.,
Appendicitis
NOT cause significantanemia, unlike the
hookworms. !
Diff fr Ascaris: Noheart & Lung
migration
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Notes:
Adult worms
live in the cecum and ascending colon.
Anterior portion is threaded into the mucosa.
Female worms shed between 3,000 20,000 eggs/day
Lifespan is 1 year
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Laboratory Diagnosis
Needed to confirm yoursuspicion based on History& PE.
1. Direct Fecal Exam
2. Kato Technique(qualitative) & Kato-KatzTechnique (quantitative)
3. Concentration Techniques(Sedimentation/FlotationMx)
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Laboratory Diagnosis
DIRECT FECAL SMEAR
2mg of Feces + 1 gtt NSSLPO/MPO
KATO TECHNIQUES
20-60mg feces
qualitative tech, MASSexamination
KATO KATZ TECHNIQUE
QuantitativeEgg counts/gram feces
determine egg reduction aftertreatment
Determine intensity of ascarisinfection.
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TREATMENT
DOC: MEBENDAZOLE
500mg SD - light infxns500 mg x 3 doses - heavy infxns
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PREVENTION
Treatment of infected individualsSanitary disposal of human wastes by construction of toilets
and their proper useFrequent handwashingHealth EducationThorough scalding and washing of uncooked vegetables
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Enterobius vermicularis
(pinworm/seatworm)
Oxyuris vermicularis
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MORPHOLOGY ADULT WORM
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MORPHOLOGY EGGS
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LIFE CYCLE
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The eggs are distributed in the environment. Infection can be acquired by ingestion/inhalation of eggs.
The adult worm invades the colon.
At around 12mn-4am, the gravid female migrates to the
perianal area. Here, the female worm ruptures to release
eggs causing pruritis (thats why affected individuals
scratch their perianal area at night.
Fully gravid female migrates down the colon and anus
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Fully gravid female migrates down the colon and anus
(crawls on perianal and perineal skin)15-43 days after
ingestion of infective stage ova. (rupture of eggs caused
pruritus)
Eggs found in the environment
Transmission: anus to mouth by finger contamination
(by scratching; contamination by carriers on soiled bed
linen; airborne eggs; retrofection(female worm after
laying eggs will crawl back making it difficult to cure)
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PATHOLOGY
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CELLOPHANE/SCOTCH TAPE
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CELLOPHANE/SCOTCH TAPE
SWAB
CELLOPHANE/SCOTCH TAPE
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CELLOPHANE/SCOTCH TAPE
SWAB
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TREATMENT
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STRONGYLOIDES STERCORALIS
Common Name:THREADWORM;
Smallest Nematode of
Man
Habitat: Small Intestine
Cochin China
Diarrhea
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EPIDEMIOLOGY
Tropics, especially in Southeast Asia.
Its geographic pattern is similar to that of hookworm becausethe same type of soil is required.
More of a focally transmitted worm than a soil transmittedhelminth because it is infective shortly after passage w/ thefeces
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LIFE CYCLE
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MAJOR PATHOLOGY AND SYMPTOMS
1. Major clinical features areabdominal pain, diarrhea, andurticaria, with eosinophilia.
2. Skin shows recurringallergic, raised, itchy, redwheals from larval penetration.
3. Migration of larvae:
Primary symptoms are in thelungs; bronchial verminous(from worms) pneumonia.
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MAJOR PATHOLOGY AND SYMPTOMS
4. Intestinal symptoms include abdominal pain, diarrhea,constipation, vomiting, weight loss, variable anemia,eosinophilia, and protein-losing enteropathy.Light infections are often asymptomatic; gross lesions are
usually absent.The bowel is edematous and congested with heavy infection.
5. S. stercoralis has caused sudden deterioration and death inimmunocompromised persons because of heavy
autoinfection and larval migration throughout body(hyperinfection), with bacterial infection secondary to larvalspread and intestinal leakage.
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BAERMANN TECHNIQUE
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BAERMANN TECHNIQUE
LAB DIAGNOSIS
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LAB DIAGNOSIS
1. Recovery of the rhabditiform (noninfective) larvae is
normally from the stool concentrate. Caution: Filariform
(infective) larvae can also be recovered in the stool.
A minimum of four (4) stools are recommended beforeindicating that the patient is not infected (routine formalin,
ethyl acetate sedimentation concentration);
2. If the stool specimens are negative, examination of duodenal
contents is recommended (duodenal aspirates, Entero-Testcapsule); however, the overalL sensitivity of the method varies.
LAB DIAGNOSIS
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LAB DIAGNOSIS
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METHOD OF DIAGNOSIS
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METHOD OF DIAGNOSIS
DIAGNOSTIC CRITERIA
Identification of encysted larvae in biopsied muscle;
Serologic testing (ELISA) 3 to 4 weeks after infection.
A history of eating undercooked pork or bear
Fever, muscle pain, bilateral periorbital edema, and rising
eosinophilia
DIAGNOSTICS
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DIAGNOSTICS
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Capillaria philippinensis
( d WORM)
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(pudoc WORM)
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Capillaria philippinensis
(Pudoc Worm)
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PATHOLOGY
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The first proven caseof human infection with Capillariaphilippinensis occurred in 1963in a patient from thePhilippines who died 3 days after admission to thehospital with a diagnosis of malabsorption syndrome.
Although the significance was not recognized until 4 yearslater, C. philippinensis eggs were found in the stools andautopsy showed parasitism of the large and smallintestines.
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LIFE CYCLE
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Although the exact mode of transmission is unknown,experimental infection is transmitted through small fish that serve
as the intermediate host; often, whole, small fish may be ingested.
Development to the infective stage in the fish takes at least 3
weeks.
In areas of the Philippines where this infection occurs, people alsoeat raw shrimp, crabs, and snails.
They also tend to defecate in the fields or water where the fish,
shrimp, crabs, and snails are obtained, thus completing the life
cycle.
The worms live burrowed into the mucosa of the small bowel,mainly the jejunum.
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THANK YOU!
The harder thestruggle, the
greater the glory.