worms

Dr Putra Hendra SpPD

UNIBA
BATAM
Infectious Agents

Bacteria
Viruses
Fungi
Protoctists / Protozoa
Helminths
 Types of parasites
 Protozoa
 Single celled, Organized cellular structure
 May ingest solid particles
 Require aquatic environment
 Reproduce by binary fission at some point in life cycle
 Helminths (worms)
 Multicellular, Organized internal structure; includes
 Platyhelminths (flatworms)
 Nematoda (roundworms)
 Ectoparasites
 Insects and arachnida found on the skin.
 KECACINGAN
(Soil-Transmitted Helminths / STH)

Cacing Gelang Cacing Cambuk

Ascaris lumbricoides Trichuris trichiura

Cacing Tambang
Necator americanus Ancylostoma duodenale
Siklus Hidup STH
 DAMPAK CACINGAN
Investasi cacing

Darah dihisap
Anemia
KH & Protein dihisap Lemas

mengantuk
BBLR Perdarahan
Gizi buruk Malas belajar/ ibu bersalin
sering bolos

Prestasi belajar Mati Mati

menurun

Produktivitas
menurun

Sosek rendah
 Trematodes
Flat worms
Cestodes
Helminth
Tissue type
Round worms
(Nematodes)
Intestinal
type
8
 NEMATODES

NEMA: thread EIDOS: bentuk

Nematohelminthes dapat berbentuk :

bulat, silinder, spindle .
Contoh:
ENTEROBIASIS = OXYURIASIS ( pin worm)
ASCARASIS = round worm
ANCYLOSTOMIASIS = hook worm
TRICHINOSIS
TRICHURIASIS = whip worm
 Classification – Intestinal Nematodes
Ascaris lumbricoides (round worm)

Necator americanus (american hook worm)

Usus kecil
Ancylostoma duodenale (hook worm)

Strongyloides stercoralis

Trichinella spiralis (trichina worm)

Capillaria philippinensis

Enterobius vermicularis (pin worm)

Caecum dan
Vermiform appendix Trichuris trichiura (whip worm)

20/04/08 Dr Ekta, Microbiology

 Cara infeksi Nematodes
1. Ingestion (mulut)
• Embryonated eggs contaminating food & drinks, e.g.
A.lumbricoides, E. vermicularis & T. trichiura
• Growing embryos in an intermediate host (infected
cyclops) e.g. D.medinensis
• Encysted embryos dalam daging babi yang terinfeksi :
Trichinella spiralis

2. Penetration kulit – larvae filariform melubangi kulit :

A.duodenale, S.stercoralis, N.americanus

3. Gigitan nyamuk : filarial worms

4. Inhalation debu terinfeksi embryonated eggs e.g.

A.lumbricoides, E.vermicularis
 Ascaris lumbricoides

 Infeksi cacing paling sering pada manusia

 Diperkirakan51 juta anak terinfeksi

biasanya pada daerah yang masyarakatnya
kurang mampu

 Anak yang terinfeksi kondisinya lebih buruk

daripada orang dewasa
Ascaris lumbricoides
Ascaris lumbricoides
 Ascaris lumbricoides
Adult worms live in the lumen of the small intestine (1). A female may
produce approximately 200,000 eggs per day, which are passed with the
feces (2) .
Unfertilized eggs may be ingested but are not infective. Fertile eggs
embryonate and become infective after 18 days to several weeks(3) ,
depending on the environmental conditions (optimum: moist, warm, shaded
soil).
After infective eggs are swallowed (4) , the larvae hatch (5), invade the
intestinal mucosa, and are carried via the portal, then systemic circulation
to the lungs (6) .
The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar
walls, ascend the bronchial tree to the throat (7), and are swallowed .
Upon reaching the small intestine, they develop into adult worms (1) .
Between 2 and 3 months are required from ingestion of the infective eggs
to oviposition by the adult female. Adult worms can live 1 to 2 years.CDC
 Gejala ascariasis
 Tak bergejala
 Stage 1: Larva cacing melekat pada dinding usus.
 Stage 2: Larva cacing migrasi ke paru: demam dan sesak
 Batuk dan pneumonia
 Stage 3: worms enter the small intestine and mature into
worms and remain there to feed
 Abdominal symptoms
 Abdominal discomfort
 Intestinal blockage - may be partial or complete
 Partial intestinal blockage
 Total intestinal blockage
 Severe abdominal pain
 Vomiting
 Restlessness
 Disturbed sleep
 Worm in stool
 Worm in vomit
 Symptoms & Complications
 Symptoms produced by Migrating larvae
1. Pneumonia (loeffler’s syndrome) – fever,
cough, dyspnoea, blood tinged sputum that
may contain larva, urticarial rash &
eosinophilia

2. Visceral larva migrans – if larvae enter

systemic circulation (from pulmonary
capillaries) to reach other organs like brain,
spinal cord, heart, kidney.
20/04/08 Dr Ekta, Microbiology
 Life cycle
Adult worms (intestine)

Throat, swallow, Unembryonated

small intestine eggs (stool)

Right heart, lung, Embryonated eggs

respiratory in 2-3 weeks in soil
passage, (infective form)

Penetrate Ingestion of
Rhabditiform
intestine, reach eggs
larva hatches
20/04/08 liver Dr Ekta, Microbiology
 Komplikasi

 Paru: Larvae migration through the lung

parenchyma  mechanical and immune-mediated
damage:
 Pulmonary microhemorrhages
 Inflammation & exudation of fluid
 Pulmonary infiltrates
 Cough, dyspnea, wheeezing, mild hemoptysis
(Loffler pneumonia)
 PEM, Vit. A deficiency (night
blindness)

Intestinal obstruction (particularly in

children 1-5 years),
intussusception & volvulus

Penetration through intestinal ulcer

(perforation) – peritonitis

Hypersensitivity reactions to
worm Ags (toxic body fluids) –
urticaria, edema of face,
conjunctivitis, irritation of URT

20/04/08 Dr Ekta, Microbiology

6. Ectopic Ascariasis – due to
migration of worm up into the
stomach. It may
 pass up through the
oesophagus at night & comes
out through mouth or nose,
 enter larynx to cause
asphyxia.
 migrate to other organs and
cause appendicitis,
cholecystitis, biliary colic,
cholangitis, pancreatitis
20/04/08 Dr Ekta, Microbiology
 Ascaris lumbricoides
Laboratory Findings/Diagnosis

 Diagnosis is established by stool examination for

characteristic ova. Each adult female produces so
many eggs that a single stool specimen is adequate

 Migration of larvae through the lungs is assocaited

with peripheral eosinophilia and pulmonary infiltrates on
chest radiograph

 In endemic areas, any child presenting with signs

suggestive of intestinal obstruction should be evaluated
for Ascariasis
 Ascaris lumbricoides
Treatment
 Mebendazole (100 mg twice daily X 3 days) or

 Albendazole (400 mg as a single dose)

(The above are not generally given to children < 1 yr)

 Pyrantel pamoate (11 mg/kg up to 1 gm/day, X 3 days)

 In cases of partial bowel obstruction caused by

Ascaris: alternative therapy with piperazine citrate,
which paralyzes the worms may abrogate the need of
surgical intervention
ANKYLOSTOMIASIS
 Hookworms
 Sekitar 1 juta orang menderita ankilostomiasis

 Merupakan penyebab utama iron deficiency

anemia di negara sedang berkembang

 Anak-anak paling rentan terkena komplikasi karena

diet tidak tdak cukup
Jenis cacing yang paling sering menginfeksi
manusia:

(1) Ancylostoma duodenale

(2) Necator americanus
Adult females:10-13 mm (A. duodenale), 9-11 mm (N.
americanus)
Adult males: 8-11 mm (A. duodenale), 7-9 mm (N.
americanus).

A smaller group of hookworms infecting animals can invade and

parasitize humans (A. ceylanicum) or can penetrate the human
skin (causing cutaneous larva migrans), but do not develop any
further (A. braziliense, Uncinaria stenocephala).
 Hooks in
the mouth

Mouth of an
Hookworm
Life Cycle: A. duodenale & N. americanus
 VPH aspect  zoonosis
Children habits play with soil
CLM = Cutaneous Larva Migrans
Hookworm
larvae
under the
skin
Hookworms
in the
intestine
 Hookworms
 In the bowel, adults attach by their mouth to the
intestinal mucosa and begin to feed

 Equipped with teeth, cutting plates or both, powerful

esophageal muscles, and hydrolytic enzymes, the
hookworm digests the plug of tissue within its buccal
capsule

 Potent anticoagulants and inhibitors of platelet function

are released and cause profound bleeding from
lacerated capillaries in the lamina propria

 Adult worms mate in the small intestine, and the

females deposit fertilized eggs in the lumen
Ancyclostoma
duodenale.
 Hookworms
Clinical Manifestations

 Skin penetration by third stage larvae  an intensely

pruritic dermatitis called ground itch (localized to site
of hookworm entry)

 Adult hookworms in intestine:

 Nonspecific GI tract symptoms
 Blood loss secondary is proportional to worm burden and
develops 10-20 weeks after infection
 A. duodenale infection is usually associated with greater loss
than occurs with N. amricanus
 Hookworm anemia results when blood loss exceeds the host’s
iron reserve and dietary intake
 Occasionally, severe hookworm anemia leads to heart failure
 Symptoms produced by larvae
 Lesions in the skin:
1. Ancylostome dermatitis or Ground itch –
occurs at the site of entry (more common in
necator), lasts for 2 to 4 weeks

2. Creeping eruption – reddish

itchy papule along the path
traversed by filariform larvae
(larva migrans)

 Lesions in the lungs – bronchitis &

bronchopneumonia.
20/04/08 Dr Ekta, Microbiology
 Clinical features of hookworm
anemia
 Extreme pallor (kuning
jerami)
 Epigastric tenderness with
dyspepsia
 Constipation
 Muka bengkak
 Pedal edema
 Growth retardation

20/04/08 Dr Ekta, Microbiology

 Symptoms produced by adult worm

 Epigastric pain, diarrhoea & vomiting

during early phase of infection.

 Microcytic hypochromic (Iron deficiency)

anaemia – due to chronic blood loss:
a single adult hookworm sucks 0.2ml of
blood/ day
 Hemorrhages from punctured sites

20/04/08 Dr Ekta, Microbiology

 Laboratory Diagnosis
 Stool examination –
microscopy: non bile
stained egg, segmented

 Occult blood in stool –

positive

 Blood examination –
anaemia, eosinophilia
20/04/08 Dr Ekta, Microbiology
 Hookworms
Treatment
 Mebendazole (100 mg twice daily X 3 days) or

 Albendazole (400 mg as a single dose)

 Mebendazole is poorly absorbed and may not eradicate

developmentally arrested Ancylostoma larvae residing in
extraintestinal issues. Therefore periodic follow up stool
examination may be necesessary

 Alternate Treatment:
Pyrantel pamoate (11 mg/kg up to 1 gm/day, X 3 days)

 Re-infection in endemic areas occur so commonly that the effect

of single course of treatment is of questionable benefit

 Iron supplementaion reverses mild to modertae hookworm anemis

 Pencegahan ankilostomiasis
 No evidence of naturally acquired resistance

 Children in endemic areas are constantly exposed to infective

third-stage larvae

 Interest in development of a vaccines aimed at preventing

hookworm infection/disease in children in the developing world

 Most promising vaccine candidates: family of proteins called

ASP’s (Ancylostoma–secreted proteins) which are secreted by the
infective larval stage

 Immunization with recombinant hookworm ASP has been shown to

prevent tissue migration in a murine model of ancylostomiasis
TAENIASIS
 Taenia saginata & Taenia solium
Epidemiology
T. saginata:
Widespread in cattle breeding areas of the world. Prevalence >10%
in some independent states of the former Soviet Union, in Near
East, and in central and eastern Africa.
Lower rates in Europe, Southeast Asia, & South America

T. solium:
Prevalent in Mexico, Central and South America, Africa, Southeast
Asia,and the Philippines

Infections in USA and Canada are found in immigrants

from areas where taeniasis is endemic, and in travelers
who consume undercooked meats in endemic areas
 Tapeworms
Taenia saginata and Taenia solium
Segmented worms, called tape worms, cause human
illness in either of two stages in their life cycle:

(1) Adult stage: Cause gastrointestinal symptomatology

(2) Larval stage: Causes signs and symptoms referable to
enlarging larval cysts in a variety of tissues

Humans are the only definitive hosts for T. saginata

(the beef tapeworm) and T. solium (the pork tapeworm)
Taenia saginata - The Beef Tapeworm
Taenia solium - The Pork Tapeworm
 Taenia saginata & Taenia solium
Clinical Manifestations
Cysticercosis occurs in humans after the ingestion of T. solium eggs

Embryonic metacestode migrates from the intestine and can lodge in

a number of tissue sites such as the brain, muscle, and eyes with
proclivity for the brain

The clinical course largely depends on the endurance of the parasite

inside the tissue and on the ensuing inflammation

In the brain parenchyma, the intruding cysticercus might be

destroyed within a few days by host immune mechanisms or remain
viable in the brain for > 10 years
 Taenia saginata & Taenia solium
Clinical Manifestations
Cysticercosis can affect humans at any age
Most common during the 3rd and 4th decades of life
About 10% occur in children

In infants initial signs of cysticecosis in infants is generalized seizure

CT with contast or T2-weighted MRI  isolated cystic lesion in the
brain parenchyma

Typically the lesion disappears spontaneously 2-3 months later, but in

some  granuloma  cacification (permanent sequela)
Isolated lesion is most common; some children have two-several cysts

Cystcercotic encephalitis is a severe form of CNS cystcercosis

that occasionally occurs in children, particularly adolescent girls
scolex
India Ink Technique

Note : less than 13 lateral uterine

branches (one side) .

 cysticercus

 Surrounded by fibrous capsule

 Containing an invaginated scolex

 Bladder-like, fluid –filled cyst

 Multiple,0.5-2cm in size
(3) Brain type:

The symptoms are related to the

site of infection.
headache,
nausea,
vomiting,
epilepsy,
paralysis
Epilepsy
Differences between T. solium and T. saginata
1. Body length

T. solium T. saginata
 Morphology
T.saginata T.solium

Size 4-8 m 2-4 m

4 suckers,
Scolex 4 suckers
rostellum & hooklets
Mature proglottid
2 lobes 3 lobes
Ovary

Testes 300-400 150-200

Gravid proglottid:
Uterine branches
15-30 7-12
 T.saginata T.solium

D.H Human Human Human

I.H Cattle Swine Human

Tissue(brain, eye,
Habitation Small intestine Small intestine
skin etc.)

Cysticercus
Infective stage Cysticercus bovis Egg
Cellulosae

Disease Taeniasis Taeniasis Cysticercosis

 Taenia saginata & Taenia solium
Laboratory Findings/Diagnosis
 CT and MRI are the most relaible tools for the diagnosis of
neurcysticercosis

 Serologic tests are unreliable (cross reactivity with antigens of

other parasites)

 Serology is highly specific for CNS inection when tests are

performed on CSF
 Taenia saginata & Taenia solium
Treatment
 Intestinal T. solium infection:
Praziquantel - (5-10 mg/kg once)

 Neurocysticercosis:
 Albendazole - 15 mg/kg/day (maximum, 800 mg/day)
divided into two doses X 8 days
 Two months later, if repeat imaging studies show
cysts: Praziquantel in a total dose of 75mg/kg divided
in three doses for 15 days. Repeat imaging studies
in two months
 Enterobius vermicularis
(Pin Worm, Seatworm)
Adult worms Male 2 - 5 mm
Female 8 -13 mm, oviparous

Eggs 60 µ, non bile stained

Plano-convex with coiled
embryo

Infective form Embryonated egg

Mode of transmission Ingestion,

Autoinfection
Site of localization Large intestine –
caecum & appendix
20/04/08 Dr Ekta, Microbiology
 Enterobius vermicularis.

Enterobius Enterobius
Enterobius egg in vermicularis female. vermicularis
feces. male.
 Life cycle – E. vermicularis

20/04/08 Dr Ekta, Microbiology

 Trichuris trichuriura.
These whipworms cause 800 million infections per
year worldwide. Trichuriasis occurs in the southern
United States and Latin America.

Female whipworm, Trichuris trichiura.

 Trichuris trichiura:

1.Inhabits the caecal region.

2.Live free in lumen of colon .
3.Larvae have migratory cycle in
lung
4.Larvae cause Loeffler`s
syndrome.
 Strongyloides stercoralis

Adult worms 2 - 2.5mm, ovoviviparous,

eggs laid in the tissues

Free living worms Moist soil

Infective form Filariform larvae

Mode of transmission Penetration / autoinfection

Site of localization Wall of Small intestine,

mainly duodenum & jejunum

20/04/08 Dr Ekta, Microbiology

Trichinella spiralis (Trichina Worm)

Adult worms (smallest Male 1.4 – 1.6 mm

nematode infecting man)
Female 3 - 4 mm, viviparous

Infective form Encysted larvae (100µ) in

striated muscles of pig

Mode of transmission Ingestion of improperly

cooked pork

Site of localization Small intestine

Commonly involved Diaphragm, Intercostals, Deltoid,

muscles Pectoralis major, Biceps
20/04/08 Dr Ekta, Microbiology
 Trichinella spiralis

Muscle can be squeezed between 2 plates of glass to

reveal microscopic larvas.
Life Cycle – T spiralis

Encysted larva in pig

muscles (infective form)
Eating under-
Larva deposit and cooked pork
encyst in striated
muscles Larva released in
small intestine
40 hrs
Larva enters
circulation Female deposits Develop into
larva in intestinal adult worms
mucosa
20/04/08 Dr Ekta, Microbiology
 Pathogenicity
 Trichinelliasis / Trichinosis – clinical features depends
on the stage:
1. Stage of intestinal invasion: 5-7 days, pain in abdomen,
nausea, vomiting, diarrhoea

2. Stage of larval migration: fever, urticarial rash, splinter

hemorrhages, periorbital & facial edema

3. Stage of encystation: asymptomatic in light infections;

myalgia, weakness in heavy infections

 Complications – during migration:

 myocarditis, encephalitis

20/04/08 Dr Ekta, Microbiology

Differential diagnosis
SYMPTOM &SIGN
 Symptoms Parasite

Abdominal pain and distension Giardia

Cryptosporidium
Amoebiasis
Ascaris, hookworm, taenia
Diarrhoea +/- malabsorption Giardia
Cryptosporidium
Strongyloides
Diarrhoea with blood loss Amoebiasis
Trichuris
Hookworm
Tenesmus, prolapsed rectum Trichuris
 Intestinal parasites: Symptoms
Symptom Mechanism Parasite

Anaemia Blood loss Amoebiasis

Hookworm
Trichuris
S mansoni

Malabsorption Giardia
Diphyllobothrium

Malnutrition Heavy infestation

 Intestinal Parasites : Symptoms

Symptom Mechanism Parasites

Skin rash Papulovesicular Hookworm

Creeping eruption Strongyloides
Peri-anal rash and Enterobius
pruritus

Respiratory Pulmonary Ascaris

symptoms migration Hookworm
Strongyloides
Toxocara
 Intestinal Parasites : Surgical Symptoms
Symptom Mechanism Parasite

Intestinal obstruction Worm bolus Ascaris

Appendicitis Obstruction Ascaris

Jaundice, biliary Biliary obstruction Ascaris

colic

Prolapsed rectum Tenesmus, weight Trichuris

loss

Intestinal perforation Transmural necrosis Amoebiasis

and peritonitis
Komplikasi rectal prolapse

1. Oxyruriasis.
2. Strongyloidiasis.
3. Trichuriasis.
4. Ancylostomiasis.
 Loeffler`s syndrome is
caused by :
1. Adult Ascaris in liver
2. Fasciola in liver
3. Adult Ascaris in intestine
4. Ascaris larva in lung
5. Schistosoma eggs in liver
Penyebab Visceral larva migrans
1. Ascaris lumbericoid.
2. Trichuris trichiura
3. Toxocara canis
4. Fasciola hepatica
5. Wucheraria bancrofti
Penyebab komplikasi
intestinal obstruction

1. Ascaris lumbricoides.
2. Enterobius vermicularis.
3. Ancylostoma duodenal.
4. Strongloides stercoralis.
 Drugs used for treating human intestinal
nematodes (single dose unless otherwise stated

Ascariasis Hookworm enterobius tricuris strongyloides

Piperazine ++ + ++ - -

Pyrantel pa ++ ++ ++ - -

Albendazole ++ ++ ++ + +

Mebendazole ++ ++ ++ + +

Thiabendazole n/a n/a n/a n/a ++

Ivermectin n/a n/a n/a n/a ++

85