Professional Documents
Culture Documents
MEDICAL
HELMINTHOLOGY
Introduction to
Medical Helminthology
HELMINTHES
NEMATHELMINTHES PLATYHELMINTHES
Nematodes live as
1. The free-living, are widely distributed in water and
soil
2. The parasitic spesies, live in plants, mollusks,
annelids, arthropods and vertebrates
Over 80.000 spesies are parasite of vertebrate
Classification Based on
The existence of phasmid (a caudal chemo
receptor)
The habitat of the adult worm
NEMATODES
General characteristics
HABITAT
IMMATURE INTO
INFECTIVE
SOIL TRANSMITTED HELMINTHS
IN INDONESIA
HABITAT
Lumen of the intestine :
Jejunum
Media ileum
Infection by Trichuris trichiura
( TRICHURIASIS )
Distribution
Trichuriasis - cosmopolitan
Primarily in hot and humid areas
prevalence 80-90 %, especially among underfives
and school children
Habitat
Caecum, appendix, colon (proximal end)
Mode of infection oral
Infective eggs embedded under fingernail (hand to
mouth infection)
Ingested with contaminated food/drinks (carried by
insect vector: cockroach, flies)
Infection by Hookworm
GEOGRAPHIC DISTRIBUTION Cosmopolitan,
especially :
Tropical equator
Coal/tin mines, coffee/rubber plantations
Ideal soil for egg development :
Sandy soil
Clay soil
Muddy soil hindered from excessive
dryness or wetness
HABITAT
Small intestine (jejunum)
In heavy infection : duodenum, colon
Infection by
Strongyloides stercoralis
Jejunum (proximal )
In human body
C
Eggs hatch
(Proximal intestine)
Eggs in
Feces
HOOKWORM
LIFE CYCLE
In human body
Larvae entered
Pulmonary
Adult in intestine
( jejunum )
Larvae entered
Blood stream
Eggs in
feces
Filariform l arvae
penetrate skin Immature
egg
In Soil
Infective larvae
Mature
Filariform larvae egg
Immature
egg
Rhabditiform larvae Hatch in soil
Strongyloides stercoralis
LIFE CYCLE
Life cycle in human body
A
Larvae enter
Lung
Adult in
duodenum, especially
Larvae entered Proximal duodenum
Blood stream
Filariform larvae
Rhabditiform larvae
Infective stage
B in soil
Egg
Development
Rhabditiform
larvae
Disease : Trichuriasis
Heavy infection worm migrate to colon,
rectum
Prolapsus recti, worm found in mucosal
lining (due to frequent defecation)
Infecion by Trichuris trichiura
PATHOLOGY AND CLINICAL SYMPTOMS
Disease: Ancylostomiasis
Synonym: Uncinariasis, necatoriasis
infection by A. duodenale are more
serious than N. americanus
Chronic infection rarely produce acute
manifestation
Tissue damage and symptoms are caused
by :
Larva stage
Adult worm
Infection by HOOKWORM
PATHOLOGY CAUSED BY LARVA STAGE
Patient
Glositis atrofik pada with atrophic glossitis
anemi hipokrom
also show fingernail
mikrositer yang
deformity (koilonichia)
disebabkan infection
Fingernail becomes thin and
berat HOOKWORM
Tampak lidah concave
halus with elevated ridge
dan kurang papila
source : Atlas Parasitologi Kedokteran, Zaman P. Alih Bahasa : Anwar C.; Mursal Y.
Strongyloides stercoralis
CLINICAL FEATURES
Disease : Strongyloidiasis, Strongyloidosis,
Cochin China diarrhea
Level of infection :
Mild - asymptomatic
Moderate
Heavy and chronic
In moderate infection
Female worm embedded in the
mucosal wall of duodenum
Burning sensation and stinging
pain in the epigastrium
Nausea, vomiting, diarrhea and
constipation
In heavy and chronic infection
Loss of body weight; Anemia
Dysentery (chronic); Slight fever
May be accompanied by secondary
bacterial infection where worm inhabits
the entire intestinal epithelium up to the
distal colon)
Ascaris lumbricoides
Diagnosis
Identify the eggs found in feces using
following methods :
Direct smear method
Concentration method
Sedimentation method
Identify larva found in sputum
Identify adult worm found expelled from
anus, mouth, nostril
Quantitative lab method to measure
level of infection
- Stoll method
- Kato Katz method
Additional : chest X-ray
Infection Trichuris trichiura
Diagnosis
Identify egg worm found in fecal
sample
Identify adult worm from prolapsed
rectum (by proctoscopy)
Measure level of infection by counting
Number of eggs per gram feces with Stoll
method and Kato katz method.
Number of female worm expelled through
deworming
Infection by HOOKWORM
Diagnosis
Identify eggs from feces sample
Identify larva from :
Fecal culture
Old feces sample
Infection by
Strongyloides stercoralis
Diagnosis
Find and identify
Rhabditiform larva :
From fresh feces
Gastric (duodenal) juice
Eggs :
In heavy diarrhea
After administration of
laxative
Ascaris lumbricoides
Mass treatment
BasedTreatment
on prevalence of
Drug available
Ascariasis in one area :
Pyrantel pamoate
prevalence > 30 %, treatment 3x/year
Mebendazol
prevalence (20-30) %, treatment 2x
Oxantel pamoate
/year
Piperazine
prevalence (10-20) %, treatment 1x
/year Albendazole
prevalence < 10 %, individual
treatment in positive cases only
Ascaris lumbricoides
ASCARIASIS
PREVENTION
Drugsavailable:
Elimination of source of infection
Improved
Oxantel pamoate personal hygiene (hand
Mebendazol (drugtoilet
washing, of choice)
training)
Through washing of sold
vegetables
Health education
Provision of sanitary public toilet
HOOKWORM
ANTIHELMINTHICS
Tetrachlorethylen
Mebendazole
Albendazole
Pyrantel pamoate
Bitoskanate
Bephenium hidroxynaphtoate
PREVENTION
Same as with Ascariasis but
with the addition of :
wearing shoes during work
in plantation or mine area
Infection by
Strongyloides stercoralis
TREATMENT AND PREVENTION
Drugs given
Thiabendazole
Mebendazole
Pyrvinium pamoate
PREVENTION for Strongyloidiasis
Similar to the prevention of hookworm
Autoinfection is prevented by means of :
Avoid constipation
Anal hygiene
NON-SOIL TRANSMITTED HELMINTHS
1. Enterobius vermicularis
2. Trichinella spiralis
Enterobius vermicularis
A. MORPHOLOGY
> Enterobius vermicularis = Oxyuris vermicularis = pinworm.
> In its life, this worm (ovipar) develops from:
egg larva worm.
> Its egg is oval, assymetry, that contains embrio.
> This worm has lateral ala cephalic in anterior tip.
> One female worm can produce 11.000 eggs in one day.
> The female worm will die after producing eggs.
> The male worm will die after copulation.
B. LIFE CYCLE of Enterobius vermicularis
Female & male worms do copulation in cecum & around (appendix,
ascending colon & ileum)
Pregnant female worms migrate at night & produce eggs in anus &
around (anal area)
After several hours, eggs become mature & infectious, then come to host,
via:
F. TREATMENT
> Mebendazole, thiabendazole, etc.
G. PREVENTION
> Washing hand before eating
> Cutting long fingernail, etc.
Trichinella spiralis
A. MORPHOLOGY
> Trichinella spiralis = porkworm.
> In its life, this worn (vivipar) develops from larva worm.
> Its larva can become cyst (circular larva which is covered by
hyaline capsule).
> This worm has stylet mouth to invade intestine or muscle
tissue.
> One female worm can produce about 1.350-2.000 larvas.
> The male worm will die after copulation.
B. LIFE CYCLE of Trichinella spiralis
Female & male worms do copulation in mouse/pig/person duodenum to
cecum
Pregnant female worms enter to intestinal villi and then lymphatic sinus
Larva is brought by lymphatic flow, to thorachic duct, right heart, lung, left
heart, and then to around body
Host (person/pig/etc) can die
Larva enter to mouse/pig/person muscle tissue & make cysts (larva can live
until 30 years in muscle)
Cyst wall rupture & larva release & larva become mature (be worm) in health
person duodenum
The worm can also pass placenta & mammary
Trichinella spiralis
C. SPREADING
> Cosmopolite (spread around the world).
F. TREATMENT
> Thiabendazole.
G. PREVENTION
> Cooking meat (esp. pig muscle) perfectly
> Destroying mouse, etc.
BLOOD AND TISSUE
NEMATODE
THERE ARE THREE GROUPS :
Filaria dan Dracunculus
Larva Migrans (TROPICAL MEDICINE)
Rarely found nematode :
- Angiostrongylus cantonensis
- Capillaria hepatica
- Gnatostoma spinigerum
FILARIA AND DRACUNCULUS
Wuchereria bancrofti
Brugia malayi
Brugia timori
Loa loa
Onchocerca volvulus
Acanthocheilonema
perstans
Mansonella ozzardi
Dracunculus medinensis
FILARIA
LIFE CYCLE
LARVAE MIGRATE TO
FINAL LOCATION AND FEMALE
DEVELOP TO ADULT PRODUCE
MICROFILARIAE
MICROFILARIAE
HUMAN INFECTED
TO BLOOD
WHENVECTOR BITES
OR SKIN
HUMAN
DEVELOPMENT
IN VECTOR
FILARIA
TOPICS
(As problem of Public Health in Indonesia)
Wuchereria bancrofti
Brugia malayi
Brugia timori
Wuchereria bancrofti
Brugia malayi
Brugia timori
Life Cycle of B malayi
THE DEVELOPMENT IN THE MOSQUITO : 10 12 DAYS
MICROFILARIAE APPEAR IN THE BLOOD :
Wuchereria bancrofti : minimum after 8 months
Brugia malayi : minimum after 3 months
THE ADULT MAY LIFE AND PRODUCE MICROFILARIAE FOR
MORE THAN 18 YEARS
LIFE SPAN OF MICROFILARIAE APPROXIMATELY 1 YEAR
LYMPHATIC FILARIASIS LIFE CYCLE
Adult worm
Microfilariae
HUMAN
BODY
MOSQUITO
Infective larva (L3) BODY
Larva L1
Mansonia, Anopheles,
Larva L2 Culex, Aedes
MAIN MOSQUITO VECTORS
W. bancrofti Anopheles sp
B. malayi Mansonia sp
HABITAT
Vessel and lymph node
(bellow the diaphragm)
Can live 10-20 years
Microfilaria in blood,
penetrate placenta
3 times metamorfosa
DISTRIBUTION :
Urban bancroftian filariasis, vektor Culex
fatigans
Rural bancroftian filariasis, vektor Aedes,
Anopheles dan Mansoni
Wuchereria bancrofti
Periodicity
Clinical
Nocturnal Periodicity
Sub periodic nocturnal
Diurnal Periodicity
Sub periodic diurnal
Non periodic
CHRONIC TROPICAL
ASYMTOMATIC FILARIAL
NONE LYMPHATIC PULMONARY
MICROFILAREMA FEVER
PATHOLOGY EOSINOPHILLIA
Grading of lymphoedema
Grade 1
Reversible pitting
oedema
Acute manifestations
Characterised by recurrent attacks of fever
associated with inflammation of lymph nodes
(adenitis) and /or lymph vessels
(adenolymphangitis, ADL)
Involvement of genitalia lymphatic in male
funiculitis, epididymitis or orchitis
Lasting for 4-5 days
Repeated episode important in the progression
of disease
Acute manifestation: ADL
Acute Filarial Lymphangitis
Cord-like structure with retrograde lymphangitis:
painful, red and tenderness
Systemic reaction mild, distal oedema rare
Recurrent at same site common
ADL with secondary bacterial infection
Most common form of ADL
Associated with fever, chills, myalgia and headache
Cellulitis and oedematous, subside after each attack
Acute adenolymphangitis
(ADL)
Subcutaneous abscess may form and
rupture releasing chylous fluid
Chronic manifestation
Major signs
Hydrocoele
Chyluria
Rupture of lymphatic lining the bladder leading to passage of
lymph in the urine
May resolve spontaneously
Lymphocytes in urine
Lymphoedema
elephantiasis
Chronic manifestation
Major signs
Hydrocoele
Chyluria
Lymphoedema
Swelling due to collection of lymph fluid in soft
tissue
Pitting oedema, may or may not be reversible
Thickened skin
elephantiasis
Chronic manifestation
Major signs
Hydrocoele
Chyluria
Lymphoedema
Elephantiasis
Irreversible, non-pitting oedema with fibrotic and
verrucous skin changes (thickening, folding,
hyperkeratosis, pigmentation, ulceration)
Skin & soft tissue infection common
Grading of lymphoedema
Grade 2
Irreversible oedema
No skin changes
Grading of lymphoedema
Grade 3
Irreversible oedema
Skin thickened
Grading of lymphoedema
Microfilaraemic carrier
No sign and symptom of infection
Source of infection to others
Evidence of sub-clinical infections:-
40% with sub-clinical hematuria/proteinuria: low grade
renal damage. Complete reversal after clearing Mf
Lymphoscintigraphy: markedly dilated, tortuous lymphatics
and abnormal lymph flow
Secondary bacterial infection of chronic
lymphoedema
CLINICAL:
Main symptom : fever, limphangytis,
limphadenitis
Elephantiasis : lower extremity bellow knee,
elbow,inguinal, rarely scrotum
THERAPY :
Hetrazan, po 0,1 gr, 3-4 x/day, as long as 10 days
PREVENTION :
Pentachlorophenol (dowicide G), kill water plant
Pistia stratioides, Eichornia, Salvinia
Brugia malayi
ELEPHANTIASIS BY B. malayi
Chrysops
Onchocerca valvulus
Causes onchocersiasis or river blindness
Intermediate host and vector blackfly or buffalo gnat (genus Simulium)
Since microfilariae are found in the skin, the specimen of choice for the
diagnosis of onchocersiasis is a skin biopsy or skin snip.
1. CLINICAL DIAGNOSIS
2. PARASITOLOGICAL DIAGNOSIS
Blood Specimen should be obtained at the time or the day
when the peak concentration of microfilariae is expected
3. IMMUNOLOGICAL AND POLYMERASE CHAIN REACTION
(PCR)
4. ULTRASONOGRAPHY
TREATMENT
DEC :
Microfilaricidal Host are Eliminated
Adult Some are Eliminated
INVERMECTIN (MECTIZAN)
Microfilaricidal Host are Eliminated
Adult No Effect
ANTIFILARIAL DRUGS
Diethylcarbamazine citrate
(DEC, HETRAZAN, BANOCIDE, NOTEZINE)
DEC :
Is a Microfilaricidal agent also capable of Killing a
Proportion of the Adult Wuchereria bancrofti,
Brugia malayi, and Brugia timori
INVERMECTIN (MECTIZAN)
Is a Potent Microfiraricide but has no Microfilaricidal
effect
Blood Trematoda
(Schistosoma sp.)
There are four species of schistosome which
are infective to humans:
Those egg will hatch and release free-swimming larva called Miracidia
Inside the snail they will undergo asexual reproduction, and will become
sporocysts
After penetration, they will loose their tail and become Schistosomule
Egg will penetrate the tissue and are passed with the faeces
S. mansoni
Clonorchis sinensis
Dicrocoelium dendriticum
Opistorchis felineus
Opistorchis viverini
Fasciola hepatica
Clonorchis sinensis
Epidemiologiy
- China, Japan, Korea, Taiwan, Vietnam
Habitat
- Biliary tract, pancreatic tract
Host
- definitive : human, cat, dog
- vector 1 :
Water snail genus of Bulimus, Thiara, or species
Melanoides tuberculatus
- Vector 2 :
Fish family of
Cyprinidae, Salmonidae,
Gobiidae, Anabantidae
Morphology
- Elongated, flat,
transparent, bulging
on posterior
- Oval egg, thickened
on posterior, found
within faeces
LIFE CYCLE
Swallowed by vector1
EGGS within MIRACIDIUM
(water snail)
faeces (cilliated larvae)
SPOROCYST
Mating EGGS
REDIA
Grow mature in
biliary tract
CERCARIA
Crossing fish (vector2)
Swallowed by skin
METACERCARIA
definitive host forming METACERCARIA
(cyst) in fish skin/muscle
Diagnosis
- Eggs within faeces
- Immunology diagnosis
Prevention
- Avoid eating raw fish must be completely cooked
Dicrocoelium dendriticum
Epidemiology
- Cosmopolite for lamb & other herbivores in Asia, Africa,
Europe & America
Morphology
- Mature form: flat, slender
- Eggs: dark brown, thick wall, contain completely-grown
mirasidium
Host
- Definitive: lamb
- Vector 1: snail genus of Abida, Zebrina
- Vector 2: ant, species Formica fusca
Life Cycle : comparable to C. sinensis
Fasciola hepatica
Epidemiology
Is the first trematode
found
Causes fasciolatic
hepatic
Is cosmopolite mainly
in country with large
farm (mostly sheep),
infection in human
often happens in
Cuba, France, England,
and Aljazair.
Habitat and host
Big size, 30 x 13 mm
Integuments is scaly
Posterior end without thorn
Unique shape, like shoulder because it has
kerucut kepala
Batil isap kepala (1 mm) and stomach are
almost same in size and adjacent
Caecum is hyper branching until posterior
end
Hyper branching testis is lied between 2/4
posterior body, one is behind the other
Ovary branches, anterior to testis and smaller
Uterus is short, curved, located between
ootype and porus genital.
Egg is 130-150 x 63-90 in size and has
operculum. Immature eggs are lied in billiary
duct and exit with feces.
Life cycle
Hepatic tissues are infiltrated
Eggs are expelled within feces with eggs, immature eggs
are lied in billiary duct
Miracidia enter
intermediate host I and develop Penetrate intestinal wall,
to become sporocysts, rediae I, Enter peritoneal cavity
rediae II in 3 weeks , and cercariae
At night, in 8 hours,
become metacercariae Metacercariae penetrate
definitive hosts
Clinical Symptom
Until metacercaria penetrate Glissons capsule, these
is no complain. But trauma and necrotic lesion rise
during migration through hepatic tissues.
In heavy infection, epithelia is scraped and young
worm will return to hepatic parenchyma, form
abscess pouch, and hepatic tissues are infiltrated
with eggs.
When larvae migrates to peritoneal cavity, focus
ectopic may happen in blood vessel, lungs,
subcutaneous tissue, brain ventricles, and eyes
where abscess will be formed.
Symptoms : colic, ikterus obstructiva, cough and
vomiting, abdomen rigidity, acute epigastria pain,
leukocytosist and eosinophily until above 60%
Diagnosis
Paragonimus westermani
Disease : Paragonimiasis ,
Pulmonary distomiasis
Paragonimus westermani
Epidemiology
It is cosmopolite in
human, mainly east in
Japan, Philippine, Korea,
China, Muangthai,
Taiwan, Africa, etc.
In Indonesia, it is
autochthon infection in
animal. In human, as
import case.
Host
In intermediate hosts I,
MIRASIDIA become REDIAE I, In duodenum, encystations happens,
REDIAE II, and finally CERCARIAE penetrate intestinal wall (in 30-60 minutes)
PREVENTION
Treating patients
Cooking crab before being eaten