Super Family

TRICHOSTRONGYLOIDEA
• Trichostrongyloid nematodes are common and
pathogenic in grazing ruminants
• The abomasum and the small intestine are the usual
locations in ruminants
• Trichostrongylus infection are often asymptomatic
• In large numbers (10000 – 100000) are capable of
producing protracted and debilitating watery diarrhea
,especially in stressed or malnourished sheep, cattle and
goats
At first, the feces remain semisolid, but soon they
become watery and dark green in color (“black
scours”), staining the fleece of the hindquarters

Protracted diarrhea is sufficient to account for the

weakness and emaciation typically observed in
Trichostrongylosis
 Normal intestine Damage intestine

Cause iritation, erosion intestines and damage to

capillary vessel and ductus lymph node. Lead to
hypersensitivity at intestine, enteritis at intestine
Pre-parasitic Stages • Egg develop to larvae L3 at
optimal temperature & humidity
(22-26oC and 100% RH) : 7 days

 L1 and L2 live within soil and feces

via engulf bacteria.

 Infective larva (L3) have double

layer cuticle as protection (leftover
L2 cuticle)

 Unable to eat

 Food reservation stored in

intestine cell that
conserved during L1 dan L2
 Haemonchus contortus
The pathogenic effects of H.contortus ----- the inability of the
host to compensate for blood loss
may remove one fifth of the circulating erythrocyte
volume per day ( lambs)

The cardinal sign of haemonchosis :

Pallor of the skin and mucous membrane
A hematocrit reading of less than 15% : anemia,
weakness, shortness of breath

Loss of plasma protein results in submaxillary edema (bottle

jaw)

Feces are well formed, diarrhea occurring only in infection

complicated with Trichostrongylus and Cooperia
Life cycle of a
strongylid nematode,
H.contortus
• Shape like thread; small size
(0.5 - 3 cm)
• Very small buccal capsule
• Copulatrix bursal well
developed
• Direct life cycle – without
migrate tissue
 L3 transmission from feces to
surrounding plants/environment
 Rain water
 Wind
 Other creatures:
Man (boot)
Fungal – Pilobolus
Invertebrate – Fly,
Bug, worm
Parasitic Stage  Infective larva (L3) within
host body released outer
cuticle layer
(Moulting/Exsheathment)
 Changes of condition
environment inside organ
(rate of dissolved CO2 ) 
Activation neurosecretory
cell  Trigger L3 molting
Type of Worm Habitat Moulting
location
Molting side :
Haemonchus Abomasum Rumen
Specific species –at
contortus
Mecistocirrus digitatus proximal organ -
Ostertagia spp Adult worm habitat
Trichostrongylus axei
Cooperia spp Small Abomasum
Trichostrongylus spp intestines
Strongylus spp Colon, Small
caecum intestines
After L3 moulting worm move toward it’s habitat and
developed to adult worm (L3L4 Adult)

Hipobiosis / Arrested larval development :

larva Stagnant temporary of parasite development at
larva stage

 Effort of parasite to survive in unfavorable

condition:
- Winter season or long drought
 Host respond immune
 Super Famili
STRONGYLOIDEA
 Corona
radiata

Gigi Buccal
capsul

Oesophagus


Super Famili
STRONGYLOIDEA

Famili Famili Famili

SYNGAMIDAE STRONGYLIDAE CHABERTIIDAE

Stephanurus Chabertia
Syngamus Oesophagostomum

Sub Famili Sub Famili

STRONGYLINAE CYATHOSTOMINAE
(Strongylus besar) (Strongylus kecil)

Strongylus Cyathostomum
Cylicostephanus
Triodontophorus Cylicocyclus
Cylicodontophorus
Poteriostomum
Gyalocephalus
Genus : Strongylus
 Important parasite in horse

• Habitat : Colon and caecum

Contain buccal capsule

which well developed
 Used to gnaw mucosal / eat
vili intestine

 Few species have teeth

 S. vulgaris S. edentatus S. equinus
Colic symptom and
Blood flow from the
Colic arteri
• Life cycle pre-parasitic stages
similar with Trichostrongyloidea
Spesies Size Charactertis Prepaten Life cycle
tics period
S. vulgaris 1.5-2.5 cm Have 2 6-7 L3  Submucosal intestine (L4)
teeths months  Arteriole intestine  Artery
shaped like mesenterica cranialis  L5  Seccal
ear & colon wall  Form nodule  Adult
worm
S. 2.5-4.5 cm Without 10 - 12 L3  Submucosal intestine
edentatus teeth months  System portal  Liver (L4) 
Peritoneum  seccal & colon wall 
Form nodule purulen  Adult worm
S. equinus 2.5-5.0 cm Have 3 teeth 8-9 L3  seccal & colon wall  Nodule
shaped like months at Submucosal & serosa intestine
triangle (L4)  Peritoneum  Liver 
(2 bifid & 1 Pancreas (L5)  seccal & colon
single)

Larvae migration after L3

enter inside horse (host)
 Super Family

ANCYLOSTOMATOIDEA
 Family ANCYLOSTOMATIDAE
Hookworm
 Have mouth with buccal capsule
Teeth which well-developed

 Do not have crown yet ventral

part of mouth equip with tooth /
cutter pieces like horn
substances (chitin)

Buccal  End of anterior part

capsule usually curl toward
dorsal

 Commonly known as
blood sucker worm
 Famili
Ancylostomatidae

Sub Famili Sub Famili

Ancylostominae Necatorinae
Ancylostoma Necator, Bunostomum
Gaigeria, Globocephalus,
Agriostomum Uncinaria, Grammocephalus
Bathmostomum
Genus : Ancylostoma
 Blood sucker worm: Man,
canidae & felidae

 Habitat: small intestines

 Dispersion :
cosmopolitan (typical at
tropic & subtropic region)
•Dog, wolf, fox, wild carnivora
• Cosmopolitan
(typical at tropic & subtropic
region like North America,
Australia, Asia)

• Dog, cat, wolf, wild canidae,

sometimes man)
• Tropic & subtropic region
• Uncinaria spp.
• Dog, cat, fox at cold
climate

• Man at tropic region

• Have been reported at
dog and pig
LIFE CYCLE

Creeping
eruption
Adult hookworms live in the small intestine and shed eggs in feces and into the
environment, where they larvate, hatch, and develop into infective third-stage
larvae. This development occurs in approximately 2 to 9 days, depending on
temperature and humidity

Dogs and cats become infected with hookworms via ingestion of the third-stage
larvae from a contaminated environment, larval penetration of the skin, and/or
ingestion of other vertebrate hosts with infective larvae in their tissues. Dogs and
cats may also become infected by eating cockroaches that contain infective larvae

Transmammary transmission of larvae from the bitch to pups is an

important route of infection for A. caninum. In dogs more than 3 months of
age, some A. caninum will migrate through the lungs and enter somatic
tissue, where the larvae become dormant, or arrested. Arrested
development may also occur in the mucosa of the small intestine. These
arrested larvae are activated after removal of adult worms from the
intestine; activation also occurs during pregnancy, with the larvae
accumulating in the mammary glands and secreted in the milk.
 Unlike A. caninum, A. tubaeforme is not transmitted to nursing kittens
but is acquired only after birth through environmental contamination.
Migration of hookworms within the host is complex. After penetrating
the skin, larvae are carried by the bloodstream to the lungs where they
migrate up the respiratory tree to the trachea. Larvae are coughed up
and then swallowed, and then make their way to the small intestine,
where they mature, mate, and produce eggs. Eggs are first found in the
feces 2 to 3 weeks after infection.

Larvae that infect other animals (paratenic/transport hosts) do not

develop further in these hosts but become dormant
(hypobiosis/arrested development) in various host tissues. When a dog
or cat ingests these larvae in animal tissues, the larvae travel to the
small intestine, where they are released and mature into adult worms.
Immature and adult worms attach to the mucosa of the small intestine,
digest the tissue, inject anticoagulants, and suck blood. Worms may
detach and move to new sites and reattach. Small bleeding ulcers form
where the worms once fed.

A. caninum more pathogenic for dogs than A.braziliensis /

U.stenocephala
Hookworm are transmitted to humans by skin penetrating L3
larvae that develop in faecally contaminated soil

Adult worms attach themselves to gut villi and use teeth in their
buccal capsules to abrade the mucosal surface, then they feed on
blood---------- anemia is a prominent symptom in hookworm
disease
Three quite distinct types of hookworm disease
• Invading L3 larvae cause an allergic dermatitis with a
popular and sometimes vesicular rash that is termed
ground itch

• Lung pathology –focal haemorrhages and allergic

pneumonia

• The most important damage-------the blood-feeding adults.

Up to 200 ml of blood per day may be lost ------- by a
patient with a heavy infection
L3 larvae of non- human hookworm species can
penetrate human skin and cause “ cutaneous larval
migrans”, they move laterally in the skin. Such larvae
never develop to adult worm------- the infections are self-
limiting
Dirofilaria immitis (heartworm)

• Host : dog, cat, wolf and

fox
• Other infection- man,
horse, sealion and bear
• Habitat : right ventrikel
and A. pulmonary
• Size : 12-16 cm (male),
25-30 cm (female)
 • Dispersion at tropic,
subtropic and few
moderate climate region
• Intermediate host: Culex,
Aedes, Anopheles
mosquitoes

•Female - ovoviviparous
LIFE CYCLE
Microfilaria periodicity

Fluctuation number of microfilaria worm within

blood circulation in host at 24 hours period.

oNocturna periodic : Microfilaria found within perifer

vessel at night day.

oDiurna periodic: Microfilaria found within perifer

vessel at day.

oNon Periodic : Microfilaria found within perifer

vessel irregularly.
oMicrofilaria found within perifer vessel day or night:
§ Subperiodic nocturnal : Night >>
§ Subperiodic diurnal : Day >>
Theory regarding periodicity

• Habit to blood sucking from vector

•Changes from rate of O2 and CO2 in blood
•Dilatation blood capillary during rest time
•Released of microfilaria together in a period
•Circardia cycle from microfilaria