Intermediate Host

 Transport host

an organism that carries a parasite to another host.  The parasite undergoes no development in the transport host.

 Direct Life Cycle

no intermediate host

 Indirect Life Cycle

has an intermediate host

 Infective Stage

stage which can infect a given host; usually only one stage is infective to a given host

 Pathogenic Stage

stage causing disease, i.e. stage where multiplication of mucoorganisms occur in body

 Prepatent Period

period between the entry of an infective stage into the definitive host and the time at which a subsequent stage of the parasite within the host can be demonstrated

 Commensualism

denote two organisms which live together neither bearing a parasitic relation to the other, without harm or prejudice to either but with one or both members deriving benefit

 Mutualism or Symbiosis

mutually advantageous association of two or more organisms

 Ectoparasite

parasite that lives on the body surface of its host

 Endoparasite

parasite that lives within the body of its host.  Multiplication of bacteria of the "normal" flora of the intestinal tract is not viewed as endoparasitism

Infection

Infestation

endoparasitism

ectoparasitism

 Auto Infection

an infection in which the source of re-exposure for a host is the host itself

Incidental parasite

one that becomes established in an organism in which is does not ordinarily live

 Hypobiosis

= Arrested Development

larvae of the parasite remain dormant in the host,

 i.e. do not undergo any further development during this time

 Pathogenesis

development of any disease process

 Zoonosis

an infection or infestation shared in nature by man and lower animals

 Vectors

a substance that transports an infectious agent from infected individual or its master to a susceptible individual or its food and immediate surroundings.  An organism may or may not pass through any developmental stage within the vector

Biological vector:  some development occurs within the vector

Mechanical vector:  no development occurs; just a transport host

 Sample collection and handling -

skin scraping and time/salt solution

 Fresh as possible; representable of animal

skin scraping - need microscopic slide, slide cover, oil, scapel/blade;  create irritation to access dermis;  should see RBCs;  get from multiple sites on animal

Salt solution - floatation medium;  have to look at specimen within specific time frame as salt will break up ova

pseudoparasite

incidental parasite

spurious parasite

false; not a parasite

ex carpet wool,plant fibers

is a parasite that can grow/establish in an abnormal host

ex heartworm in people

is a parasite in an abnormal host but does not grow/establish

ex horse parasite (strongylide) egg in dog feces

 parasitism

does not necessarily meant the host will be harmed.  If a parasite has damaged the host, it has failed the law of parasitism.  It is not to the advantage of the parasite to kill the host.

 Clinical Signs of parasitism

pain - abdominal due to GIT spasms

weight loss - parasite competes for nutrients with host

lethargy, weak

diarrhea to constipation

rough hair coat to alopecia to skin lesions in extreme case

puritis (itching)

anemia

change in stool

head shaking - ear mites

peripheral eosinophilia (increase in eosinophils)

tick paralysis - toxin release

scooting, changes in behavior

jaundice/icteric

birth defects/abortion/sterility

eye problems

respiratory difficulties (coughing)

increase in primary and secondary infections

stunted growth

decrease in milk production

most drastic - Death

 Immunity to parasitic infections by host

1.  body resistance to infection

2.  inhibition of development

3.  inhibition of egg production

4.  self-cure mechanism - self limiting course possible due to histamine release or immuoglobins

 Failure of immunity of the host

1.  stress - pregnancy, parturition, lactation (ie old dogs)

2.  some parasites will coat themselves with host material

so host will not recognize them as foreign

3.  antigenic variation

4.  hypobiosis

 Nematodes

basically roundworm; cylindrical elongated with tapering ends

tough outer coating called the cuticle which functions as protection/body armor; has to be shed/molt to grow

Rhabditiform Esophagus - hourglass, non parasitic

Filariform Esopagus - club shape, parasitic

 nematodes (continued)

males usually smaller with cuticular expansion on caudal end called a copulatory bursa (grasps and holds the female)

female may be

OVIPAROUS - eggs hatch outside female

OVOVIVIPAROUS - eggs hatch inside the body of the parent

VIVIPAROUS - give birth to live young

For embryonation to occur outside need: warmth, oxygen, moisture

NOT sunshine

 Exsheathment

parasite take off the protective coating (usually during L3)and occurs in different parts of the hosts's body; requires stimuli from host's GIT to occur properly (pH, CO2, salts, temperature)

egg > hatch > L1, L2 (remain in feces and feed on fecal microflora) 

> L3 (infective stage)

if immune response by host coincides with exsheathment - no infection but parasite can go into hypobiosis

Genus Strongyloides (threadworms)

Papillosus - ruminants

Westeri - horse

Stercoralis - dog, cat, people

Ransomi - pig

Parthenogenic reproduction

non sexual, no males; females lay embryonated eggs;

this is a survival mechanism for the parasite

homogenic - direct life cycle

heterogonic - indirect life cycle

Routes of infection

percutaneous - major route "Tracheal Migration"

(capillaries > veins > lungs, cough/swallow > GIT)

parthenogenic female results; fecal oral only

Transmammary or transcolostral routes

Hyperinfection - S Stercoralis - only in people

Autoinfection - S Stercoralis - only in people

Clinical signs of Strongyloides

dermal or invasive phase

dermatitis, puritis, hyperemia; foot rot;

creeping eruptions - cutaneuous larvae migrans (CLM)

Pulmonary or migratory phase

Ruminat parasite (cow, sheep, goat)

egg typical - smooth surface, ellipsoidal and generally has an embryo in the morula stage

L1 and L2 are free living and eat fecal flora

L3 INFECTIVE occures in protective sheath

L4 occures in intestinal mucosa

Adults occur in teh intestinal lumen

Premunition

the presence of a stable population of adults in the GIT tends to inhibit further infections and further maturation of the larvae

this is a survival mechanism for the parasite, not the host

Spring Rise / Post Parturient Phenomenon

Diagnosis

find eggs in feces; most look alike

culture feces to L3

Necropsy

Name the GI roundworms

CCOOTH

C ooperia

C habertia

O stertagia

O esophagostomum

T richostrongylus

H aemonchus

Superfamily: Trichostrongyloidea

Genus: Ostertagia

host: cattle

habitat: abomasum (true stomach)

CS:  blood suckers

diarrhea, weakness, anorexia, occasional anemia and edema

because of the ability to undergo hypobiosis, there are 2 types

Type I or summer: parasites active, use anthelmintics

Type II or winter: larvae undergo hypobiosis, anthelmintics not effective

Superfamily:  Trichostrongyloidea

Genus: Trichostrongylus

host:  ruminant and horse

black scours: extensive inflammation of the mucosa of the abomasums (upper GI and small intestine) giving it a raised effect and black, smelly diarrhea (digested blood)

Superfamily: Trichostrongyloidea

Genus: Haemonchus contortus (barber pole worm)

host:  ruminants

worm is red, buccal cavity has very small dorsal lancet.  Females have barber pole effect (white egg filled uterus twisted with helix)

Direct life cycle

CS:  Severe anemia

blood loss from adult and larvae

weak, pale, poor doers, loss of appetite (decreased raw materials)

loss of albumin (plasma protein responsible for colloid oncotic pressure COP); this keeps fluid where it is supposed to be

edema - Bottle jaw: fluid accumulation in the throat latch (angle of the mandible)

Superfamily:  Trichostrongyloidea

Genus: Oesophagostomum

Species:  Columbianum

nodular worm in sheep

has Alae (cuticular fin or wing like flange that occurs at the neck of the tail; this is a diagnostic feature used for identification

on reinfection, body is sensitized; will see local inflammatory reaction where larvae have entered the mucosa

two areas of malfunction

1.  malabsorption

2.  blackage and interferes with movement and digestion

economic loses:

lost wool and meat; cannot use intestines as casing for sausage

Superfamily: Trichostrongyloidea

Genus: Oesophagostomum dentatum

hosts: pigs

Tx:  broad spectrum anthelmintics used on all GI roundworms; withholding time

Superfamily: Trichostrongyloidea

Genus: Chabertia

Species:  Ovina

hosts:  ruminants, young sheep

Ovina = the large mouth bowel worm

use pre oral digestion

Superfamily:  Strongyloidea

host:  equine

typical strongyle - smooth, ellipsoidal, elongated and embryonated (segmented), thin shelled

Large stronglyles: only 3

small strongyles: hundreds

Superfamily:  Stronglyloidea

Large stronglyes

roundworms, pathogenic; blood suckers

1.  Strongylus vulgaris:  smallest; 2 dorsal teeth

*** smallest and most pathogenic***

2.  Strongylus edentatus:  longer with 2 subventral teeth

3.  Strongylus equinus:  no teeth

Superfamily:  Strongyloidea

Small strongyles

subfamily: Cyanthostominae

problem with encysted larvae.  Anthelmintic therapy is not very useful.  This is the reason for 3 month therapy.

Triodontophorus 

Trichonema

Pathophysiology of vulgaris and thrombo embolic colic

Endoarteritis - damage to vessel interior by larvae

Clots called thrombosis form (thrombus singular, thrombi plural)

Two options:

1.  Thrombus completely occludes artery and an aneurysm develops and eventually ruptures

2.  Thrombus breaks off into pieces (embolus singular, emboli plural).  These small pieces will lodge in the small vessels, most commonly the large intestine and possibly rear legs;  the interrupted blood supply will lead to colic called thrombo embolic colic

Superfamily: Strongyloidea

Family: Stephanurida

Stephanurus dentatus

Stephanurus dentatus - kidney worm

direct life cycle

Eggs:  typical strongyle shaped and pass in urine 9-16 months after infection.  Can persist for 3 years

Animals under 2 years of age will nto show signs due to the long prepatant period

Cull gilts (female pigs that have not had a litter) over 2 years of age. 

Tx:  borad spectrum anthelminitic

Family:  Syngamidae

Genus: Syngamus trachea

the "Y" worm or "Gape" worm

Host:  poultry

Habitat:  trachea

Eggs are flat and have an operculum; capable of hatching to L3 in or out of egg

Eggs in feces

Once eggs ingested > heart, lungs, trachea where they copulate

Pre Patent Period 7 days

Superfamily:  Ancylostomatoidae

Family Ancylostomatidae - have teeth

Subfamily: Ancyclostominae - have teeth

Subfamily: Bunostominae - have cutting plates

The anterior end of the worm is hooked,

therefore "Hookworm"

The severity of infection depends on:

1.  magnitude of challenge

2.  degree of exposure to parasite

ZOONOTIC

Human cutaneous larval migrans

"Creeping eruptions" - linear, tortuous, erythematous, intensily puritic eruption of skin - larvae under skin migrating = CLM

Genus:  Ancylostoma

Species:  Caninum

Ancylostoma caninum

** know every detail of this parasite

Common name is Hookworm

Host is dog

Habitat is small intestine (causes CS - bleeding)

[large intestine - mucus]

Routes of infection

1.  Ingestion:  fecal oral

2.  In utero:  rare <2%.  Larvae remain dormant in bitch until she becomes pregnant then larvae cross the placenta

3.  Skin penetration thru circulatory system to respiratory system

4.  Transmammary:  this occurs because the arrested larvea are reactivated

5.  Arrested larvae are reactivated during the last 2 weeks of pregnancy

Severe anemia

Somatic migration - larvae migrating through muscle - little to no damage

GI mucosal trauma, anorexia, diarrhea, malabsorption, clubbed villi (reduced surface area)

Clinical forms:

1.  Peracute infection:  puppy 2nd week of life usually die from severe anemia;  see not eggs in stool as takes 15 days to see in stool

Eggs shed in feces 2 weeks after ingestion

Eggs shed in feces 1 mo after skin penetration

2.  Acute-severe anemia:  +- eggs in stool of 4-8 week old puppy

3.  Chronic:  always see eggs in stool.  Animal clinically healthy "compensated infection" RARE but possible

MUST TX EACH FORM DIFFERENTLY

Peracute - transfusion; supportive care until stable then anthelmintics

Acute:  may or may not transfuse; supportive treatment; anthelmintic

Chronic:  give anthelmintic / Heartguard+

(preventative, not tx; only works on low #) 

Milbemycin

Secondary - non compensated:  treat primary cause;

supportive care; diet changes; iron and B vitamins; worm when able to handle worming

The eggs will remain in the dirt and are infective for long periods of time,

so use concrete runs and clean with Clorox

Anthelmintics:

Periodic Drontal or Drontal+

Family:  Metastrongyloidea

Genus:  Parelaphostrongylus

Host:  white tailed deer

Pathology:  natural parasite in deer;

fatal in sheep and goats sharing pasture

Family:  Crenosomatidae

Genus:  Aelurostrongylus abstrusus

Host: cat

Habitat:  lung parenchyma (tissue)

shows improvement with antibiotics, but that is only treating secondary infection;  becomes ill again when antibiotics stopped

Family:  Filaroididae

Species: osleri, milkshi, hirthi

hosts:  mammals and ruminants

Does not require development outside of the host;  this is proven for osleri and hirthi but not milksi

Is directly infective as L1 and all 5 stages occur in the lung tissue of the dog

Unique among parasites of the domestic animals because it does not require a period of development outside the definitive host of within an intermediate host before it is infective

Can find larval stage in sputum

The drug of choice is albendazole

Superfamily:  Trichostrongyloides

Genus:  Dictyocaulus

Species:  viviparous, filaria, ainfieldi

Viviparous - cattle; the only nematode that reaches maturity in the lungs of cattle

Filaria - sheep and goats; will see coughing and a mucoid nasal dischage

Ainfiledi - horses, mules and donkeys

Verminous bronchitis:  a bronchitis that gets progressively worse even though there are not larvae in feces

Tx:  Levamisol

broad spectrum for ruminants

Order:  Oxyurida

Genus:  Oxyuris

Species:  equi

pinworm or rectal worm in the horse

Have a very long, fine pointed tail (how they get the name pinworm)

The eggs are ellipsoidal and somewhat flattened on one side with a operculum and a veriform embryo inside

*** the egg is the pathogenic stage, not the adults

eggs cement in masses on the perianal hairs and on the skin of the anus

The primary pathology is puritis caused by the eggs: severe itching of the anus and tail region

DX:  do perianal scraping for eggs but do not do a fecal sampling as the eggs will be lost in the feces

or scotch tape agains the anal region then place on a slide

Tx:  Piperazine against adults

Thiabendazole against adults and larvae

Order:  Ascarida

Genus:  Heterakis gallinarium

also called Heterakis gallani

arrowhead worms because of large cervical alae

** L2 is the infective stage

Causes no pathology

blackhead in poultry