Origin of a Parasite

Evolution of the Parasite

(Free living organism that evolved to being a parasite)

1.) Mechanism of entry {infection and reinfection}

2.) Mechanism of protection from Host’s defenses
3.) Increased reproductive capacity
4.) Streamlining {loss of non-essential structures and functions}

Parasites cannot evolve in an environment devoid of higher life forms that are potential hosts.

The survival of the parasite (lower form) is dependent on the survival of suitable hosts (higher form).

Problems with an Evolutionary Explanation

Because simple free living life forms (bacteria, protozoa, algae, etc.) are generally harder than higher life forms (mollusks,
arthropods, birds, mammals), a parasitic life is less advantageous compared to a free- living, commensal or mutualistic
existence.

In natural selection, adaptation, mutations are positively selected only when it provides an advantage in the given
environment/setting.

An organism that has acquired a mechanism of entry to a host while unable to ward off the host’s defenses will perish
taking with it the evolved gene.

Possible Origin of the Parasite (Creationist perspective)

Parasite evolved after the fall of man, sin causes deterioration of creation and parasite is a product of this.

May have been mutualistic organisms in the original creation.

Deterioration in the gene line may have caused altered behaviors that injure the host.

What happens when free living organisms accidentally go in a human body?

-Free living agent dies due to lack of ability to survive.

-Human dies due to disease.

Nematodes – round worm
Characteristics:
Non-segmented worms/helminths
-Cylindrical
-Tapered at both ends
-Complete digestive tract (Buccal cavity—> Esophagus—> Gut—> Anal opening)
-Separate Sexes
-Females are usually larger (provide increase reproductive capacity)
-Males are usually curved at the posterior and have special copulatory organs (Copulatory spicule to hold on to female
during copulation)

Intestinal Nematodes

1. Ascaris Lumbricoides (Giant Intestinal Round Worm)

-Most common intestinal nematode in the world

-Soil transmitted (soil is the essential transmitter)
Eggs will hatch in the intestines of the host after ingested. The penetrate the intestinal wall and enter the
bloodstream. Undergo heart-lung migration.
*Intestines to the blood vessels and to the Pulmonary capillaries to alveolar sacs to upper respiratory tract
through mucus and then swallowed again before they become adults in the intestines.

Un-embryonated eggs are non-infectious

Females produce Ova and passed to the feces, eggs are unfertilized in the stool meaning no males in the
intestines.

Morphology
Adult:
-male: 10-31 cm
-female: 22-35 cm
Ova:
Unfertilized egg: longer, larger (bile stained)
Fertilized: Round, shorter
Mammillary coat/layer (outermost part of the egg)
Thick shell underneath mammillary coat and then underneath that there is a finely granular embryo.

When egg loses mammillary coat then it is called a decorticated egg/ova

Clinical Manifestations
-Allergic reactions to larval migration
-Pneumonitis
ADULT WORM:
-Abdominal Pain
-Lactose intolerance
-Bowel obstruction
Erratic migration of adults may have serious effects
-Often regurgitated or passed out through the nostrils or other body openings
-biliary obstruction
-appendicitis
-pancreatitis

Diagnosis
-detection of eggs in stool

Infective Stage: Embryonated Ova

Mode of Infection: Ingestion
Adult Habitat: Small intestines
Diagnostic Stage: Ova in stool

2. Ascaris Suum
-Parasite of pigs
-Some studies suggest that it may be the same species as Ascaris lumbricoides but there remains no consensus among
taxonomists.
- morphologically the same with Ascarislumbricoides
3. Trichuris trichiura
- aka Whipworm
-Soil transmitted
-Frequently observed with Ascaris
-no heart-lung migration
Morphology
Adult: -Male posterior 2/5 of worms is thicker than anterior 3/5

-Posterior end of male is coiled with greater than 360 degrees

-Smaller than Ascaris lumbricoides

Ova: -Football shaped/ Barrel shaped with bipolar mucus plugs

Bile stained, with thinner smooth shell compared to Ascaris.

*Most easily identifiable eggs in the stool sample*

Clinical manifestations: adults attached by penetrating to the intestinal wall.

RESULTS: - Petechial hemorrhages in the intestines (increased risk of amebic dysentery)

-Enterorrhagia

-Blood-streaked stools (due to small hemorrhages)

-Diarrhea (may be present or absent)

-Dysentery

-Rectal Prolapse (chronic and heavy infections of Trichuris trichiuria in the wall of the rectum will lead to
weakening the sphincter muscles of rectum and these sphincters help keep the rectum in place so in result to this
the rectum comes out of the anal opening.)

-Anemia (due to chronic infections, loss of plasma & blood)

Diagnosis: Demonstration of ova in stool (similar to ascaris)

Infective stage: Embryonated ova
Mode of infection: Ingestion
Adult Habitat: Large Intestine
Diagnostic stage: Ova in stool
4. Hookworms
5 species
-Necator americanus (most common in man)
-Ancylostoma duodenale (most common in man)
-Ancylostoma ceylanicum*(more common in animals, occasionally causes intestinal infections in humans)
-Ancylostoma braziliense (more common in animals, Extra intestinal infections, humans can get infected but not the
intestinal form of the infection)
-Ancylostoma caninum (more common in animals, Extra intestinal infections, humans can get infected but not the
intestinal form of the infection)

*Curvature at the anterior end (hook-like shape) true for Necator Americanus but with the Ancylostoma species.

-Soil transmitted
-Blood sucking nematodes

Life cycle
-normally found in the intestines of the host.
-eggs are passed thru feces, are non-infectious
-in soil, eggs are developed,
- Rhabditiform larva is a free-living stage feeds organic materials later will malt and form filariform larva (parasitic
stage) but this does not eat, it just finds suitable host and lives as a parasite.

Filariform Larva: Could infect in two methods

-Skin penetration (Necator americanus & Ancylostoma)
-Ingestion (Ancylostoma)

Skin penetration route (similar to Ascaris lumbricoides)

Skin —-> blood stream—-> heart lung migration “necessary step” —> URT—> swallowed—> small intestine
(Adult/maturation)

Ingestion (similar to Ascaris lumbricoides)

Small intestine —-> Blood steam—- Heart lung migration “necessary step”—> URT—> Swallowed—> Small intestine
(adult/maturation)

Necator Americanus
-infects only through skin penetration

Ancylostoma duodenale
-Skin penetration, ingestion, transmammary, and probably transplacental
Morphology
Adult:
Male: posterior structure known as copulatory bursa (fan like with ribs)
Female:

Necator americanus buccal opening (semi lunar cutting disks used by adults to attach themselves to walls of intestines=
bleeding) {Right}
Ancylostoma duodenale (2 pairs of ventral teeth)
Ancylostoma caninum (3 pairs of ventral teeth)

ANCYLOSTOMA NECATOR AMERICANUS

DUODENALE

Ova:
Ovoid/ egg shape
Thin membrane (thinner than ascaris and trichuris)
Inside is the Embryo 2-8 cell stage of cell division

Rhabditiform larvae
-can be found on stool sample especially patients who are constipated. (To find Rhabditiform larva in stool is Rare but
possible)
-Specimen not processed immediately

Now, when the Rhabditiform larva worms are described, it is usually in comparison to another nematode, which is the red
worm or genus Strongyloides.

Buccal cavity is longer than genus Strongyloides.

It has an inconspicuous (not visible) or a small, genital primordium.

Genital primordium is actually the primitive or the embryonic form of the reproductive organs of the hookworm.
Filariform larvae

- Rarely seen in clinical samples actually for hookworms, almost impossible

to find Filariform larva in stool samples.
- There is a way in the laboratory to culture it.
- One way to differentiate filariform with the Rhabditiform is that it is longer
and more slender.
- There is an outer cuticle covering the larva that seals shut the buccal cavity
of the worm.
- Does not feed(find host and infect only) and relies on the energy it has stored from the rhabditiform stage.

Clinical Manifestations
-Ground itch/dew itch (found on feet due to contact w/ soil or any part that touched soil.)
-Bronchitis or Pneumonitis (due to larva migration)

Chronic and heavy infections due to many adults in intestines:

-Abdominal pain, steatorrhea (passing of stools with large amount of fats, light color and it floats)
-Diarrhea w/ blood and mucus
-Eosinophilia (increase Eosinophils in the blood samples)
Prolonged Infections:
-Iron deficiency anemia (due to blood loss, RBCs smaller than normal)
-Hypoalbuminemia (loss of protein due to hemorrhaging in the intestines)
-Cutaneous larva migrants/creeping eruptions
a condition where filaria form larva penetrates the skin but is unable to find the bloodstream and therefore unable
to proceed to the heart lung migration.
Occurs in an infection by the Three zoonotic hookworm species: Ancylostoma ceylanicum, Ancylostoma
braziliense, Ancylostoma caninum}

Diagnosis:
-Demonstration of ova in stool

Review:
Infective stage: Filariform larva
Mode of infection: Skin penetration/Ingestion (could also be transplacental, transmammary)
Adult habitat: Small intestines
Diagnostic stage: Ova in stool.
5. Strongyloides stercoralis “Threadworm”
-Taxonomically Closely related to hookworms
-Facultative parasite/zoonotic
-found in the small intestines similar to hookworms
-theorized as no males but females due to no report of identification if male from clinical samples.

Life Cycle

It is believed that females can actually produce ova without the male, this is for the parasitic life cycle.
Parasitic adults of Strongyloides stercoralis are females, can produce ova thru parthenogenesis.
Parthenogenesis is the production of offspring without the participation of the male.

Now occasionally, eggs may also be passed with the stool like that of hookworms, but the most common is that the eggs
hatch while it is still inside the intestines. It is the Rhabditiform larva that is most commonly found in the stool samples.

Rhabditiform larva whether it is in the parasitic life cycle or in the free living life cycle, it is in fact a free living larval
stage. If it is passed with the stool and then reaches a suitable environment such as soil, it will eventually transform into a
filariform larva, that is if it will proceed to a parasitic existence.

Similar with hookworms that it can penetrate the skin and be ingested —-> heart-lung migration—-> adults in small
intestines.

Primary difference:
-eggs not passed through stool because it is often already the Rhabditiform Because eggs develop faster. Eggs deposited
into mucosa of intestine not just lumen.
-Rhabditiform larva stays inside intestine and then transforms into a filariform larva.
-ALTERNATIVE LICE CYLE A. Rhabditiform larva will not leave the intestines at all. And This usually happens if the
patient is also constipated or does not have irregular bowel movement, so the Rhabditiform larva becomes a filariform
while still inside the intestines. Either it gets passed to the stool eventually, or it can penetrate the intestinal wall, reach the
bloodstream, undergo the heart lung migration, and eventually becomes an adult back in the intestines. =Auto infection or
“Internal auto infection.”
-B. Rhabditiform larva passed through stool and reaches soil. here in the soil, there is actually a potential for Rhabditiform
larva to proceed to a free-living life cycle. Instead of becoming a filariform larva, it will develop into a female or male
free-living organism and eventually release OVA that will be Rhabditiform.
-C. From this free-living life cycle, occasionally, we can also have a Rhabditiform that will become a filariform, therefore,
signaling the beginning of a parasitic life cycle (FILARIFORM IS ALWAYS PARASITIC!! NO HOST=DEATH)

Morphology
-Adult (not usually found in clinical samples especially male because they’re free-living agents)

Rhabditiform

-Buccal cavity is shorter than hookworm

-Esophageal muscle very close to oral opening
-Has conspicuous or large genital primordium. (Definitive ID)

Filariform
-Slender, longer
-Filariform of Strongyloides stercoralis demonstrates a notched tail. “Split at posterior end of tail” (Unique to this species)

Ova:
-Same shape with hookworm egg but embryo is much advance with fully formed larva.

Clinical Manifestations
-Pruritic skin papules (itchy)
-Larva currens (serpentine lesions)
-Lobar pneumonia
-Alternating diarrhea and constipation
-Cochin China diarrhea (watery and bloody intermittent diarrhea)
-Dissemination in immunosuppressed patient. (Two reasons: Immunocompromised, reinfected from internal source
“Internal auto infection” =hyper infection)

Diagnosis:
-Demonstration of larvae in stools (Most common: Rhabditiform larva)
-Harada-Mori, Baermann funnel (culture techniques, increase sensitivity of test)
-duodenal sampling
-Larvae may be found in sputum and urine (CSF or other bodily fluids) in disseminated infection in the body.

Review:
Infective stage: Filariform larva
Mode infection: Skin penetration/ Autoinfection (ingestion)
Adult habitat: small intestines
Diagnostic stage: Rhabditiform larvae in stool (sometimes Filariform larva or Ova)

****Filariform larva in stool sample means that internal auto infection has already occurred. Because if you have filaria
form larva in the intestines, it is actually already very easy for that filiform larva to penetrate the wall of the intestines and
then undergo the heart lung migration, and eventually become new adults in the intestines. ****

OTHER STRONGYLOIDES SPECIES

Stongyloides fulleborni
-Parasite of monkeys occasionally found in humans
-Eggs are passed in stool
-Larvae has been found in breast milk

S.myopotami and S. Procyonis

-infects nutria (like huge rats) and raccoons
- “Swamp itch”