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D. Mode of Transmission
Infective stage needs to be transmitted to
humans to proceed with the life cycle Soil transmitted parasites developed further
in the soil before they become infective (e.g.
Diagnostic stage host/patient needs to be Ascaris, Trichuris, and hookworms)
separated or isolated to identify or diagnose a
parasitic pattern Snail transmitted parasites developed further
in the body of the snail (e.g. Schistosoma,
flukes)
Arthropods e.g. Malarial parasite, Filarial Common Symptoms of Parasites in Humans
worms, Trypanosomes, Leishmania
● Constipation
Food animal transmitted parasite e.g. ● Gas or bloating
Tapeworms (T. solium & T. saginata), ● Diarrhea
Paragonimus, Capillaria ● Pains or aches in the back, joints or
muscles
Contact transmitted parasite e.g. ● Irritable bowel syndrome
Trichomonas vaginalis, Enterobius vermicularis ● Allergies
Portal of Entry ● Increased appetite
● Itchy ears, nose or anus
● Oral ingestion of infective stage Intimate ● Nervousness or grumpiness
oral contact; most common ● Chronic fatigue, lethargy or apathy
● Skin ● Various skin problems
⎯ active larval penetration ● Tooth grinding or clenching
⎯ arthropod vector ● Anemia
● Vector has 2 life cycles (e.g. mosquito and ● Excess weight
human) ● Forgetfulness
● Vision problems
Sexual intimacy or Intercourse sexually ● Problems sleeping
transmitted disease (e.g. Trichomonas
vaginalis, Giardia lamblia)
Transplacental from a pregnant mother to Symbiology
the fetus (e.g. Toxoplasma gondii) ● Mutualism when these non-similar
Intranasal can be deposited in the nasal organisms benefit in the association called
cavities and reach the covering of the brain mutuals
(meninges) e.g. Naegleria, Acanthamoeba ● Commensalism an association when one
organism benefits and the other neither
Airborne inhalation e.g. Enterobius benefits nor is harmed
vermicularis ⎯ Commensal benefits
⎯ Host neither benefits nor is harmed
● Parasitism when one organism harms the
Specimen Examined other, or in some sense lives at the
1. Stool sample expense of the other without killing it
2. Urine immediately
3. Sputum ⎯ In order parasitism to take place, the
4. Blood parasite should exhibit an entry to the
5. Tissue biopsy host.
a. muscle biopsy
b. rectal biopsy Effect of the parasite on the host
6. Tissue aspirate ● most common mechanism is by
a. liver aspirate interference with the vital processes of the
b. duodenal aspirate host through the enzyme system
c. pulmonary aspirate ● invasion and destruction of host tissue
d. lymph node aspirate ● deprive the host of essential nutrients and
e. cerebrospinal fluid substance
f. hydrocele fluid
7. Orifice swab Effects of the Host on the Parasite
a. vaginal swab ● genetic make-up of the host may influence
b. perianal the interaction
● nutritional status of the host Immune
processes play an important role in
host-parasite relationships
Treatment
● Deworming use of antihelmenthic drugs in
Parasite modes of entry ingestion, arthropod
an individual or a public health program
bites, penetration of intact skin or mucous
● Cure rate refers to the number of
membranes
previously positive subjects found to be
egg-negative on examination of a stool or
urine sample using standard procedure
● Selective treatment involves Spread and tropisms
individual-level deworming with selection for ● Some parasites must migrate to certain
treatment based on a diagnosis of infection locations within the host in order to
complete their life cycle.
● Non-human parasites, in humans, often fail Mechanisms for evading the host response
to migrate properly and become “dead-end ● Antigenic variation trypanosomes
infections”. ● Intracellular infection plasmodia
● Parasites migrate to a predisposing ● Encystation amoebae, cestodes
location. ● Camouflage schistosomes
● Harboring a parasite not in the infective
stage will have no effect. Trematodes require a snail as the first
● Increase in eosinophils indicate intermediate host. e.g. Echinostoma
parasitism. ● Secondary IH can be snail, snail/snail,
fish/snail, crab/snail, or water vegetation.
Tissue damage and host response ● Only helminth that requires snail (fluke
● direct destruction of tissue worm)
● hypersensitivity reactions ● For all the IH, the last IH and larva
● eosinophilia manifests the infective stage. e.g.
metacercariae
⎯ occurs with helminths, not protozoa
⎯ results from tissue migration
Parasitic cycle
a. Filariform larvae in contaminated soil penetrate the human skin, and are transported to the
lungs where they penetrate the alveolar spaces; they are carried through the bronchial tree to
the pharynx, are swallowed and then reach the small intestine. In the small intestine they molt
twice and become adult female worms.
b. The females live threaded in the epithelium of the small intestine and by parthenogenesis
produce eggs, which yield rhabditiform larvae. The rhabditiform larvae can either be passed in
the stool, or can cause autoinfection.
c. In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate
either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external
autoinfection); in either case, the filariform larvae may follow the previously described route, being
carried successively to the lungs, the bronchial tree, the pharynx, and the small intestine where
they mature into adults; or they may disseminate widely in the body.
d. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in
Strongyloides stercoralis and Capillaria philippinensis infections. In the case of Strongyloides,
autoinfection may explain the possibility of persistent infections for many years in persons who
have not been in an endemic area and of hyperinfections in immunodepressed individuals.
Filarial Life Cycle (Wuchereria bancrofti)
1. The infected vector transmits the infective-stage larvae into the human host during a blood meal.
2. The L3-stage larvae mature into adult worms.
3. The parasites develop into adults and then produce microfilariae (MF), which migrate to the
lymphatics and blood for circulation.
4. The vector once again ingests the microfilariae during a blood meal on an infected host.
5. The microfilariae then migrate to the thoracic muscles of the vector through the midgut.
6. The microfilariae develop into the L1 stage and;
7. subsequently into the L3 larvae.
8. The L3 larvae migrate to the vector's proboscis via the hemocel. The infected vector transmits the
infective-stage larvae into the human host during blood meal [1].
Classification of Helminths ● All nematoda have sensory organs/anterior
chemoreceptors (cannot be used to
● Nematodes (roundworms) differentiate) but not all have posterior or
● Platyhelminthes (flatworms) caudal chemoreceptor.
● Trematodes (flukes)
⎯ anterior ends amphids, head/cephalic
● Cestodes (tapeworms) papillae, all nematodes are provided
⎯ posterior ends phasmids, tail/caudal
papillae, selective presence (e.g.
Helminthic diseases aphasmids have caudal chemoreceptor)
Intestinal ● Anterior buccal capsule may contain hooks,
teeth or cutting plates for attachment.
● Strongyloides (autoinfection cycle)
Invasive
● Trichinosis (muscle pain, uncooked
carnivores)
● Filaria (worms in lymphatics or under skin)
● Schistosomiasis (liver or urinary tract
granulomas and fibrosis)
● Cysticercosis (cysts in brain, seizures)
● Echinococcus (massive cysts in liver or
lung)
Transmission of Nematoda
● Ingestion of fully embryonated ova
● Ingestion of encysted larvae
Hookworms ● Larval skin penetration
Human ● Skin inoculation by vectors
Filariform Hookworm
● infective stage of hookworm
● capable of skin penetration
● MOT: skin penetration 2nd larval stage
● C[apillaria]. philippinensis
● A[scaris]. lumbricoides Intestinal Roundworms
● S[trongyloides]. stercoralis
● Hookworms Anterior
B. Large intestine ● presence of any: stichocytes, teeth, cutting
plates (attachment)
● E[nterobius]. vermicularis ● at least one free-living stage (except E.
● T[richuris]. trichiura vermicularis)
Extraintestinal Adults
● lymph glands Filarial ● blood suckers
● muscle Trichinella larvae ● extent of larval migration through tissues
● meninges Angiostrongylus
Ascaris Lumbricoides
II. Caudal Chemoreceptor
● CN - giant intestinal roundworm
A. Phasmid Phasmidia, Secernentea (with ● whitish or pinkish worms
caudal chemoreceptor) ● males (10 to 31 cm)
● A[scaris]. lumbricoides ⎯ curved posterior
● E[nterobius]. vermicularis ⎯ single, long tubule
● S[trongyloides]. stercoralis ● females (22 to 35 cm) paired reproductive
● Hookworms organs (posterior two thirds)
● smooth striated cuticles
B. Aphasmid Aphasmidia, Adenophorea ● terminal mouth - three lips and sensory
(without caudal chemoreceptor) papillae
● T[richuris]. trichiura ● Adults reside but do not attach to the
● T[richinella]. spiralis mucosa of the small intestine
● C[apillaria]. philippinensis
ID: egg in various aspects: size, color, shape, shell and content.
Fertilized
● broad oval, brown
● average size 60x45 pm
● thicker shell and consists of ascaroside, chitinous layer, fertilizing membrane and mammillated
albuminous coat
● fertilized Ascaris egg, still at the unicellular stage, as they are when passed in stool
● fertilized egg of A. lumbricoides in an unstained wet mount of stool, undergoing early stages of
cleavage at 200x magnification
Unfertilized
● longer and slender than a fertilized egg
● chitinous layer and albuminous coat are thinner
● content made of many refractable granules various in size
● unfertilized egg of A. lumbricoides (prominent mammillations on the outer layer)
Decorticated
● both fertilized and unfertilized eggs, sometimes may lack their outer albuminous coats and are
colorless
● A. lumbricoides decorticated, fertile eggs in wet mounts, 200x magnification
Life Cycle
1. Site of inhabitation: small intestine
2. Infective stage: embryonated eggs
3. Route of infection: by mouth
4. No intermediate and reservoir hosts
5. Lifespan of the adult: about 1 year
2 main parts
● posterior part - 2/5 fleshy (thick)
● anterior - 3/5 attenuated (thin), female is larger (2 inches long)
Ova
● bi-polar plug
● barrel-shaped (50-54 u)
● brown with bipolar protuberances.
● barrel or spindle in shape and 50x20um in size
● has a translucent polar plug at either ends
● content of the egg is an undeveloped cell
Trichuris trichiura Life Cycle
1. It starts from the release of trichuris trichiura eggs with feces, the eggs will experience maturation
in the soil. In this process the maturation of worm eggs takes 3 weeks to 5 weeks, the mature
eggs will be infective which can then infect humans.
2. The process can be through mechanical vectors or other objects that have been contaminated.
For example, the soil has been contaminated by human feces (which contain whipworm eggs) or
vegetables that have been sprayed with fecal fertilizer. Infection will occur immediately if the feces
contain eggs that are ready to hatch, it will hatch in the intestines when the eggs are swallowed by
humans.
3. In hatching eggs, the larvae will come out through the egg wall and enter the small intestine. After
adulthood, worms that are in the distal part of the intestine will go to the colon area. The period of
growth of eggs into worms for 30 to 90 days. The female and male worms will copulate.
4. When female worms lay eggs, they will mix with feces in the large intestine and come out with
feces. Eggs will experience maturation for approximately 6 weeks. The ripening process will take
place in moist soil and shady places. The host of trichuris trichiura is humans. The life cycle of
trichuris trichiura is related to what is consumed by humans.