Parasitology

Parasitology

What is a Helminth

Parasitic worms

Biohelminths

• Heteroxenous (development involves several host species) parasitic worms

• Go through host independently of environmental factors

Geohelminths

• Monoxenous (development is restricted to a single host species) parasitic worms

• maggots become invasive in external env. under strictly defined factors – temp, humidity etc

Types of hosts

• Definitive

• Intermediate

• Paratenic

• Reservoir

• Accidental

Definitive host

• host ADULT parasite lives in

• parasite undergoes SEXUAL REPRODUCTION

Intermediate host

• host LARVAL STAGE of parasite lives in

• ASEXUAL MULTIPLICATION takes place

• 2 types : 1st and 2nd immediate hosts

Paratenic host

• Host in which the parasite STAYS IN LARVAL STAGE (no further development)

• Host transmits infection to another host

Reservoir host

• Host that harbors the parasite that it transmits to another host in an endemic area (disease constantly present)

Accidental host

• Host in which parasite is not usually found

Ectoparasite

• Parasite inhabits body surface of host

• Doesn’t penetrate tissue

• e.g. Fleas

Endoparasite

• Parasite lives within body of host

• e.g. Giardia lamblia, hookworm

Free living parasites

• Parasites that hv non-parasitic stages of active existence

• Can live independently of host

  • E.g. fleas, lice

Obligate parasite

• Cannot live without host

  E.g. Toxoplasma gondii, Plasmodium

Facultative parasite

• Live in parasitic form or free-living form

• E.g. Candida, naegleria fowleri

Accidental parasites

• Parasitize an organism other than usual host

• E.g. Heartworms, crablouse

Aberrant parasite

• live in contact with the host for only a part of their cycle or occasionally at the time of feeding

• E.g. Multilocular cyst, Toxocara

Temporary parasite

• live in contact with the host for only a part of their cycle or occasionally at the time of feeding

• E.g. mosquitoes/bedbugs

Permanent parasite

• Remains on/in body of host from early life until maturity

• E.g. headlice

Life cycle of Parasites

• simple or complicated

• with multiple morphological forms and developmental stages

Direct life cycle

• parasite requires only a single host to complete development

Indirect life cycle

• parasite requires 2 or more host species to complete development

What are the modes of transmission

• Oral (per os)

• Skin

• Vector

• Direct

• Vertical

• Latrogenic

Effects of parasite on host

• Tissue necrosis

• Trauma & physical obstruction

• Allergic reaction

• Inflammatory reaction

• Nutritive effect

• Cancerogenic effect

SUBPHYLUM SARCODINA.

a. Genus Entamoeba —> 3

i. Entamoeba histolytica

ii. Entamoeba coli

iii. Entamoeba gingivalis

PHYLUM CILIOPHORA

a. Genus Balantidium —> 1

i. Balantidium coli

What is the life cycle of Entamoeba Histolytica

1. Mature quadrinucleated cells are ingested from contaminated food (per os). This passes from stomach to small intestine

2. This then travels to the stomach but the cysts have a protective barrier that prevents its coating from being broken down

3. The cysts then travel to the small intestine and the protective coating gets broken down by digestive enzymes (in small intestine). This process is called excystation

4. This releases trophozoites (which are the pathogenic form) which are carried to the caecum.

5. The best habitat for them is the caecal mucosa, where they lodge into glandular cysts and undergo binary fission

6. Some trophozoites then become pathogenic “forma magma” which invades the submucosal layer/intestinal wall destroying tissue and forming ulcers

7. They can also enter the blood stream, causing abscesses in the liver, lungs and brain

What is the life cycle of Entamoeba coli

1. First, cysts (invasive form) originate from animal reservoirs or human carriers. Examples include pig feces, polluted water or direct contact with infected animals/humans

2. Humans ingest cysts (invasive form) from contaminated food or water

3. Excystation occurs in small intestine and cyst walls breaks due to digestive enzymes. This releases trophozoites which travel to the large intestine

4. The trophozoites feed on the intestinal contents and multiply thru binary fission

5. Trophozoites typically remain as commensals (harmless presence), but in some cases they invade the mucosa leading to inflammation and ulcers

6. But trophozoites can also penetrate the intestinal wall and cause ulcers, diarrhea, abdominal pain and weight loss.

7. Some trophozoites form cysts, which are excreted in feces. These survive in the environment + infect new hosts

Draw Entamoeba Histolylica in its different forms

Draw an entamoeba coli

Entamoeba gingivalis localization, characteristics and transmission ?

• It is found in oral cavity, transmission via oral cavity

  1. Trophozoites are transmitted thru saliva

  2. They colonize gingival tissues and feed on bacteria, WBCs and epithelial cells (lining of the gums)

  3. They multiply by binary fission

  4. They spread through oral contact (kissing, sharing utensils etc.)

• They ONLY exist as a trophozoite, no cyst stage

• Trophozoites are 10-20 micrometers, mobile w. multiple pseudopodia

• Their cytoplasm has food vacuoles w. ingested bacteria, leucocytes and epithelial cells

ORDER KINETOPLASTIDIA VS ORDER DIPLOMONADIDA

Order KINETOPLASTIDIA

• Genus Trypanosoma

  i. Trypanosoma brucei gambiense

  ii. Trypanosoma brucei rhodesiense

  iii. Trypanosoma cruzi

• Genus Leishamania

  i. Leishmania donovani

  ii. Leishmania tropica

Order DIPLOMONADIDA

• Genus Trichomonas

  i. Trichomonas vaginalis

  ii. Trichomonas tenax

  iii. Trichomonas hominis

• Genus Giardia

  i. Giardia lamblia

What is the lifecycle for Trypanosoma brucei (gambiense and rhodesiense)? —> SLEEPING SICKNESS

1. Vector Tsetse fly bites and injects metacyclic trypomastigotes (infective form) into human blood. These parasites enter the bloodstream + tissues

2. The metacyclic trypomastigotes transform into bloodstream trypomastigotes and they multiply in body fluids (blood lymph, cerebrospinal fluid) by binary fission

3. The bloodstream trypomastigotes spread to different organs

4. When another tsetse fly bites an infected person, it ingests bloodstream trypomastigotes

5. Inside the fly, parasite undergoes several transformations

• Trypomastigotes → Procyclic Trypomastigotes in the midgut (multiply by binary fission).

• Procyclic Trypomastigotes migrate to the salivary glands, transforming into epimastigotes.

• Epimastigotes multiply and fill the glands, eventually becoming metacyclic trypomastigotes (infective stage).

6. Now when infected tsetse fly bites new human, it injects metacyclic trypomastigotes, continuing the cycle

What are the symptoms of T. b. gambiense & T. b. rhodesiense

🧠 "G for Gambiense = Grows Slowly" (Chronic)
🧠 "R for Rhodesiense = Rapid Death" (Acute & Severe)

What is the lifecycle for Trypanosoma cruzi? (CHAGAS disease)

1. Vector Triatomine bug (kissing bug) bites and defecates near bite

2. Feces contain metacyclic trypomastigotes (infective stage). The parasites enter the body through bite wound (scratched in) or mucosal membranes (eye, mouth, etc.)

3. This causes local inflammation (chagoma)

4. The metacyclic trypomastigotes invade cells at the infection site

5. Inside cells, they transform into amastigotes (replicating from) which multiply by binary fission and eventually burst out of cells transforming into trypomastigotes which enter the bloodstream.

6. Another Triatomine bug bites the infected person, ingesting trypomastigotes. The infected bug defecates near its next bite wound, spreading the parasite.

7. The cycle continues.

What is the lifecycle for Leishmania donovani (Kala-azar) AND Leishmania Tropica ?

1. The sandfly (PLEBOTOMUS PAPATASII) injects promastigotes through human skin, which travel into blood stream

2. Macrophages ingest (phagocytose) promastigotes, but instead of killing them, the parasite survives

3. Inside macrophages, promastigotes transform into amastigotes (intracellular stage)

4. Amastigotes divide inside macrophages, macrophages burst releasing new amastigotes which infect other macrophages

5. Another sandfly bites the infected person and ingests macrophages containing the amastigotes

6. Inside the sandfly’s gut, amastigotes change back into promastigotes

7. They multiply in the sandfly’s midgut and move to its proboscis (feeding organ)

8. The infected sandfly bites another human, injecting promastigotes into skin and the cycle repeats

What are the 3 genus names of the order Trichomonas and their localizations?

• T. vaginalis – vagina & uterine cervix in females

• T. tenax – oral cavity

• T. hominis – caecum

What are some morphological characteristics of Trichomonas sp.

• No cystic stage

• Pear shaped

• 4 anterior flagella and the 5th one running along the undulating membrane and axostyle

What is the lifecycle for Trichomonas vaginalis?

1. Trophozoite in vaginal, prostatic secretions and urine

2. Trophozoite reproduces by longitudinal binary fission

3. Spread through sexual intercourse (no intermediate host)

4. Trophozoites move to the vagina or urethra of new host

5. The disease name is Trichomoniasis

What are the symptoms of Trichomonas vaginalis?

• Foul smelling, yellow-green vaginal discharge

• Itching, burning and painful urination (dysuria)

• Strawberry cervix

• Men —> Often asymptomatic but may cause mild symptoms

• Increased risk of HIV transmission (due to inflammation)

• Infertility in both sexes

What is the life cycle of Giardia Lamblia?

1. Injection of cyst from contaminated water, food or surfaces (Common in areas w. poor sanitation)

2. Excystation occurs in small intestine which hatch into 2 trophozoites

3. The trophozoites multiply by binary fission and colonize the duodenum

4. As trophozoites move to the large intestine, they encyst again to survive outside the body

5. Trophozoites attach to the villous epithelium of the small intestine

6. They damage absorption, release toxins and cause diarrhea

7. Cysts are excreted in feces and can survive in the environment.

8. Trophozoite can also be excreted but do not survive outside the body

What’s the name of the disease caused by Giardia Lamblia?

Giardiasis

What are the symptoms of Giardia Lamblia?

• Watery foul-smelling diarrhea

• Malabsorption —> weight loss, fatty stools (steatorrhea)

• No blood in stool (non invasive)

For Class Haematozoa, Genus Plasmodium, what are the 4 diff. types of plasmodiums

i. Plasmodium vivax

ii. Plasmodium malariae

iii. Plasmodium falciparum

iv. Plasmodium ovale

Class Coccidia, Genus Toxoplasma, what is the name of the parasite?

• Toxoplasma gondii

Plasmodium Vivax

1. The definitive host, Female anopheles mosquito injects sporozoites (localised in their salivary glands) into the bloodstream of the intermediate host human

2. The invasive form, Sporozoites travel to the liver within minutes

Liver Stage

1. The sporozoites invade hepatocytes

2. Schizonts form —> divide and release merozoites

3. P. vivax & P. ovale ONLY: Some sporozoites become hypnozoites, which can stay dormant in the liver and reactivate later, causing relapses.

Blood Stage

1. The merozoites (pathogenic form) invade RBCs and become Ring Form trophozoite

2. Ring Form → Amoeboid Form → Mature Trophozoite.

3. Mature Schizonts develop, burst RBCs, releasing more merozoites → infect new RBCs.

4. This cycle repeats every 48 hours, causing fever spikes (tertian malaria).

Sexual stage

1. Some merozoites turn into gametocytes (male: microgametocytes, female: macrogametocytes).

2. These do not cause symptoms but wait for a mosquito to ingest them.

Mosquito Stage (Sporogony)

• Mosquito takes a blood meal, ingesting gametocytes.

• Male microgametocyte produces 8 flagellated microgametes.

• Female macrogamete fuses with a microgamete → zygote.

• Zygote elongates into a motile ookinete, which penetrates the mosquito’s stomach wall.

• Oocyst forms and undergoes division, releasing sporozoites.

• Sporozoites migrate to the mosquito’s salivary glands → ready to infect a new human host.

Definitive Host: Mosquito (where sexual reproduction occurs).

Intermediate Host: Human (where asexual reproduction occurs).

Disease: Tertian Malaria (fever every 48 hrs).

Key Feature: Relapses due to hypnozoites in the liver.

Destruction of erythrocytes

• Releasing of cellular components

• Hemolysis – anemia, antigenic variation

Lab. diagnosis • Different stages of parasite (trophozoites, schizonts, and

gametocytes) demonstrated in blood

• PCR

• ELISA

• Symptoms:

  • Cyclic fevers & chills (tertian fever).

  • Anemia (due to RBC destruction).

  • Splenomegaly (enlarged spleen).

    Diagnosis: Blood smear (Ring Form, Schizonts, Enlarged RBCs with Schüffner’s Dots).

• Treatment:

  • Chloroquine (for blood stages).

  • Primaquine (for hypnozoites in liver, to prevent relapse).

2 types of merozoites, one affects liver one effects RBCs

Bradizotes = slow parasites

Tachizotes go to RBCs n interact w receptor on RBCs, first recognition occurs, erythrocytes engulf parasites (vaculoe inside). This is first stage of endo - Ex aka. ring trophozoite

The parasites then start to produce pseudopodia,

Plasmodium Vivax

1. Asexual Phase (Schizogony) – In Humans 🔹 Pre-Erythrocytic Schizogony (Liver Stage)

• Sporozoites enter the bloodstream when an infected mosquito bites.

• They travel to the liver and infect hepatocytes.

• Inside hepatocytes, they transform into schizonts, which undergo multiple rounds of division.

• In P. vivax (and P. ovale), some sporozoites become hypnozoites (dormant stage) and remain in the liver for months/years before reactivating.

• Schizonts rupture, releasing merozoites into the blood.

2. Endoerythrocytic Schizogony (Blood Stage – RBC Infection) 🔴

• Merozoites invade red blood cells (RBCs) and undergo the following transformations:

  1. Ring Form (Immature Trophozoite): Small, with a vacuole and nucleus at one pole.

  2. Amoeboid Form (Mature Trophozoite): Enlarged, irregular shape, showing motility.

  3. Schizont: Undergoes nuclear division, forming many merozoites.

• Schizont bursts, releasing merozoites → Invade new RBCs and repeat the cycle.

• This RBC destruction causes fever cycles (tertian fever, every 48 hours).

3. Sexual Phase (Gametogony) – In Humans & Mosquitoes 🔹 Gametocyte Formation (In Humans)

• After multiple rounds of RBC infection, some merozoites differentiate into gametocytes:

  • Macrogametocytes (Female) – Larger

  • Microgametocytes (Male) – Smaller

• Gametocytes remain in the blood and wait to be ingested by a mosquito.

🔹 Mosquito Stage (Sporogony – Sexual Reproduction)

• When an Anopheles mosquito bites an infected human, it ingests gametocytes.

• Microgametocyte (Male) produces 8 motile microgametes (Exflagellation).

• Macrogametocyte (Female) matures into a macrogamete.

• Fertilization occurs → Forms Zygote.

• Zygote elongates into a motile ookinete → Penetrates mosquito’s stomach wall.

• Ookinete transforms into an oocyst, which matures and releases sporozoites.

• Sporozoites travel to the mosquito’s salivary glands → Mosquito becomes infective.

Life cycle Toxoplasma gondii

Definitive host Cats - The Starting Point

• Sexual reproduction (schizogony & gametogony) in cat’s small intestine → produces oocysts.

• Oocysts are shed in feces and contaminate soil, water, food.

Environmental & Intermediate Host Infection

• Oocysts mature in soil/water and become infective.

• New hosts/ Intermediate host (humans, pigs, sheep, rodents) ingest oocysts from contaminated food, water, or surfaces.

• Oocysts release sporozoites → invade epithelial cells + host cell ruptures releasing trophozoites in blood n lymph

• transform into tachyzoites/ chronic tissue cysts produces within muscles and tissues .

Tissue Cysts & Reinfection

• Tachyzoites spread via blood & lymph, infecting organs.

• Acute phase: Active infection (esp. dangerous in pregnancy or weak immunity).

• Chronic phase: Tachyzoites → bradyzoites (slow-growing form) inside tissue cysts (muscles, brain).

• If another animal eats infected tissue (e.g., a mouse eaten by a cat, or humans eating undercooked meat), the cycle repeats.

• Cats get infected again → new oocysts shed in feces → cycle continues.

Key Ways Humans Get Infected

✔ Ingesting oocysts (contaminated food, water, unwashed veggies, cat litter).
✔ Eating undercooked infected meat (pork, lamb, etc.).
✔ Mother-to-baby transmission (congenital toxoplasmosis).
✔ Blood transfusion/organ transplant (rare cases).

Disease name: TOXOPLASMOSIS

Lab. diagnosis • Microscopic Examination

• Smears and Sections

• Specimens

• Blood, Sputum, CSF, bone marrow

• Tissue biopsy

• Serological tests – IHA, IFA, ELISA (IgM/IgG)

• PCR & DNA probes

Class Trematoda (Flukes), Genus Fasciola, Discrocoelium, Opisthorchis, what is the name of the parasites ?

1. Genus Fasciola

• Fasciola hepatica

2. Genus Dicrocoelium

• .Dicrocoelium dendriticum

3. Genus Opisthorchis

• Opisthorchis felineus

Class Trematoda (Flukes), Genus Schistoma, What are the 3 parasites?

• Schistoma haematobium

• Schistoma japonicum

• Schistoma mansoni

Fasciola hepatica

Definitive Hosts: Humans, Sheep, Cattle

🐌 Intermediate Host: Snail (Lymnaea species)

Life Cycle in 3 Clear Phases

1. Eggs & Snail Infection (Water Stage)

   • Unembryonated eggs are shed in feces into water.

   • In water, eggs develop into embryonated eggs → hatch into miracidia (larvae).

   • Miracidia penetrate a snail (Lymnae species) and develop through stages:

   • Sporocyst → First & Second Generation Rediae → Cercariae (infective stage).

   • In snail, miracidia progress through

     sporocyst, first generation rediae, second

     generation redia to become cercariae

2. Cercariae to Metacercariae (Water to Plants Stage)

• Free-swimming cercariae leave the snail and attach to water plants (e.g., watercress, grass).

• They encyst and become metacercariae (dormant, infective form).

3. Infection & Maturation in Host (Animal/Human Stage)

• Host ingests contaminated water plants (sheep, cattle, or humans).

• Metacercariae hatch in the duodenum, penetrate the intestinal wall, and travel to the liver.

• Inside the liver, they mature into adult flukes, feeding on tissue and causing disease (liver rot in animals).

• Eggs are laid in bile ducts → passed into feces → cycle repeats.

🛑 Key Ways Humans Get Infected

✔ Eating raw water plants (e.g., watercress, unwashed veggies).
✔ Drinking contaminated water containing metacercariae.

🐑 Definitive Hosts: Cow, Human, Sheep, Goat

🐌 Intermediate Hosts:

1. Land Snail (Zebrina or Helicella)

2. Ant

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Life Cycle in 3 Clear Phases

1. Snail Infection & Cercariae Release (Land Stage) 🐌

   • Embryonated eggs (already containing miracidia) are shed in feces onto land.

   • Snail ingests eggs → Inside the snail, miracidia hatch and go through:

   • Sporocyst → 1st Generation Redia → 2nd Generation Redia → Cercariae.

   • Cercariae are released from the snail via its respiratory pore in slime balls (a protective mucus secretion).

2. Ant Infection (Second Intermediate Host) 🐜

• Ants eat the slime balls containing cercariae.

• Inside the ant, cercariae develop into metacercariae (infective stage).

• Some metacercariae migrate to the ant’s nervous system, making the ant climb up grass blades at night and latch on → This increases chances of ingestion by grazing animals (sheep, cows, etc.).

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3⃣ Host Infection & Maturation (Inside Animal/Human) 🐑👤

• Definitive host (sheep, cow, goat, or human) ingests the infected ant.

• Metacercariae excyst in the duodenum, travel to the bile ducts and mature into adult flukes.

• Adult flukes lay eggs → Passed in feces → Cycle repeats.

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🛑 How Humans Get Infected

✔ Accidentally eating infected ants on raw vegetables.
✔ Consuming contaminated food or water.

4 subphyla of Phylum Arthropoda

• Trilobitomorpha

• Chelicerata (ticks and mites)

• Crustacea

• Hexapoda (insects)

Complete metamorphosis

• Typical of higher insects

• Life cycle : Egg—> larva —>pupa —> imago (adult stage)