BIOL 4106 - Exam 2

Life Cycle of Hematozoa Apicomplexans

Infective stage for vertebrate host: Sporozoite

Infective stage for vector: Gametocytes

Three Phases of Apicomplexan Life Cycle

Merogony (Host)

• Multiple nucleus division → merozoites

Gametogony

• (Part one: Host)

  • Merozoites → gamete

    • Microgamete: male

    • Macrogamete: female

• (Part two: Vector)

  • Fertilization; microgamete → macrogamete

  • Results in an ookinete (zygote) → oocyst

Sporogony (Environment)

• Replication within oocyst → sporozoites (INFECTIVE STAGE)

• Must ingest sporulated oocyst

Malaria Life Cycle

Sexual Phase

• Occurs in female Anopheles mosquitos

Asexual Phase - Two Locations

• Extraerythrocytic

  • Sporozoites will attach to hepatocytes (Circumsporozoite protein)

  • Merogony (nuclear division) → merozoites

  • Merozoites rupture hepatocytes

• Erythrocytic

  • Merozoite → ring stage → trophozoite → schizont → merozoites

  • attach to RBC and enter via apical complex looking for receptors

    • P. vivax uses Duffy Antigen which is lost in Sickle Cell Anemia people (those people can’t get it)

  • Eats hemoglobin (toxic to the parasite)

  • Ring stage → gametocyte for infective stage of the mosquito

Schüffner’s Dots

Dotted appearance of trophozoites seen in P. vivax and P. ovale ameboid trophozoites infected RBC when stained with Giemsa

Maurer’s Clefts

Large course dots were observed in P. falciparum infections containing older ring-form trophozoites and asexual stages.

Maurer’s clefts resemble the Schüffner’s dots but are usually larger and coarser.

Band / Basket form

[P. malariae]

Trophozoites have compact cytoplasm and a large chromatin dot.

Occasional band forms and/or “basket” forms with coarse, dark- brown pigment can be seen.

Clinical Presentation of Plasmodium falciparum

Malignant tertian malaria

Clinical Presentation of Plasmodium vivax

Benign tertian malaria

Clinical Presentation of Plasmodium malariae

Quartan malaria

Clinical Presentation of Plasmodium ovale

Very Benign tertian malaria

Benign Malaria

All four Plasmodium spp.

Treatable

No signs of severe organ dysfunction

Symptoms:

• Headaches

• Extreme fatigue

• Mild jaundice (destruction of hepatocytes)

  • Malarial hepatitis

• Splenomegaly (RBC get stuck during blood filtering)

Malignant Malaria

[P. falciparum]

Most serious and can be fatal

Severe organ dysfunction

• Hyperparasitemia

• Anemia (Hemolysis & Bone marrow suppresion)

• Cerebral malaria

• Hypoglycemia

• Hemoglobinuria (Blackwater)

• Acute respiratory distress syndrome

• Low BP

• Jaundice

  • Heme → bilirubin; liver cannot break it down fast enough and deposits in tissue

Recrudescence

[P. malariae → chronic infection]

From not finishing your meds or drug resistance to malaria with a very low level RBC infection and asymptomatic

Relapse

[P. ovale and vivax]

Cleared merozoites in the blood but still have hypnozoites in the liver

Reinfection

Was effectively treated but had a new infection

Paroxysm

Cold shiver → Hot → Sweat (Malaria)

Deep vascular schizogony

[P. falciprium]

Sticky RBC with profusions (knobs) by mature trophs

• Deadly → Cerebral Malaria

Fetal Death from P. falciprium

Lack of oxygen

• Mom’s anemia

Hyperthermia

• Mom’s high fever

(Baby doesn’t get infected)

Hemozoin crystal

A dark-brown granular pigment from undigested toxic heme from hemoglobin

Gametophytes differential

Plasmodium falciparum is a banana-shaped while the rest are circular

Vector for Babesia

Ixodes scapularis

Vector for Malaria

Female Anopheline mosquitoes

Merozoites per Sporozoite in the liver

P. vivax 6-8 days 10,000 merozoites per sporozoite

P. ovale 9 days 15,000 merozoites per sporozoite

P. malariae 12-16 days 2,000 merozoites per sporozoite

P. falciparum 5-7 days 40,000 merozoites per sporozoite

Pathology from Malaria

Synchronized rupture of RBCs by merozoites that starts paroxysm

• Can release hemozoin and other parasite metabolic wastes

Can result in spikes of fever, chills, onset of malaise (discomfort) & headache, and anemia (ruptured RBC’s = blood cell loss)

Hallmarks of P. falciparum

Ring form: 2 distinct chromatin dots in ring

Gametocyte: Crescent or banana shaped within RBCs

Multiple infections of a single RBC (more than 1 ring per cell)

Normal sized RBCs

Diseases caused by P. falciparum

Cerebral Malaria

Blackwater fever (renal failure → death)

• Massive intravascular hemolysis of RBCs causing a spillover of hemoglobin into the urine (hemoglobinuria)

Hallmarks of P. vivax

Enlarged RBCs (ameboid shape)

Schuffner’s dots

All stages found in peripheral blood

Fasciola hepatica

Sheep Liver Fluke → Liver Rot

Intermediate Host: Lymnea sp (aquatic snail)

Definitive Host: humans, sheep, cattle

Infective Stage: metacercaria

Transmission: fecal-contaminated water with metacercaria

• Ex: watercress

Life Cycle:

Ova → miracidium* → sporocyst → redia → cercaria → metacercaria** → adult fluke

Niche: Liver & Bile Duct

Disease: Fascioliasis - migration of flukes

• Hepatomegaly

• Liver abscesses → jaundice

• Eosinophilia

• Scarring and fibrosis of liver and bile ducts

Morphology:

• Leaf shaped, large cone projection (anterior cone and shoulders)

• Extensive vitellaria

Fasciola gigantica

Liver fluke

Morphology: similar to F. hepatica but LARGER

Different snail vector

Distribution: Asia, Africa, Hawaii

Fascioloides magna

Liver fluke

• Cycle similar to F. hepatica

Niche: Liver

Definitive Host: Herbivores — deer, sheep, cattle

Morphology: similar to F. hepatica except NO anterior cone or shoulders

Fasciolopsis buski

Intestinal fluke - common in humans and pigs

• LARGEST fluke to infect humans (DH)

• Biology similar to F. hepatica

• Feed on intestinal epithelial cells

Niche: small intestine

Intermediate Host: Snail

Transmission: metacercaria in underwater vegetation

• Ex: Water chestnuts, bamboo, etc.

  • Boiling can kill metacercaria

Disease: causes ulceration, hemorrhage, and abscesses of small intestine

HALLMARK:

• Intestinal ceca not branched (wavy)

• Acetabulum large and close to oral sucker

Clonorchis sinensis

Chinese liver fluke

Reservoir: dogs and cats

1st Intermediate Host: aquatic snail

2nd Intermediate Host: freshwater fish

DH Infective Stage: metacercaria in 2nd IH (FW fish)

Definitive Host: human, dog, cat

Niche: lumen of bile duct (bile duct epithelium)

Infections of Clonorchis sinensis

Light infection: asymptomatic

Moderate to Heavy infections: clinical disease presentation → cholangiocarcinoma (bile duct cancer)

Dx of flukes

Eggs in stool

Heterophyes heterophyes

Morphology: Very tiny flukes

Niche: small intestinal villi

Distribution: Africa, Asia, Middle East, and FAR EAST (Far East is called Metagonimus yokogawai)

1st IH: snail

2nd IH: fresh / brackish water fish

Disease: gastric distress, malaise, fatigue, diarrhea → heart failure, eggs in brain and spinal cord, death

Dicrocoelium dendriticum

Lancet fluke

• Life cycle on LAND ONLY

Distribution: Not Africa or South America

1st IH: Cionella lubrica (LAND snail)

2nd IH: Formica fusca (common brown ant)

Definitive Host: ruminants like cattle, sheep, and deer

Niche: bile ducts of DH

Prosthogonimus machrorchis

Oviduct fluke of birds

1st Intermediate Host: snail

2nd Intermediate Host: dragonfly nymph

Definitive Host: bird

Paragonimus westermani

Human lung fluke

Distribution: Japan, China, Vietnam, Thailand, Cambodia, Africa, Central and South America

Paragonimus kellicotti

Distribution: North America

Definitive Host: multiple mammalian animals, including humans

1st Intermediate Host: aquatic snail

• Live in fast-moving streams

2nd Intermediate Host: crustacean (crayfish or crab)

Schistosomatidae Characteristics

Blood fluke

No second intermediate host

Distribution: USA

Definitive Host: humans, birds, fishes, and turtles

Infective Stage: Cercaria

• Does not have redia or metacercaria

Mature in blood vascular system of definitive host

Dioecious (separate sexes)

Identify based on egg

Schistosoma haematobium

Eggs in urine have a terminal spine

Distribution: Africa and Middle East

Niche: veins of urinary bladder plexus (veins draining urinary bladder)

• Blood in urine (hematuria)

• Can cause bladder cancer

Schistosoma mansoni

Eggs in feces have large lateral spine

Distribution: Africa (Egypt and Sudan), Middle East, South American, and Caribbean

Niche: veins draining large intestine (Inferior Mesenteric Veins)

Schistosoma japonicum

Eggs in feces with rudimentary spine

Distribution: Far East = China, Malaysia, Philippines, Indonesia (eradicated from Japan)

Niche: veins draining small intestine (Superior Mesenteric Veins)

Schistosomiasis

Caused by the eggs

Tranverse through wall of vein → tissue of intestine or bladder → lumen to go out with feces or urine

• S. mansoni & S. japonicum: gut wall to gut lumen to go out with feces

• S. haematobium: bladder wall to bladder lumen to go out with urine

2/3 of eggs don’t make it to the lumen of intestine or bladder

• Trapped in intestinal or bladder wall

• Some get lodges in capillaries of liver

Trapped eggs secrete soluble egg antigens (SEA’s) which are hydrolytic enzymes which trigger inflammatory and immune responses

• Chronic, granulomatous fibrosis lesions in tissues containing trapped eggs (swirly)

Monecious

Hermaphroditic

Majority of platyhelminths

• Self fertilize

• Cross fertilize between two hermaphroditic individuals [Paragonimus sp.]

Dioecious

Separate sexes [Schistosomes sp.]

• Female lives inside male and cannot survive without him

Fill in the arrows

Dendritic

Ovum

An egg that encloses the embryo (miracidium)

• Operculum - opening at one end of egg through which larva will escape

Miracidium

Infective stage for IH

Ciliated free-swimming larva hatched from ovum

• Will lose cilia after ingestion

Some can penetrate; some need to be ingested

Sporocyst

From metamorphosis of miracidium as it elongates to form a sac-like structure

• No mouth, no digestive system, absorbs nutrients from the host

• Germinal sac

Embryos develop asexually within

Can produce generations of sporocysts: daughter sporocysts, redia, or cercaria (depending on species)

Redia

Either bursts out of sporocysts or leave by birth canal

Active in host (crawls around)

Rudimentary digestive system and actively feeds on host tissue

• Muscular pharynx and short sac-like gut

Can develop embryo to form daughter redia or cercaria

• Cercaria goes out of birth pore

Cercaria

Infective stage for DH [Schistosoma sp.]

Free-swimming with a tail or no tail

• Has a mouth and digestive system but doesn’t feed

• Penetration gland

Considered a juvenile fluke

Metacercaria

Ingested by DH (except Schistosoma)

• DH does not need to feed on IH

Encysted form

General Life Cycle of Trematodes

Ovum → miracidium → sporocyst → redia → cercaria → metacercaria → adult fluke

Prosthogonimus machrorchis

Babesia bigemina

Cattle, deer, and rarely humans

Distribution: Central and South America

Vector: Boophilus annulatus (North American Cattle Tick)

Babesia canis

Infects dogs by tick bites that can be fatal

Distribution: Worldwide

Vectors:

• Rhipicephalus sanguineus (Brown dog tick)

• Dermacentor variabilis (American dog tick)

Babesia microti

Infects rodents and humans

Distribution: USA, Northeast and Midwest

Vector: Ixodes scapularis (deer tick)

Life Cycle:

Sporozoites enters vertebrates via saliva → RBC (no hemozoin) → merogony → merozoites → gametogony → gametocytes → blood meal → syngamy (gametocytes fuse) → kinete → sporogony → sporozoites

How to identify babesia sp./babesiosis

If there are any symptom for tick-related diseases

Mild malaise

Maltese crosses