1. Leishmania is classified in the phylum _________. What order?
Metamnoda. Order Kinetoplastida. Many spp, several human spp. Cause disease called leishmaniasis.
What is the common name of the vector for Leishmania
Sandfly
What genera of vector transmit Leishmania in the Old World and New World
Old world includes N. Africa, Asia and Europe. Transmitted by genus Phlebotomus.
New World includes Mexico and South America. Transmitted by genus Lutzomyia.
What two parasite forms occur during the life cycle? Draw a generalized life cycle.
Amastigote and promastigote. Fly takes a blood meal and ingests amastigotes. In insects guts where it transforms into promastigote. Attaches to gut wall and then proliferates and undergoes binary fission. Promastigotes moves to sandfly mouth parts. Next blood meal, promastigotes infects host. Now Inside human. Promastigote enters macrophage via phagocytosis. Promastigote inside parasitophorous vacuole (inside macrophage). Fuses with lysosome--> low pH. Transform into amastigote, which are acidophilic. Optimal pH 4-5.5. Binary fission. Host cell ruptures-->releases amastigotes which enter other macrophages==> spread of infection in body.
Inside what cells does the parasite live in humans
Macrophage.
What is found inside a parasitophorous vacuole
The promastigote. Fuses with lysosome which has a low pH.
By what process does the parasite multiply
Binary fission.
Why do reservoir hosts make control of the parasite difficult
Rh are dogs and rodents. These are common part of our lives and are not as severely affected as humans to these parasites, makes it harder to spot.
What are the types of pathology associated with leishmaniasis and treatment for leishmaniasis?
Three types of pathology. Cutaneous leishmaniasis, mucuocutaneous leishmaniasis and visceral leishmaniasis. Pentostam is used to treat all forms of pathology.
2. What is another name for cutaneous leishmaniasis
Oriental sore, relatively mild pathology.
What species cause this pathology in the Old World and New World
Old world- Leishmania tropica. Vector is Phlebotomus. New World- Leishmania mexicana. Vector is Lutzomyia.
Do these species cause secondary lesions
No
Draw life cycle
Sandfly bites. Promastigotes in skin. Into macrophages. Happens at site of bite. Damage caused by parasite in this area causes a nodule of skin to form. Ulcerates, erupts and spreads. Leads to secondary bacterial infections. Can heal without treatment-->can lead to disfiguring scar.
What is meant by learned way to vaccinate
Innoculate in less conspicuous areas of body--> Immunity. If you want to find material to do some immunizing, use periphery material. Amastigotes are all around the periphery.
Why don't the amastigotes spread through the body
Amastigotes cannot grow at core body temperature.
How can infection be diagnosed
Margin of lesion--> check for amastigotes.
3. What species causes mucocutaneous leishmaniasis
Braziliensis. Western hemisphere.
Where does the primary skin lesion form
Forms at site of bite.
Name two types of secondary lesions and describe the pathology they cause and where prominent
Secondary lesions caused by amastigotes in macrophages at mucocutaneous junctions of skin.
Chiclero ulcer- occurs in Mexico and Central America. Lesion on ear- on pinna. Cartilage not highly vascularized. Don't have a very strong immune system here. Infection remains for years. Pinna erodes.
Espundia- rainforest of central and South America. Serious disfigurement. Long, chronic. Skin lesions spread. Invades mucous membranes. Nose affected in 80% of cases. Facial cartilage is destroyed. Nose and soft palate destroyed. Into larynx and trachea, if these become destroyed then voice and breathing can be damaged.
4. What species causes visceral leishmaniasis
Leishmania donovani
Who were Leishman and Donovan
Physicians in India who discovered the agent of the disease at around the same time. Published discovery practically simultaneously.
Why are amastigotes also called LD bodies
Because they were discovered by Leishman and Donovan.
What is the life cycle
Amastigotes throughout body. Macrophages. Spleen and bone marrow. Compensatory macrophage production. To detriment of RBC production. Spleen and liver-->hepatosplenomegaly. Enlargement. Anemic and emaciated. Macrophage released while immature-->Ineffective.
Why does the immune system become worn down in this infection
Increase macrophage production to detriment of RBC production. Eventually keep making so many macrophages that are released when immature and thus not effective. Immune system tanks.
What is the pathology
Fever, progressive wasting. Anemia, immune deficiencies. If left untreated--> death in 2-3 years.
How is infection diagnosed
Amastigotes in tissues. Blood/nasal smear. Bone marrow. Spleen puncture. Xenodiagnosis- where you're taking tissue samples to inoculates lab animals.
5. How can sandflies be controlled
Short flight range- insecticide inside houses. Adult sandflies use low growing bushes as resting spots.
How can humans be protected from sandfly bites
Repellants, bed nets and sprayed fly screens.
6. What is the significance of Leishmania-HIV coinfection
It's an emerging disease in developing countries. Significantly decreases immune responses in host.
7. Describe key features of phylum Ciliophora
Cilia. 2 nuclei. macronucleus- controls trophic activities. Micronucleus- controls reproductive functions.
What is the one species in the phylum Ciliophora that infects humans
Balantidium coli in humans and pigs. Largest protozoan parasite of humans.
Is Balantidium coli large or small compared to other protozoans in humans
Largest.
8. Draw a B. coli trophozoite and label the following: peristome, cytostome, food vacuoles, cytopyge, contractile vacuoles, macronucleus, and micronucleus. PICTURE.
LOOK AT PICTURE IN PHONE
Which structure is lined with coarse cilia
Peristome- lined with coarse cilia. Draws in any food material that is going to be ingested. Leads into cytosome. Area of membrane for ingestion.
Which structure ingests food
Cytosome, it's the area of membrane for ingestion.
Why are contractile vacuoles unusual in a parasitic organism? What is the function of cytopyge?
contracticle vacuoles for osmoregulation. Unique among parasitic protozoa.
Also there is the cytopyge where wastes are eliminated.
What are the functions of the macronucleus and micronucleus
macronucleus- controls trophic activities. Micronucleus- controls reproductive functions.
9. What stimulates encystment in B. coli
Dehydration.
What is the transmission stage
Cysts. Transmission stage is ingested by next host. Excyst in SI. Then move down to LI.
What pathology is there
Many cases are asymptomatic. Trophs ingest starch and cellular debris. Some cases produce hyaluronidase.
10. How does hyaluronidase contribute to pathology by B. coli
It digests the host intestinal epithelium. -->Flask shaped ulcer. Hemorrhage. Secondary bacterial infections. Necrosis. Sloughing of tissue-->diarrhea and dysentery= balantidial dysentery. Occasional perforation of LI-->peritonitis-->death. Secondary foci--> liver and lungs.
What type of ulcers can form in the intestine
Flask shaped ulcer. Hemorrhage. Secondary bacterial infections. Necrosis. Sloughing of tissue-->diarrhea and dysentery= balantidial dysentery.
11. How can B. coli infections be treated and controlled
Control via sanitation. Treatment via metronidazole.
12. Describe various characteristics of an ideal antiparasitic drug.
Effective against intended pathogen. Should be less harmful to host cells than to parasite. Kills 100% of parasites of all life cycle stages within host. Broad spectrum-- effective against a wide range of parasites. Rapid acting, less time for parasite to interact with drug and develop possible resistance. Ease of administration in terms of taking it and length of time. Safe, no harmful side effects. Affordable. Long shelf life. Safe for environment.
How is the use of ivermectin detrimental to the environment
Used in animals also. Feces in environment-->ivermectin in soil and water. Soil invertebrates killed. End up in milk and meat.
1. What characteristics do members of the phylum Apicomplexa share
All parasitic. All have apicalcomplexa and complex life cycles.
What is the function of each of the components of the apical complex
Rhoptries and micronemes- secretory organelles. Penetration of host cells.
Conoid and subpellicular microtubules - structural.
Worldwide, how many people are infected with and how many die from Plasmodium
~Half the world is at risk. 2010~216 millioncases. 655,000 deaths (mostly children).
What are the four species of Plasmodium which infect humans
Plasmodium vivax, P. ovale, P. malariae and P. falciparum.
2. Trace an overview of the life cycle of the Plasmodium parasite in the vertebrate and mosquito hosts
Sporozeite transmission stage to human-->blood-->liver-->RBC-->gametocyte (transmission stage to mosquito-->stomach of mosquito-->hemocoel-->salivary glands-->sporozeite develop in salivary glands and transmission stage to humans.
What species of mosquito transmits malaria
Genus anopheles
Is it the male or female mosquito
Female
What stage of the parasite is infective to humans
Sporozoiete.
Why do sporozoites invade hepatocytes and no other cells
Because they bind to receptors (circumsporozoite protein) only on hepatocytes and no other cell.
What is the exoerythrocytic cycle
Stage that involves the liver, this is where the parasite multiplies. Prepatent time of development, meaning that infection before evidence of organism.
3. How does the mosquito transmit the parasite to the human host
Infected female anopheles spp mosqutio-->blood meal. Probes skin for capillary. Injects salivary secretas-->prevent clotting and sporozeites injected.
Once the sporozoite invades the hepatocyte, it transforms into a ____
Trophozoite that feeds on host cell cytoplasm for one week. Then mature. Undergoes shizogony
This stage feeds for approximately one week and then undergoes a process of asexual reproduction known as ____.
Schizogony- asexual reproduction.
What occurs in the two steps of this process
i. nuclear division. Numerious daughter nuclei formed known as schizout or cryptozoite. ii. cytoplasm divides-->merozoites have formed.
What is the end product of this reproduction
Merozoites form which then burst out of hepatocytes.
This stage leaves the liver, enters the blood and initiates which cycle
Erthrocytic cycle.
4. What is the function of MSP-1
Initial interaction between merozoite and RBC is random. Merozoite surface protein - 1 (MSP-1) interacts with protein on RBC surface-->binding.
How does the apical complex function during the invasion of an RBC
Merozoite orients apical complex to RBC. Secretions invade RBC; invasion is an active process meaning parasite pushes against RBC membrane and forms a pit, which closes up around it. Inside the RBC it morphs into a trophozoite. It will feed on the host cell cytoplasm, forming a large food vacuole.
How did the signet ring stage get its name
Parasite inside RBC, feeding on cell cytoplasm and forming a large food vacuole looks like a signet ring.
What is hemozoin
Trophozoite grows and food vacuole becomes less noticeable. Hemozoin becomes apparent (end production of hemoglobin digestion).
Does schizogony occur during the erythrocytic cycle
Yes. Schizogony is where the parasite multiplies. i. Nuclear divison forming blood shiznots. ii. cytoplasmic divison (segmenter) merozoites are produced.
What is released when as infected RBC ruptures
Releases merozoites and parasites metabolic wastes. These merozoites then infect other RBCs.
What does synchrony mean in a malaria infection
Occurs in an infected individual. Merozoites tend to develop at same time. Release of merozoites from host cells is synchronous. Massive release of merozoites and waste productions into blood stream-->stimulates host immune response. Fever and chills. Periodicity of sympmtoms varies between spp.
How is this related to the fevers associated with infection
Massive release of merozoites and waste productions into blood stream-->stimulates host immune response. Fever and chills. Periodicity of sympmtoms varies between spp.
What is the fate of micro- and macrogametocytes
Some merozoites enter RBC and undergo gametogony-->microgametocytes and macrogametocytes. These are the transmission stages to mosquito. Macro becomes female, micro male.
5. What stage of Plasmodium is infective to the vector
Gametocytes.
What happens to the macrogametocyte in the vector
Nucleus shifts and turns into macogamete (female)
Name and explain the process which the microgametocyte undergoes in the vector.
What stimulates this process?
Undergoes exflagellaton. Nucleus divides into 8 daughter nuclei. Each of which develops a flagellum. These then break apart and now you have 8 microgametes (male).
The stimuli for exflagellation is decreased temperature and higher pH (mosquito pH in stomach higher than human).
What two cells join during fertilization and what stage is produced
Microgamete(male) swims until finds macrogamete (female). Penetrates--> fertilization. Produces ookinete.
Where does the ookinete go
The ookinete is mobile. It penetrates the stomach wall of mosquito into its hemocoel side and attaches.
It transforms into a(n) _________ on the hemocoel side of the mosquito stomach
Oocyst
How many sporozoites develop in one oocyst
Oocyst nucleus divides-->sporoblasts-->Divide and produce sporozoites--> 10,000 from one oocyst.
How do the sporozoites get to the salivary glands
Sporozoites break out of oocyst. They then migrate through body and enter salivary gland.
How does feeding behavior change in an infected mosquito
They feed more frequently-->increased chance of transmission-->PITT. They inject sporozoites into humans.