Parasitology

Front 1

Give the difference between direct host and intermediate host?

Back 1

Direct host: particular organism in which the parasite develops to its sexually mature, adult stage.

Intermediate host: organism in which growth, development and sexual multiplication of parasite occurs.

Front 2

Describe the process of sedimentation and what is it used commonly to detect?

Back 2

Based on faster falling down of heavy parasitic eggs compared to other particles. It's used to detect eggs of trematodes and some nematodes. (Fascial hepatica - trematodes and ascoris Sumi - nematodes)

Steps:

1. Rub 3g of faeces on tea strainer dipped in water. Wait 10 min for sedimentation. Pour off water over sediment.

2. Add water again. Wait 10 mins. Repeat three times.

3. Add clean water to sediment and transfer to crystal glass dish.

4. Stain with malachite green and place under microscope.

Front 3

Describe the process of flotation and what is it used to detect?

Back 3

-Based on flotation of oocytes of protozoans and eggs of some nematodes in a hypertonic solution.

- Pour in NACL with water into a test tube and place a sample of faeces in the solution.

-slowly fill to the top and then place a cover slip on top.

-wait 20 minutes.

-Place cover slip on a slide and look at it under microscope.

Front 4

Describe McMasters method and its uses:

Back 4

- Qualitative method.

- McMasters method used for the estimation of eggs, oocytes and cysts per one gram of faeces. Allows for the prediction of infection intensity. Also for evaluation of drug efficacy.

-4g of faeces is inoculated with 60 ml super saturated NaCl. mix until it is suspended. Suspension filtered by a tea strainer + stirred for 3 minutes.

-Discard sediment. Fill McMasters chamber with the faecal suspension.

-Allows us to determine the number of eggs per 1 gram faeces.

Front 5

Describe some of the methods used for serological testing of parasite antigens and detection of antibodies against parasite antigens.

Back 5

- stripe tests. - taxoplasm gandii

- complement tests - trypanosoma

- direct aggluation - tricomonas

- immunofluorescence- cryptosporidium

- western blotting- faenia solium

- immunochromographic - leishmania

Front 6

Give me the difference between "prepatent time of infection" and " patent time of infection"

Back 6

1. Prepatent time of infection: the time taken from development of infection until commencement of the production of offspring. E.g: eggs, larvae, oocytes, cysts.

2. Patent time: time from when off spring are produced. It is the time by when the infection can be detected by traditional methods.

Front 7

Possible methods of infection?

Back 7

-ingestion

- inhalation

- vectors such as flies.

- penetration of skin e.g: hookworm

- direct contact

- sexual transmission

Front 8

Explain what is coprological examination?

Back 8

Coprological methods such as sedimentation and floatation involve examine the faeces of animals to identify and count parasitic eggs, oocytes, and cysts for example.

Front 9

Why is the life cycle of parasites important to vets?

Back 9

- veterinarians must know the life cycles of parasites to achieve success in their treatment and transmission etc. It also informs them how to control infections.

- they know the clinical signs, pathogenicity and know the methods of detecting the infection.

Front 10

Give the differences between:

1. Intensity of infection

2. Extensity of infection

3. Prevalence of infection

Back 10

1. Intensity of infection: number of individuals of particular parasite species in each infected host in a sample. Severity of the infection.

2. Extensity of infection: how wide spread an infection is in a group of examined individuals.

3. Prevalence of infection: number of individuals of a host species infected with a particular parasite species.

Front 11

Lifecycle of cryptosporidium

Back 11

1- Unsporulated oocyst is shed in faeces.

2- ingestion occurs and sporulation occurs in host. Sporozoites enter enterocytes.

3. The trophozoites rapidly schizont, forming 4-8 merozoites

4- two different types of oocysts are produced:

•The first, a thin walled oocyst that releases it sporozoites in the intestine.

•The second - a thick walled oocysts that's passed in the faeces.

Front 12

Life cycle of eimeria melagrinitis (same as e. Tenella

Back 12

1. Oocysts are shed in faeces. Sporulation takes place outside host. 1-3 days. Sporulated oocysts are infectious.

2. After oral ingestion by host, it enters the gizzard and creates sporozoites.

3. Sporozoites invade gut cells by moving from top of villi downwards.

4. When these sporozoites invade gut cells, trophozoites form, which is the feeding stage of the parasite.

5. Trophozoites develop into multinucleated schizont to proliferate. This schizont releases merozoites which have the ability to become infective trophozoites or gametes.

6. Male and female gametes fuse, producing an oocyst which is shed in faeces.

Front 13

Life cycle of giardia

Back 13

1. Ingestion of food that contains fecal contamination, having cysts.

2. Trophozoites exist in small intestine and may divide by binary fission.

3. Trophozoites are attached to the surface of intestinal villi.

4. Fully developed cysts have 4 nuclei and 2 sets of organelles.

5. The cysts are immediately infective for the host.

6. Giardia have a direct life cycle and have no intermediate hosts.

Front 14

Life cycle of trypanosoma brucei

Back 14

1. Tsetse fly takes a blood meal. These infected metacyclic trypomastigotes transform into blood stream trypomastigotes.

2. The trypomastigotes multiply by binary fission in bodily fluid and then make their way into the blood stream.

3. Tsetse fly takes a blood meal and metacyclic trypomastigotes transform into procyclic trypomastigotes in tsetse fly midgut.

4. Procyclic trypomastigotes leaves midgut and transform into epimastigotes.

5. Epimastigotes multiply in salivary glands and transform into metacyclic trypomastigotes.

Front 15

Life cycle of taxoplasma gondii

Back 15

1. Unsporulated oocysts are shed for 1-2 weeks. Oocysts take 1-5 days to sporulate in the environment and become infective. Intermediate hosts e.g birds ingest oocysts become infective.

2. Oocysts transform into tachyzoites in neural and muscle tissue and develop into tissue cyst bradyzoites.

3. Cats become infected after consuming intermediate hosts that harbour these tissue cysts.

Front 16

Life cycle of leishmania

Back 16

1. Transmitted by bite of female sandfly that is previously infected.

2. Female sandflies inject infective stage during blood meal.

3. Promastigotes that go into wound are phagocytes by surrounding macrophages.

4. Promastigotes transforms into amastigote which then multiples.

5. Sand fly takes a blood meal and ingests macrophages infected with mastigotes.

6. These amastigotes transform to promastigotes in the gut.

Front 17

Lifecycle of trypanosoma equiperdum

Back 17

1. It has direct life cycle meaning it has one host. It can be sexually transmitted and does not require a vector.

2. Trypanosoma s are not continually present in the genital tract of the horses so it's transmission isn't during every sexual contact the infected horse/donkey has with uninfected animals.

Front 18

Life cycle of histomonas melagridis

Back 18

1. Cecal worms produce eggs within the bird host, containing h. Melagridis

2. Cecal worms are shed in the environment and their eggs develop into larvae in the soil.

3. Earthworms ingest these cecal worms larvae containing h. Melagridis

4. Histomonas released from nematode larvae in ceca or direct infection replicate rapidly.

5. Migrate to submucosa and lead to extreme necrosis.

6. Moves to the liver where causes necrotic lesions.

Front 19

Life cycle of eimeria truncata = renal cocci

Back 19

1. Oocysts are shed in faeces.

2. Within 1-5 days , zygote divides and forms 4 sporocysts with each having two infective sporozoites.

3. These infective oocysts are consumed in contaminated environment.

4. Parasite reaches kidneys and junction of ureters where gametogony occurs.

5. Death may occur secondary to kidney failure.

6. Life cycle continues as infected hosts she'd oocysts to the environment.

Front 20

Life cycle of isopera suis/ felis

Back 20

1. Isopera suis shed as oocysts in faeces . Immature oocysts contain zygote.

2. As immature oocyst reaches external environment it is composed of two sporoblasts.

3. As it is ingested it changes into mature oocyst with two sporo cysts in each containing 4 sporozoites and this is the infective stage of the isopera.

4. Sporozoites are released and penetrate cells of host intestinal mucosa.

5. Schizogony occurs and sporozoites form trophozoites. After a few days the trophozoites divide by multiple fission to form schizont

6. Schizont consists a lot of merozoites.

7. When schizont is mature, host cells and schizont rupture, allowing merozoites to escape to neighbouring cells.

8. Schizogony finishes as merozoites give rise to male and female gametocytes in gametogony.

9. Macro gametocytes (female) are penetrated by a microgamete (male) resulting in a zygote, an Unsporulated oocyst.

10. Unsporulated oocyst shed in faeces and the process continues.

Front 21

Define Parasite

Back 21

A parasite is an animal that lives completely at the expense of plants, animals or humans is defined as a parasite.

Front 22

Paratenic host in transmission of diseases

Back 22

Mouse- Taxocara canis and uncinaria stenocephala

Front 23

Diagnosis, Control and Symptoms of Trypanosoma Brucei

Back 23

Diagnosis: Blood exam, capillary and venous, examine CSF , serological ELISA

Control: tsetse fly traps, destruction of nests.

Symptoms: Horse, dog and mules suffer acutely , sleeping sickness, anaemia, fever edema, can invade immune system.

Front 24

D+C+S Trypanosoma Equiperdum

Back 24

Diagnosis: smears of vaginal discharge, complement fixation test, Elisa , Trypanosoma not always in blood.

Control: test breeding, quarantine + culling if rampant.

Symptoms: fever, loss of appetite, swollen genitals, loss of ligament of genitals , facial paralysis and silver dollar later stages, later stages after ,4 weeks.

Front 25

DCS Leishmania

Back 25

D: amastigotes in biopsies, bone marrow, blood and sight of infection, PCR, Elisa snap

C: chemical control but limited success, vaccination in South.

S: fever, eye inflammation , alopecia around eyes, musculocutaneous ulcers, excessive development of claws, urinary problems and kidney failure.

Front 26

Trichomonas Foetus DCS

Back 26

D: direct swab/ microscopy

C: AI insemination, reduce contact with cats.

S: cattle abortion, bulls don't show symptoms, purulent endometriosis, disease in reproduction tract cats, diarrhea in kitten.

Front 27

Neospora caninum DCS

Back 27

D: Dogs: blood sample, muscle weakness + paralysis cattle: Elisa

C: stop dogs eating placenta, don't let dog eat foetus, suspension of dog contact.

S: paralysis of hind limb, muscle weakness, onset in puppies 1-6 months, transplacenta

Cattle: mummified foetus, foetus death + underdeveloped

Front 28

D,C,S Giardia

Back 28

D: long diarrhea, flotation test, biopsies, snap, Elisa

C: good sanitation, prevent contamination

S: diarrhea, weight loss, abdominal pain

Front 29

Histomonas DCS,

Back 29

Rt-PCR

C: good biosecurity, rear turkeys on ground not inhabited by chickens for 2 years,

S: primary lesion, necrosis of tissue, ulcerations

Front 30

Isopera

Back 30

D: flotation

C: good hygiene and biosecurity. Reduce coprophagy

S: diarrhea, weight loss, abdominal discomfort