Parasites, Lect 28: Micro Exam 2

Front 1

What kingdom are parasites part of? Subdivided?

Back 1

Prt of animalia,which are then subdivided into protozoa and metazoa

Front 2

Compare and contrast protozoa vs. metazoa

Back 2

Protozoa
single celled, containes organelles, has nucleus with chormatin and karyosome, and are motile

Metazoa
are helminths and arthorpods
-multicellular have tissue organ systems
-more complex than protozoa

Front 3

What are helminths? Subdivisions?

Back 3

Helminthes are further divided into nematodes, trematodes, and cestodes.
• Commonly known as “worms” (nematodes = roundworms, trematodes = flukes or flatworms, cestodes = flatworms)

Front 4

What are some organelles in protozoa?

Back 4

membrane bound nucleus, ER, food storae granules, digestive vacuoles

they also have cilia, flagella, or use a pseudopods (sliding motion)

Front 5

What kind of respiration do protozoa and metazoa use?

Back 5

protozoa - facultative anaerobes
metazoa - have large nutirtional requirements, but primarly use anaerobic respiration.

Front 6

What do helminths have that mediate their attachment to host? What does this assist in?

Back 6

a. Nematodes have biting mouthparts designed for sucking blood from injured intestinal tissue and to facilitate attachment to the host intestine.
b. Trematodes have two muscular suckers that also mediate ingestion of nutrients and attachment.
c. Cestodes do not have digestive systems, therefore food is absorbed from the host intestine through the body wall of the worm; muscular suckers mediate attachment.

Front 7

How do protozoa and helmniths replicate?

Back 7

protoza: binary fission
helminth replication: sexual; worms lay eggs. progeny are NOT produced in humans

Front 8

Where do we find parasites?

Back 8

found worldwide!
-some have climate or life cycle requirements.


2. Resource-poor countries have higher infection rates due to:
a. Multiple infections & high probability of re-infections
b. Large number of immunocompromised and malnourished
c. Poverty & poor sanitation

Front 9

Describe the routes of entry through with humans get parasitic infections

Back 9

a. Always exogenous.
b. Must enter the body by passing through anatomic barriers.
i. Routes of entry:
a. ingestion
b. direct penetration of the skin
c. arthropod vectors (ex: bites from ticks, mosquitoes, etc.)

Front 10

What are some general virulence factors for parasites?

Adhesins, Toxic products, antigenic variation

Back 10

a. Adhesins
i. Adhesins on parasites bind to human cell surface structures (examples: glycoproteins, glycolipids, complement receptors, Duffy blood group antigen)
• This can result in tissue tropism seen with certain parasites.
ii. Non-specific attachment
iii. Mechanical or biting mouthparts can facilitate attachment.

b. Toxic products
i. Enzymes that destroy proteins (proteases) and phospholipids (phospholipases) can
cause host cell destruction leading to gross tissue pathology, and inflammation***.

ii. Other enzymes (proteinases) can degrade host antibodies, thus weakening the
immune reaction against the invading parasites.

c. Antigenic variation, antigenic mimicry, and antigenic masking may be used by
parasites to evade immune recognition. Ex. African sleeping disease

Front 11

What does disease severity depend on?

Back 11

Parasitic infections are often chronic and symptoms are generally caused by the immune response.
a. Disease severity depends on:
i. Inoculum size
ii. Number of organisms acquired over time
iii. Site of exposure
iv. duration of exposure

others: temperature on outside of skin, size of teh parasite,

Front 12

What are 2 major ways parasites cause disease?

Back 12

1. mechanical/chemical damage: due to biting mouthparts or rupture of infected cells cause inflammation (fever, chills)

2. Hypersensitivity reactions - immune response.
All 4 kinds can occur. eggs in particular lead to large inflammation.

Front 13

How can parasites elicit immunosuppression?

Back 13

Can be generalized or parasite specific. antien overload, antigenic competition, activation of T regularotry cells, induction of supressive cytokines.

Parasitic infections -- mostly CHRONIC.

Front 14

Why is diagnosis of parasitic infections difficult?

Back 14

1. pure culture isolation CAN"T be acheived
2. all diagnosis are made by morphological observations - microscipong exams of pts samples (blood, stool, muscle biopsy, skin lesion scrapings).
3. proper diagnosis relies on awareness of the physician
4. antigen, antibody and nucleic acid detection works but are uncommon

Front 15

What part of the parasite is an important diagnositc aid?

Back 15

the parasite's life cycle
-eggs have unique characteristics

timing of specifmen collection due to nocturnal periodicity

Front 16

Describe some anti-parasitic agents used in treatment

Back 16

a. Specifically targeting parasites isn’t as easy as targeting bacteria with antibiotics
because parasites and humans are both eukaryotes!

b. Complex life cycles of parasites and multiple stages of infections complicate the
effectiveness of chemotherapeutic agents.

c. Chronic or prolonged infections are generally difficult to get rid of because
chemotherapeutic agents cannot be used for prolonged periods of time.

Front 17

How can parasitic infections be prevented?

Back 17

To prevent infections, parasites must be prevented from entering the human body.
a. Ingestion of parasites can be prevented by sterilizing food and water supplies that may
be contaminated.

b. Direct penetration of the skin can be prevented by avoiding skin contact with
contaminated water or soil.

c. Protection from arthropod vectors such as clothing, netting, and repellents can be
used to prevent bites from infected arthropods.

Front 18

Describe the properties and structure of Giardia lamblia

Back 18

1. Giardia is a flagellate.

2. Has 2 forms: trophozoite and cyst.
a. Trophozoites are the active, replicating form.
b. Cysts can withstand harsh environmental conditions.
i. Encased by a thick, protective cell wall.
ii. Metabolically “slow”/inactive.
iii. Resistant to standard chlorine concentrations used in water-treatment facilities. (kind of like a spore)

Front 19

Replication, epidemiology of Giardia lamblia

Back 19

1. use binary fission
Epidemiology

1. Giardia species have worldwide distribution
a. Typically found in streams, lakes, and mountain resorts.

2. The reservoir hosts are beavers & muskrats.
3. Organism may be acquired by:
a. Contaminated water (inadequately treated)
b. Contaminated, uncooked vegetables/fruits
c. Person-to-person transmission via fecal-oral route

Front 20

Pathogensis of Giardia lamblia
1. Transmission?
2. Attachment?
3. Steps in infection/life cycle

Back 20

1. Oral route of transmission by ingestion of cysts.
a. Both cysts and trophozoites can be found in feces and are infective.

2. Attachment in the intestine establishes infection.
a. Attaches to the intestinal villi with an adhesive disk.
b. Attachment causes localized mechanical tissue damage, which causes the disease giardiasis.

3. Steps of Infection/Life Cycle
a. Human ingestion of 10-25 cysts (from contaminated water/food)
b. Gastric acid stimulates excystation (transformation from cyst to trophozoite form)
c. Trophozoites multiply in the small intestine & live on the intestinal villi
d. Villi become flattened, but necrosis does not occur
e. Encystation occurs in the small intestine and cysts pass out of the body in feces

Front 21

What are some clinical findings of Giardia lamblia?

Back 21

1. Approximately 50% of infections are asymptomatic.
2. Symptomatic disease symptoms range from mild diarrhea to severe malabsorption syndrome.
3. Incubation period is approximately 1-4 weeks.
4. Characteristic symptom: sudden, foul-smelling, watery diarrhea.

Front 22

How is lab diagnosis made for Giardia?
2. Treatment
3. prevention

Back 22

. Laboratory Diagnosis
1. Stool samples are examined microscopically for the presence of trophozoites and cysts.
a. Giardia has a characteristic appearance.
i. Flagella are present, as are two nuclei with large central karyosomes, a large ventral sucking disk for attachment of the flagellate to the intestinal villi, and two oblong parabasal bodies below the nuclei.
ii. The morphology gives the appearance that the trophozoites are looking back at the viewer (looks like a face).

G. Treatment
1. Drug of choice is metronidazole.
2. Spontaneous recovery will occur in 10-14 days.

H. Prevention
1. Chlorine cannot kill Giardia, therefore filtration of the water supply is necessary.
2. Hand-washing will prevent the “outbreak” form of Giardia (person-to-person spread).

Front 23

Blood and tissue protozoa
What are some general characteristics?

Back 23

1. non-motile
2. acquire nutrients through simple diffusion
3. require 2 hosts
4. have sexual and asexual reproductive stages

Front 24

Malaria?

Back 24

caused by blood and tissue protozoa. Very complex life cycle, and different forms

Front 25

What are types of replication for plasmodium species?

Back 25

a. Schizogony: asexual reproduction
i. Occurs during human infections

b. Sexual reproduction
i. Can only occur within mosquitoes.
ii. Is necessary for the maintenance of malaria.

Front 26

Where can we find the following species of plasmodium?
a. P. vivax
b. P. ovale
c. P. malariae
d. P. falciparum

Back 26

a. P. vivax: tropics, subtropics, & temperate regions
b. P. ovale: tropical Africa (also Asia and S. America)
c. P. malariae: subtropical & temperate regions
d. P. falciparum: tropical and subtropical regions exclusively (responsible for majority of
deaths)

Front 27

How is plasmodium transmitted?

Back 27

1. through arthorpod vector, the Anopheles mosquito

Front 28

Describe the multiple steps in the infection/life cycle of the plasmodium.

Back 28

a. Sporozoites are injected into the blood by the mosquito.
b. Sporozoites enter the parenchymal cells of the liver.
c. Schizogony occurs during the “exoerythrocytic cycle.”
i. Can also have a dormant hepatic phase when the sporozoites do not divide (hypnozoites). They can become activated months or years later, leading to relapse.
d. Hepatocytes rupture leading to the release of merozoites.
e. Erythrocytic cycle begins when merozoites infect red blood cells.
i. attach to specific receptors on red blood cells (erythrocytes, RBCs)
ii. specific receptor is the Duffy blood group antigen
f. Asexual replication continues through a series of stages inside the RBC
i. Ring
** Following ring formation, some organisms will become male and female gametocytes
ii. Trophozoite (active metabolism and ingestion of host cytoplasm + digestion of
hemoglobin)
iii. Schizont (formed by multiple rounds of nuclear division).
g. Schizont ruptures and releases up to 24 merozoites from the RBC.
h. Merozoites can infect new RBCs, i

Front 29

Clinical findings, lab diagnosis, treatment and prevention of plasmodium species

Back 29

E. Clinical Findings
1. Symptoms are flu-like: headache, muscle pain, sensitivity to light, nausea, and vomiting.
2. Incubation period is ~2 weeks.
3. Characteristic symptoms include “paroxysms.”
a. increase of symptoms, sudden attack of pain, or periodic attacks of disease including chills, fever, sweating, shaking, malarial rigors
b. occur every 48 hrs (coinciding with blood stages and schizont rupture)
c. Cyclical nature of paroxysms is due to release of merozoites & toxic cellular debris into the circulation.

F. Laboratory Diagnosis
1. Microscopic examination of blood specimens.

G. Treatment
1. Combination of supportive and chemotherapeutic measures.
a. Chloroquine treatment is a common chemotherapy.

H. Prevention
1. Chemoprophylaxis in endemic areas.
2. Protection from mosquitoes: clothing, netting, repellents.
3. Control of mosquito breeding.

Front 30

Describe imortant factors of the enterobius vermicularis (pinworm)

Back 30

A. Important Properties/Structure
1. Eggs are 55 x 25 mm; worms are white and ~1 cm.

B. Life Cycle
1. Ingested eggs hatch in small intestine and larvae migrate to large intestine.
2. Larvae mature into adult male and female worms in large intestine.
3. After fertilization by males, female worms produce and deposit eggs on perianal skin (as many as 20,000!).
4. Eggs mature to infective form in a few hours. Autoinfection can occur.

C. Epidemiology
1. Transmission by ingestion of embryonated eggs (e.g. hand-to-mouth, via fomites,
inhalation and ingestion of egg-contaminated dust).
2. Immunity negligible.
3. Worldwide distribution, most common parasitic worm in U.S., especially in school-age
children.
4. Family usual unit of infection; institutionalized populations may have high rate.

D. Clinical Findings
1. Usually asymptomatic. In heavy infections or in sensitized persons, severe anal
itching associated with nocturnal migration of worms (enterobiasis). Itching may cause
insomnia/fatigue, seconda

Front 31

Descirbe the important properties and structure of Schisotosomes (helminths- trematodes)

Back 31

1. Cercaria is the infective form.
a. Released from snails, free-swimming, pentrate the skin.
i. NOT ingested via contaminated food like other trematodes.

2. Male and female worms can be distinguished by differing morphology.

Front 32

How do schisotosomes replicate?

Back 32

1. Cycles of sexual and asexual replication.
a. Adult worms produce eggs inside human hosts.
2. Eggs released into fresh water will hatch, releasing motile miracidia.
3. Miracidia invade snail hosts, where they replicate resulting in release of thousands of
infectious cercariae.

Front 33

What is the epidemiology of schisotosomes?

Back 33

1. Second most important parasitic infection following malaria; 200 million incident cases
per year.

2. Geographic distribution of Schistosoma species depends on the availability of a suitable
snail host.
a. S. mansoni is widespread: found in Africa, Saudi Arabia, Madagascar, Brazil,
Venezuela, and Puerto Rico.

3. Reservoir hosts include primates, marsupials, and rodents.

4. Humans come in contact with schistosomes via water (swimming, bathing).

Front 34

Describe the life cycles of schistosomes

Back 34

a. Schistosomes penetrate the skin, enter the circulation, and mature in the intrahepatic portal blood.

b. Adult worms in humans reside in veins and submucosal venules.
i. Worms migrate to different body sites depending on species.
ii. S. mansoni and S. japonicum are found in mesenteric veins draining the large intestine and produce intestinal schistosomiasis.
iii. S. haematobium is found in urinary bladder veins and causes vesicular schistosomiasis.

c. Eggs are produced once the worms reach their final locations, and are excreted in
feces or urine.
i. Example: S. mansoni eggs are moved progressively toward the lumen of the intestine and are eliminated with feces.

Front 35

Describe the clinical findings of schistosomes

Back 35

1. Allergic reactions & skin rashes at the site of penetration.

2. Katayama syndrome occurs concurrently with egg-laying.
a. Symptoms include fever, chills, cough, joint pain, skin rash, abdominal pain, and swelling of the lymph nodes and spleen.
b. Result of massive release of parasite antigens, leading to immune reactions and immune complex formation.
c. Occurs 1-2 months after infection and can persist for to 3 months or more.

3. Presence of eggs in tissues can lead to granuloma formation.
a. chronic, leads to scarring and permanent tissue damage

4. Excellent at immune evasion.
a. There is little host immune response to their presence in the blood vessels.
b. Chronic infections can last for 20-30 years.

Front 36

Describe teh treatment and prevention of schistosomes

Back 36

F. Treatment
1. The drug of choice is praziquantel.

G. Prevention
1. Control of snails and improved sanitation can help stop transmission in endemic areas.