Test 1 Study Guide

Question 1

Phoresies

Answer 1

“traveling together” or “to carry” A smaller organism, termed the PHORONT, is carried mechanically by a HOST

Question 2

Parasitism

Answer 2

Where one member, the PARASITE, lives in or on another organism, the HOST, at the expense of that organism.

Question 3

Commensalism

Answer 3

When one symbiont, the COMMENSAL, benefits and the other animal is neither helped nor harmed.

Question 4

Mutualism

Answer 4

Each member, a MUTUALIST, depends upon the other; obligatory or facultative.

Question 5

Intermediate host

Answer 5

Some development in host, but does not reach sexual maturity; often asexual stages.

Question 6

Definitive host

Answer 6

Host in which parasite reaches sexual maturity and reproduces.

Question 7

Reservoir host

Answer 7

Non-human animals that serve as sources of infection to humans.

Question 8

Protozoan structure and function of organelles.

Answer 8

Single cell, more than one nucleus

Glycocalx: glycoprotein surface coat that provides important binding sites to host cells and immunity.

Kinetoplast: The kinetoplast is a disc made of circular
mitochondrial DNA (kDNA) that exists near the
kinetosome of the kinetoplastids.

Dictyosomes: The golgi apparatus is a source of skeletal plates in some ameba and the microfilaments in microsporidian parasites.

Pellicle: In some references the pellicle is
defined as separate layer of microtubules found beneath the plasma membrane

Trichosomes:

Extrusomes: These are an unusual membrane bound organelles which originate in the dictyosome and come to lie beneath the cell membrane. When stimulated they fuse with the cell membrane and release their contents to the exterior.

Toxisomes: When the released material is a defensive toxin Extrusomes are named Toxisomes.

Kinetocysts: When used in food capture they are called kinetocysts.

Haptosomes: When the material is used to paralyze preys, Extrusomes will be called haptosomes.

Contractile vacuoles: Ingested food particles are passed to a food vacuole.

Axoneme: The axoneme arise from a kinetosome (basal body), which is similar to the centriole and lie
at the bottom of flagellar pocket or reservoir.

Ectoderm: The ectoplasm is in the gel state and functions in maintaining the shape.

Endoderms: The endoplasm is found in the sol (semiliquid) state, and contains the nucleus, mitochondrion and Golgi apparatus.

Locomotory organelles: Pseudopodia, flagella, and cilia. Flagella and cilia are called undulipodia.

Question 9

Structure and names of main kinetoplastid life cycle stages.

Answer 9

amastigote: The parasite is more spherical in shape and has no free flagellum. The kinetoplast is usually detectable as a darkly staining body near the nucleus.
promastigote: The kinetoplast is towards the anterior end and a free flagellum with no undulating membrane emerges.
epimastigote: The kinetoplast is more centrally located, usually just anterior to nucleus. The flagellum emerges from the middle of the parasite and forms a shorter undulating membrane than observed in trypomastigotes.
trypomastigote: The kinetoplast is located on the posterior end of the parasite. The flagellum emerges from the posterior end and folds back along the parasite’s body. This attachment of the flagellum to the body forms an undulating membrane that spans the entire length of the parasite and the free flagellum emerges from the anterior end.

metacyclic trypomastigote: Infective trypomastigotes.

metacyclic promastigotes: Infective promastigotes

LD bodies: Leishman-Donovan body. The intracytoplasmic, nonflagellated leishmanial form of certain intracellular parasites, such as species of leishmania or the intracellular form of Trypanosoma cruzi.

Question 10

Life cycle of Trypanosome parasites.

Answer 10

Trypomastigotes in blood

ingested by reduviids

migrate to posterior portion of midgut

divide by longitudinal binary fission as epimastigotes

8-10 days later, migrate to rectum and transform into metacyclic trypomastigotes

two routes of infection
during feeding, bug defecates to clear gut and parasites deposited on skin near bite; rubbed into wound by victim or infected bug ingested by vertebrate

binds to fibronectin receptors of phagocytic cells; engulfed, especially those of reticulo-endothelial system initially

transform into amastigotes
divide by binary fission, eventually destroying cell

cycle continues and disseminates throughout body as new cells engulf amastigotes

occasionally transformation in to trypomastigotes, which circulate in blood

Question 11

Life cycle of Leishmania parasites.

Answer 11

amastigotes in tissues and fluids in dermis

sandfly sucks blood and ingests amastigotes

within midgut, amastigotes transform into promastigotes and divide by longitudinal binary fission

move up to esophagus and amass

when sandfly takes another blood meal, infective stage is promastigote.

promastigotes ingested by macrophages and other phagocytic cells

transform into amastigotes

binary fission, destroying cell in process

Question 12

Vectors of Leishmania

Answer 12

Phlebotomine sandflies (Diptera: Psychodidae) are the intermediate host and the vector of the disease.

Question 13

Vectors of African Trypanosomes

Answer 13

tsetse fly (Glossina sp)

Question 14

Vectors of American Trypanosomes

Answer 14

kissing bugs (Hemiptera: Reduviidae)

Question 15

Etiological agents of East African Trypanosomiasis.

Answer 15

East African trypanosomiasis is caused by the parasite Trypanosoma brucei rhodesiense, which is carried by the tsetse fly.

Question 16

Etiological agents of West African Trypanosomiasis.

Answer 16

African Trypanosomiasis, also known as “sleeping sickness”, is caused by microscopic parasites of the species Trypanosoma brucei. It is transmitted by the tsetse fly (Glossina species), which is found only in sub-Saharan Africa.

Question 17

Etiological agents of American Trypanosomiasis.

Answer 17

Trypanosoma cruzi, is a parasitic protozoan that is the causative agent of Chagas disease (American trypanosomiasis).

Question 18

Etiological agents of mucocutaneous leishmaniasis.

Answer 18

L. braziliensis

Question 19

Etiological agents of cutaneous Leishmaniasis.`

Answer 19

L. mexicana complex
L. tropica
L.mjor

Question 20

Cell-mediated immunity

Answer 20

Cell-mediated immunity is an immune response that does not involve antibodies. Rather, cell-mediated immunity is the activation of phagocytes, antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen.

Question 21

Humoral immunity

Answer 21

Humoral immunity is the aspect of immunity that is mediated by macromolecules - including secreted antibodies, complement proteins, and certain antimicrobial peptides - located in extracellular fluids.

Question 22

Antigenic variation

Answer 22

Antigenic variation or antigenic alteration refers to the mechanism by which an infectious agent such as a protozoan, bacterium or virus alters the proteins or carbohydrates on its surface and thus avoids a host immune response, making it one of the mechanisms of antigenic escape.

Question 23

Diagnosis for Trypanosomiasis

Answer 23

Diagnosis is achieved by demonstration of parasites in smears of blood, lymph cerebrospinal fluid and fixed tissues.

Blood inoculated in animals and xenodiagnoses by lab reared triatomic bugs are also good routine diagnostic tools.

Complement fixation and other immunological tools are commonly used.

Question 24

Diagnosis for Leishmaniasis

Answer 24

Diagnosis is based on clinical examination and demonstration of parasites in lymph and bone marrow smears or spleen biopsies.

Serological methods, such as rK39 and DAT are useful in diagnosis.

Question 25

Symptoms of Trypanosomiasis.

Answer 25

Pathogenesis starts with an acute phase due to entrance of metacyclic trypanosomes into cells of subcutaneous tissue and spread of parasite to lymph nodes and formation of pseudocysts. The local inflammation at the site of parasite inoculation results in a red nodule called Chagoma. In 50% of cases inoculation occur in eye lid and conjunctiva, causing Romana sign. Pseudocysts rupture cause acute inflammation with degeneration and necrosis of nerve cells in the vicinity, especially ganglion cells. The symptoms of the chronic phase are due to central and peripheral nervous system dysfunction. Most serious is the loss of heart muscles tone, which result in cardiac death.

Question 26

Symptoms of Leishmaniasis.

Answer 26

The sores may start out as papules (bumps) or nodules (lumps) and may end up as ulcers (like a volcano, with a raised edge and central crater); skin ulcers may be covered by scab or crust. The sores usually are painless but can be painful.

Question 27

Treatments of Trypanosomiasis.

Answer 27

Due to intracellular location of the parasites, chemotherapy is still a major challenge for research.

Question 28

Treatments of Leishmaniasis.

Answer 28

Treatment by Pentostam (Sodium Stibogluconate) and Miltefosine.

Question 29

Vector control

Answer 29

Vector control is any method to limit or eradicate the mammals, birds, insects or other arthropods which transmit disease pathogens.

Question 30

Physical and Chemical Frist lines of Defense

Answer 30

The first line of defence (or outside defence system) includes physical and chemical barriers that are always ready and prepared to defend the body from infection. These include your skin, tears, mucus, cilia, stomach acid, urine flow, ‘friendly’ bacteria and white blood cells called neutrophils.

Question 31

Innate, humoral and cell-mediated immunity

Answer 31

Innate, or nonspecific, immunity is the defense system with which you were born. The humoral immune system deals with antigens from pathogens that are freely circulating, or outside the infected cells. Cell-mediated immunity occurs inside infected cells and is mediated by T lymphocytes.

Question 32

Blood immunity cells which cells are phagocytic which cells are responsible for acquired immunity

Answer 32

eosinophils, neutrophils, macrophages, lymphocytes, basophils, plasma cells which cells are phagocytic (neutrophils and macrophages) which cells are attracted to parasite infection sites (eosinophils) which cells are responsible for acquired immunity (B and T lymphocytes) T helper cells - they help activate B cells to secrete antibodies and macrophages to destroy ingested microbes, but they also help activate cytotoxic T cells to kill infected target cells.

Question 33

Lymphoid Tissue (Lymph nodes, Thymus, spleen, GALT, Tonsils)

Answer 33

Thymus - High growth and activity until puberty, then begins to shrink. Site of T-cell maturation Lymph nodes - Small, encapsulated, bean-shaped organs along lymphatic channels and large blood vessels of the thoracic and abdominal cavities Spleen - Nestled below the diaphragm and left of the stomach. Structurally similar to lymph node; filters circulating blood to remove worn out RBCs and pathogens GALT—gut-associated lymphoid tissue (Peyer’s patches)

Question 34

Signs and symptoms of inflammation

Answer 34

The blood at the site of wound clots. Seepage of plasma and migration of white blood cells out of blood vessels occur. The neutrophils are released into the wound site and vasodilation occurs. There is redness at the site of the wound.

Question 35

Pyrogen and fever

Answer 35

Fever is initiated by circulating pyrogens which reset the hypothalamus to increase body temperature; signals muscles to increase heat production and vasoconstriction

Question 36

Components of specificity and memory of Acquired immunity (T cells and B cells)

Answer 36

B (humoral immunity): activated B cells produce antibodies. T cells (cell-mediated immunity): activated T cells modulate immune functions and kill foreign cells.

Question 37

Antibody-Antigen Interactions: Agglutination

Answer 37

Agglutination – Ab aggregation; cross-linking cells or particles into large clumps

Question 38

Amneustic response

Answer 38

renewed rapid production of an antibody following second or later contact with the provoking antigen or with related antigens.

Question 39

Monoclonal antibodies

Answer 39

an antibody produced by a single clone of cells or cell line and consisting of identical antibody molecules.

Question 40

Artificial, natural, active, and passive immunizations.

Answer 40

Active immunity results when a person is challenged with antigen that stimulates production of antibodies; creates memory, takes time, and is lasting Passive immunity preformed antibodies are donated to an individual; does not create memory, acts immediately, and is short term Natural immunity acquired as part of normal life experiences Artificial immunity acquired through a medical procedure such as a vaccine

Question 41

Antibody-Antigen Interactions: Opsonization

Answer 41

process of coating microorganisms or other particles with specific antibodies so they are more readily recognized by phagocytes. Carried out by antibodies called “opsonins”

Question 42

Antibody-Antigen Interactions: Neutralization

Answer 42

Antibodies fill the surface receptors on a virus or the active site on a microbial enzyme to prevent it from attaching

Question 43

Antibody-Antigen Interactions: complement fixation

Answer 43

Activation of the classical | complement pathway can result in the specific rupturing of cells and some viruses

Question 44

Antibody-Antigen Interactions: precipitation

Answer 44

Aggregation of particulate antigen