[Discussion] MODULE 1 UNIT 3 Flashcards
often cause anemia
trypanosomiasis and malaria
can result in bowel obstruction
Ascariasis
can cause diarrhea
amoebiasis
balance between host and parasite is tipped in favor of the parasite
disease
balance shifts in favor of the hosts ability to inhibit the parasite, the it will be damaged and eliminated
parasite
- refers to the number of parasites in or on the host- determines the likelihood of the parasitic disease.
Parasite Load
- the greater the number of parasite infective stages that enter the host, the greater will be the pathological damage.
Parasite Load
- However, a few parasites that have reproductive phase within the host can also have a considerable effect on the host.
Parasite Load
- reflects the ability of a given parasite to infect a specific organ or sets of organs
Tissue tropism
- after entering the host, the parasite migrates to these parts of the body where conditions are suitable for temporary or permanent residence.
Tissue tropism
infecting all or most organs
tropic
to a given tissue or even to certain tissue niches
restricted
Human African trypanosomiasis (HAT) agents
T. brucei rhodesiense and T. brucei gambiense
parasite remains in the peripheral blood and lymphatic system
First stage of Human African trypanosomiasis (HAT)
parasite crossing into the cerebrospinal fluid and ultimately into the brain parenchyma
Second stage of Human African trypanosomiasis (HAT)
refers to the manner of development of a disease
PATHOGENESIS
robs the host of essential nutrients and substances
Infection
Depleting or denying the host of these leads to (?) and in the process causing damage to surrounding tissues.
malnutrition
- Effects of Malnutrition
stunted growth, wasting, hunger, or more specific signs of micronutrient deficiency.
is more likely to occur in individuals with larger burdens of parasites
Malnutrition
attach to the intestinal mucosa by means of teeth or cutting plates.
Hookworms
Aside from the bleeding at the site of attachment, these parasites ingest human blood, which results in irondeficiency anemia.
Hookworms
prevents absorption of nutrients due to it covering the intestinal mucosa
Giardia lamblia
Physical trauma, or destruction of cells, tissues or organs brought about by parasite attachment, feeding, blockage, or migration by is common in parasite infections.
Traumatic or mechanical damage
Enzymes elaborated by many parasites do not only make it possible for them to digest available food in the immediate environment and to transform this nutrient into their own protoplasm but also to degrade tissues or cells to promote invasion and spread of parasites.
Lytic necrosis
vigorous inflammatory response
shares some features with other infectious diseases,
unique aspects of pathophysiology
exacerbate the impact of systemic inflammation on individual organs
Malaria
normal secretions and excretions of parasites and the products liberated from dead parasites accumulate in the host tissues
Toxic and allergic phenomena
Parasites provoke tissue reaction that consists of cellular proliferation and infiltration at the site of the parasite and may involve increase in certain types of cells – lymphocytes, neutrophils, and macrophages.
Stimulation of host’s tissue reaction
consists of a cellular reaction to the presence of parasite which is eventually surrounded by epitheloid cells and multinucleated giant cells and as it dies off
Stimulation of host’s tissue reaction
is deposited within the cell
calcium
may block fluid flow and lead to necrosis of the surrounding tissues
calcium
A parasite may open pathways in the skin or gastrointestinal tract for the entry of other pathogens in the tissues.
Secondary invasion
In one documented case, a 3-yr old was found to have a co-infection of Ascaris lumbricoides as well as Vibrio cholerae
Secondary invasion
is a distinctive host response to parasitic infections - especially in helminth infections.
Eosinophilia
elevated serum IgE leve
Eosinophilia
Eosinophils and IgE play a critical role in
antibody-dependent cellular cytotoxicity (ADCC)
particularly important mechanism against parasites
antibody-dependent cellular cytotoxicity (ADCC)
This immunity with parasitic infections differ significantly from that in viral and bacterial infections.
Acquired immunity
is much less efficient and not absolute
Immunological protection against parasitic infections
more antigenically complex
Parasite host defense
factors contributing to Parasite HD
• Large size.
• More complex structure.
• Metabolic diversity.
• Complicated life cycle.
• Have evolved to be closely adapted to the host.
This immunity, either complete or partial, may be maintained only while the parasites are present.
premunition (or concomitant immunity)
parasites inhabit body sites that are inaccessible to immune response.
Seclusion
parasites persist in the lumen of the GIT, oral cavity, or urinary tract
Seclusion
Some parasites can avoid exposing themselves to immune response by becoming
intracellular
inhabit erythrocytes and are able to avoid the effect of antibodies.
Plasmodium spp.
Unless the integrity of the (?) is breached by injury or inflammation this barrier protects lumen-dwelling parasites, many of which are surrounded by a protective tegument, or (?), from most of the effective humoral and cellular immune mechanisms of the host allowing survival and the opportunity to reproduce.
intestinal mucosa
cuticle
Those that parasitize (?) possess mechanisms to avoid destruction.
macrophages
proliferate in macrophages in various organs because they are able to inhibit the fusion of lysosomes with the parasite-containing phagosome.
Amastigotes of Trypanosoma cruzi and Leishmania spp.
To avoid forces of immune response
Antigenic variation
It may occur with developmental changes in parasite.
Antigenic variation
It may occur with developmental changes in parasite.
Antigenic variation
Even more intriguing is the ability of some parasites to vary the antigenic characteristics of a
single developmental stage
A number of parasites are able to coat themselves with host molecules. In this way, they are able to hide their own antigenic surface from the immune system.
Antigenic disguise
- Resemblance between parasite antigen and host antigen
Molecular mimicry
Some parasites have the genetic information to synthesize antigens identical to those of its host.
Molecular mimicry
The larval stage of (?) in the hydatid cyst has been found to carry P blood group antigen
Echinococcus granulosus
can acquire antigenic molecules from the host.
tegument of Schistosoma spp. adult
Parasites produce substances that are transported to their tegument that mimic substances naturally found within the host.
Molecular mimicry
In this case the antigenic determinants of the parasite are so closely related chemically to host (?)components that the immunological cells cannot distinguish between the two and an immune response cannot be raised.
“self”
Parasites liberate antigenic surface components and, later, regenerating them.
Antigen shedding
The antigens shed are able to combine with and neutralize antibodies before they reach the target parasite.
Antigen shedding
Parasites can reduce the immune function by destruction of immunologic mediators.
Immunosuppression
this means that the host shows depressed immune responses to antigens in general, including those of the infecting pathogen.
Immunosuppression
produce anticomplementary chemicals
Tapeworm larvae
splits the Fc component of attached antibodies, rendering it incapable of activating complement
Trypanosoma cruzi
There are three complement pathways:
classic, alternative, and lectin
To avoid lysis, (?) relies on molecules which block the initial steps of classic/lectin or alternative pathways, and CRIT, T-DAF, CRP, and host-derived microvesicles that disrupt or block C3 convertase assembly.
T. cruzi
responsible for African sleeping sickness
induce polyclonal B-cell activation leading to the production of nonspecific immunoglobulins
eventual exhaustion of the antibody-producing capacity of the host
Trypanosoma brucei species
can absorb vitamin B12
Diphyllobothrium latum
concave on its ventral surface = suction
Giardia lamblia
cysteine proteinases (digest cellular materials and the mucosa of the large intestine) = ulcers and abscessed pockets
Host can resist the large symptoms if few in number
Entamoeba histolytica
found to carry P blood group antigen
Echinococcus granulosus
Lysis of the red blood cells in malaria
Plasmodium spp
inhabit erythrocytes and are able to avoid the effect of antibodies
Plasmodium spp
pass through several discrete developmental stages, each with its own particular
Plasmodium spp
can acquire antigenic molecules from the host
Schistosoma spp
may immunologically hide from the host by masking themselves with host blood group antigens and immunoglobulins
adult schistosomes
may cause urinary bladder cancer
Schistosoma haematobium
the migrating larvae may carry viruses and gram-negative bacteria from the intestines to the blood and tissues
strongyloidiasis, trichinosis, and
ascariasis
Bolus = intestinal/bowel obstruction
Amoebiasis
migrate and enter the appendix, ciliary and pancreatic ducts, or the common bile duct, perforate the intestinal wall, or may penetrate the parenchyma of the liver and even the lungs
Ascaris lumbricoides
responsible for African sleeping sickness
Trypanosoma brucei species
induce polyclonal B-cell activation leading to the production of nonspecific immunoglobulins
exhaustion of the antibody-producing capacity of the host
Trypanosoma brucei species
have the capacity to express more than 100 different surface glycoproteins
Trypanosoma brucei species
splits the Fc component of attached antibodies, rendering it incapable of activating complement
Trypanosoma cruzi
proliferate in macrophages in various organs
Trypanosoma cruzi and Leishmania spp
able to inhibit the fusion of lysosomes with the parasite-containing phagosome
Trypanosoma cruzi and Leishmania spp
produce anti-complementary chemicals
Tapeworm larvae
attach to the intestinal mucosa by means of teeth or cutting plates
Hookworms
iron-deficiency anemia
Hookworms
