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63 Terms
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African Sleeping Sickness
Phase IV: Caused by Trypanosomes.
severe headaches, emaciation, mental dullness, apathy (toxicity in spinal fluid causes lethargy), drowsiness/coma, death (heart failure, meningitis, misfortune, ect.).
Tryps never invade host cells, but damage them, host agglutinates (clump together) erythrocytes
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Pathogenicity
Is linked with the parasite's ability to evade nonspecific resistance mechanisms, specific acquired immune responses, and to prevent induction and expression of host immunity. (ex. Histomonas meleagridis and black head disease in turkeys and other domestic birds- causes sever necrosis in the liver and other submucosa tissue.)
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Glossina
Species of flies (tsetse) that transmits African trypanosomiasis.
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Waterbottom sign
Phase III: Large bulge at the base of the cervical spine. Caused by Trypanosomes collecting in lymph nodes and channels (lymph nodes enlarge). No cell invasion, but a proliferation of endothelial cells, leukocytes infiltrate; fever, headache, delayed sensation to pain, weakness. Duration of phase several years w/ *T. gambiense*; 4 mos. to 1 yr. w/*T. rhodesiense*
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Chagas disease
Transmitted through *T.cruzi* via African kissing bug*.* Wild and domestic animals serve as reservoirs. Has two phases the acute (Romana’s) and chronic.
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Romana’s sign
edema of eyelid/swelling of preauricular lymph nodes. Acute phase (invasion of cells/tissues) can be rapidly fatal, most common in young children, but disease may stay “dormant” for years and then show acute symptoms
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*Trypanosoma*
Parasitic in a species of vertebrates. Kineoplastides, unicellular, monophyletic.
*Trypanosoma brucei* - sub species *T. b. brucei*, *gambiense* and *rhodesiense.* (morphologically indistinguishable but present differently clinically). Can cause African Sleeping Sickness.
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Parasitism
The most common way of life on the planet. A relationship in which one of the species (the parasite), harms or lives at the host's expense ---> ex. tissue damage, causing an acute immune response, co-opting nutritive resources, etc.
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Hyperparasitism
When parasites have parasites.
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Endoparasite
An internally infective form (ex. cat tapeworm)
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Ectoparasite
An externally infective form (ex. fleas)
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Obligate Parasite
Must be parasitic to complete the life cycle (tapeworm)
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Facultative Parasite
Not normally parasitic, but may become so if they enter the host. (ex. The amoeba *Naegleria* *fowleri* normally found in ponds, can enter humans & cause death by massive brain destruction.)
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Accidental Parasite
Parasitic individual enters the "wrong" host; will not survive, but can cause damage to the "accidental" host. (ex. dog hookworm can cause cutaeneous larval migrans in humans (aka creeping eruption)
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Parasitoid
Immature insect species enter host, develop & feed on host, finally kill the host
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Definitive host
Host in which the parasite reaches sexual maturity & reproduces
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Intermediate host
A host is required for development ( ex. mice and squirrels in cat tapeworms)
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Paratenic/transport host
A host that may house a larval form of a parasite, transferred from its intermediate host, may function as an "ecological bridge." ( ex. thorny headed worm of owl develops to infective stage in insects. \*\*ex. the nematode species complex *Trichinella* *spiralis* can occur in almost any warm blooded vertebrate)
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Ecological niche
Can be measured by quantifying aspects of a habitat (multi-dimensional).
A parasitic species niche could consists of:
* where adult lives * where larval forms live * where dispersal stages exist (ex. ground, pond, stream, ect.)
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Relative density
Average number parasites per host in a single population (=the sample mean)
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Prevalence
Number of hosts in a sample parasitized by a single species.
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Macroparasites
(Tapeworms, nematodes) occur as aggregated (overdispersed) populations, not as normal (bell shape) distributions
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Overdispersed populations
Distribution pattern of macroparasites (tapeworms/nematodes)
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Microparasites
ex. parasitic protozoans; do not follow the macroparasite distribution patterns
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Transmission adaptations
ex. larvae of the trematode *Leucochloridium* (found in snails) are elongated and have pigmented brown and green bands, pulse, and look like caterpillars (and thus "tasty" to birds) the definitive host.
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Co-evolution
Process in which two species evolve in response to changes in the environment/ each other. Will influence each others fitness and evolution.
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Susceptible
Condition when host cannot eliminate parasite
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Antibody
Immunoglobulin protein that binds with an antigen. Made of: Four polypeptide chains (two “light” & two “heavy” chains). Variable regions at the end of each chain determine the antigen the antibody will bind with. Antigen binding is a PHYSICAL event, specificity akin to “lock and key”
The action of enzymes and substrate constant region of the heavy chain determines the CLASS of antibody.
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Innate defense
First line of defense, non-specific response, non-adapted
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Acquired immunity
Adapted immunity, immunity gained from the development of antibodies in response to antigen exposure.
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Immunodiagnosis
A variety of tests have been developed to use the host’s immune response as a method of diagnosis. (ex. ELISA)
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ELISA
Enzyme-Linked Immuno-Sorbent Assay
1. known antigen placed in a test well 2. potential host serum was added, then rinsed 3. enzyme-linked antibody added, then rinsed 4. enzyme-substrate added 5. if the enzyme binds to the substrate (pos. color test), there is an indication of antibody/antigen interaction
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Phagocytosis
Phagocyte cells eat/consume the invader. ‘Non-self’ method of recognition. Vertebrates possess both fixed (ex. macrophages) and mobile (ex. neutrophils, eosinophils, basophils & monocytes) phagocytes.
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Cytokine
Proteins important in immune cell communication & transportation.
Interleukin-1: produced by activated macrophages, involved in inflammatory responses and activation of T and B cells. IL- 4 & IL-6: growth factor for B cells
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Antigen
Foreign substance that stimulates immune response (commonly proteins). /Any substance that prompts an immune response.
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Trophozoite
Feeding, growing stage (vegetative), found generally in gut of host \*ectoplasm- thin, clear outer plasm \*endoplasm- granular, dense, has inclusions (food vacuoles, nucleus, organelles)
\*endosome is central part of the nucleus (a general term for aggregation of nuclear particles), structure differs among species (of taxonomic use)
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Cyst
A capsule-like sac or wall that encloses parasites in the dormant or infective stage.
They have a characteristic number of nuclei (ex. *Entamoeba* *histolytica* has 4, *E. coli* has 8)
Life cycle: trophozoites dwell in colon of humans (mainly), dogs, pigs, & monkeys, cysts survive in warm, moist environments, mature cysts include 4 nuclei (a metacyst)
Pathology: hydrolyzing of host tissue (intestinal lesions in cecum, appendix, & colon) form flask-like ulcers, potential penetration of sub-mucosa, muscle layers and serosa (perforated colon), blood transfer of amebas to ectopic sites (formation of secondary lesions, ex. on liver, lungs) dysentery dehydration (can alone be fatal)
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*Entamoeba* *histolytica*
Diagnosis: Demonstration of cysts or trophs in stools, immunological or liver tests, molecular ID tests.
Epidemiology: promotion of disease: bad water supplies (cyst can live up to a month in cool water), unwashed food, contamination by flies & roaches, use of human excrement as fertilizer
Treatment: Metronidazole (Flagyl) is drug of choice (but carcinogenic), tetracycline/diiodohydroxyquinoline also used, ornidazole and tinidazole cure liver abscesses
Prognosis: good- if treated
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Night soil
Human __excrement__ collected at night from buckets, __cesspools__, and __outhouses__ and sometimes used as manure.
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Zoonosis
Transmission of animal parasites to humans.
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Red Queen Hypothesis
Each species has to run (evolve) as fast as possible just to stay a float, because predators, competitors, and parasites continuously evolve. “resource competition”
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Immune evasion
A strategy used by pathogenic organisms and tumours to evade a host's immune response to maximize their probability of being transmitted to a fresh host or to continue growing, respectively.
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Genetic Arms Race
Many hosts (es. vertebrates) have sophisticated immune systems, thus strong selection was most likely a result of individuals that developed phenotypes for such immunological “weaponry.” (ex. different/ interesting methods of invasion/ infection) (ex. *Trypanosoma* *spp*. display a continuous variation of antigenic coats & as the host mounts antibodies against one, another proliferates)
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Monoxenous
One host (ex. amoebas)
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Heteroxenous
Two hosts (ex. human kinetoplasts)
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Pseudopod
A temporary protrusion of the protoplasm, as of certain protozoans, usually serves as an organ of locomotion or absorbing food. “false foot”
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Flagellum
A slender threadlike structure, especially a microscopic __appendage__ that enables many __protozoa__, bacteria, __spermatozoa__, etc. to swim.
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Reservoir host
The infectious agent in which the parasite normally lives/grows and multiples. May or may not be the transmission source. Can often show no symptoms.
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Undulating membrane
(in trypanosomes) holds flagellum in relatively fixed position.
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Kinetoplast
(unique to order Kinetoplastida) a single large mitochondrion, associated with kinetosome, contains own DNA
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*Giardia* *lamblia (Giardia* *duodenalis*)
“Beaver Fever,” lacks mitochondria, placed “between” prokaryotes & eukaryotes on the evolutionary tree.
Aerotolerant anaerobes. 2 nuclei, multi flagellated.
Life cycle: cyst ingested by host, mature cysts contain “twinned” flagellates, excystation in small intestine, reproduction by binary fission to AMAZING numbers (14,000,000,000 cysts released in a single stool sample), trophs can be found outside only in watery stools
Symptoms: mucus production, intense diarrhea, dehydration, intestinal cramping, fatty stools, loss of weight (parasite feeds on mucus secretions)
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Kinetoplastida
A group of flagellated protists belonging to the phylum Euglenozoa, and characterised by the presence of an organelle with a large massed DNA called kinetoplast.
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Amastigote
Flagellum very short, body small, diagnostic of *Leishmania.*
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Trypomastigote
Kinetoplast near posterior of body, flagellum placed along the surface of the body (undulating membrane), continuing free anterior to body, diagnostic of *Trypanosoma.*
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Epimastigote
Kinetoplast near posterior of the body, undulating membrane short, in the life cycle of *Trypanosoma*
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Promastigote
Flagellum placed and directed forward (“normal”), in the life cycle of *Leishmania*
Kinetoplast is anterior to the flagellum and no undulating membrane.
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*Leishmania donovani*
Causes kala-azar and Dum-dum fever.
Morphology: amastigotes of *Leishmania* spp. look similar (rounded, 2- 3 μm, w/ large nucleus & kinetoplast), test for id. may be serological or molecular.
Life cycle: sandflies (*Phlebotomus* spp.) arthropod host takes in amastigotes from an infected vertebrate---> transformation into promastigotes + multiplication in gut move anteriorly in fly- --> infected into new host---> engulfed by macrophage---> binary fission and host cell rupture ---> new cell infection
Pathology: destruction of phagocytic cells (tremendous amt. of cells produced to fight infection, the destroyed), damaged caused by secondary bacterial infections, enlargement of spleen & liver (hepatosplenomegaly, see Fig. 5.22!!), body emaciation, eventually, bone marrow function is lost, death if untreated (90-95% of cases)
Treatment: injection of antimony compounds such as Pentostam, but some strains may be resistant to drugs, plant derivatives may show promise (see pg. 79). Anti-leishmanial activity has been shown for plants of the dogbane family. Miltefosine reported to cure 98% of visceral leish cases, may also be effective against cutaneous forms.
Prognosis: good if drugs and care are given, incomplete treatment may lead to Post-kala-azar dermal leishmanoid some 2 to 3 yrs. after, condition responds to treatment.
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*Phlebotomus*
Transmittal sandfly species of *Leishmania*. Not all flies make good hosts
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Hepatosplenomegaly
Enlargement of both the liver and spleen
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Oriental Sore
Old World cutaneous *leishmaniasis*.
*Leishmania tropica/L. major-* Similar life cycle to L. donovani. Amastigotes reside in cells associated with skin near area of fly bite. Symptoms: small red sores, near the bite.
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Mucocutaneous Leishmaniasis
Lesion around mucus membranes, increases in size, and often leads to a disfigurement.