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Terms in this set (330)
Vehicles by which infections are transmitted from one host to another; organism (often arthropod) that transmit a pathogen from reservoir to hostVectorAnimal that is not the normal host of the parasite it is harboringAbberantSome parasites may develop on only one host; other may develop on multiple hostsHost specificityOne that lives *on* the surface of the host.EctoparasiteOne that lives internally *in* the host.EndoparasiteNot required to feed on host to survive; accidentalFacultative parasiteMust have host to live; cannot complete life cycleObligate parasiteInvades/obstructs tissues; bitesMechanical damageInterferes with metabolism; consumes food/nutrientsPhysiologic damageParasite completes entire life cycle in one host speciesDirect life cyclesMore than one host species is required to complete life cycle
*Usually 2 - 3 hosts*
- Definitive host
- Intermediate host
- Paratenic hostIndirect life cyclesPercentage of infected individuals in an area at a specific time (number of EXISTING cases divided by the TOTAL population)PrevalenceRate at which NEW infections are occurring in a population (number of NEW cases divided by the POPULATION AT RISK)IncidenceIllnessMorbiditysimultaneously illnesses
- MorbidityCo-morbidities_____________ can range from Alzheimer's disease to cancer to traumatic brain injuryMorbidities____________are NOT deaths. Prevalence is a measure often used to determine the level of morbidity in a populationMorbiditiesDeathmortalityNumber of deaths due to a disease divided by total populationMortality rateStudy of all ecologic aspects of a disease to explain its transmission, distribution, prevalence, and incidence in a population
*Host factors*
*Pathogen factors*
*Environmental factors*EpidemiologyAge, gender, and socioeconomic status are examples of ________ ________host factors2 types of pathogen modes of transmission are...?direct/indirectDo parasites have a common ancestor?noA _________ is any group of organisms that is given a formal taxonomic nametaxonWhat is binary Fission?One individual dividing into two"Opportunistic"-- Not normally a parasite (doesn't require a host to survive) but will become parasitic if opportunity arises.facultative parasiteWhat's the vector of African trypanosomiasis in Africa?Tsetse fly (Glossina spp.)A free living amoeba that causes Primary Ameobic Meningoencephalitis (PAM).Naegleria fowleri or Balamuthia mandrillaris"Living together"--close interrelationship b/t two different organisms for long periods of time.SymbiosisA host that serves as a source for the parasite to be transmitted to the usual host.reservoir hostA subspecies of *Trypanosoma brucei* that's zoonotic.T.b. rhodescienseCan cause disease in a host.pathogenIndicate the type of lesions(s) of *L. braziliensis*.mucocutaneousName the vector that transmits *Cutaneous Leishmaniasis* by *L. tropica*phlebotomus sand fliesVector of *Mucocutaneous Leishmaniasis* by *Leishmania brazilienes* in central and south america.Lutzomyia sand fliesMain route of *T. vaginalisis*sexual transmissionOne organism (parasite) benefits, and one organism (host) is harmed.parasitismCommon name of vector of Leishmaniasissand flyName 2 of the 3 distinguishing features of the trypomastigotes stage- free flagellum
- undulating membrane
- kinetoplastThe infective stage trichomonads.TrophozoiteIndicate the type of lesion(s) for *L. major*cutaneousIs the infective stage of Giardia lamblia.cystIs a blood and tissue flagellate that can be identified by an undulating membrane, anterior flagellum, and posterior kinetoplast relative to the nucleus. The onset of this disease occurs w/in weeks to months.Trypomastigotes of Trypanosoma brucei rhodescienseThe genus Trypanosoma during the trypomastigotes stage, the kinetoplast is located *(anterior/posterior)* to the nucleus.posteriorThe vector of Chagas' disease in the Americas.Kissing bug (triatoma spp.)Indicate the type of lesion(s) for *L. donovani.*visceralIndicate the type of lesion(s) caused by *L.tropica*cutaneousThe number of anterior flagella of *Pentatrichomonas homisis*5Indicate the type of lesion(s) caused by *L. mexicana*cutaneous*WHO AM I??*
- Single nucleus
- Single flagellum
- Heteroxenous
*During one stage of their lives they live in blood and/or tissues of vertebrate*
*During other stages they live in gut of bloodsucking invertebrates*
- Hemoflagellates
*Laboratory culture media require blood*TrypanosomesIn the initial stage of Trypanomiasis infection, where are trypanosomes found?trypanosomes are restricted to lymph and blood systemsIn the later stage of Trypanomiasis infection, where are trypanosomes found?seen in brain parenchyma and cerebrospinal fluidTrypanosomes are a group of ______________ _____________ distinguished by having one flagellum.
*All members are exclusively parasitic, found primarily in insects*kinetoplastid protozoa*WHO AM I??*
Parasitic protist species that causes *African trypanosomiasis (Sleeping Sickness) in humans* and *nagana in animals in Africa*Trypanosoma bruceiWhat are the 3 subspecies of *Trypanosoma brucei*?brucei
gambiense
rhodesienseWhat are the 2 hosts of *Trypanosoma brucei* ?Insect vector and mammalian hostIn Trypanosoma brucei, the bite of tsetse fly injects ________ ________.metacyclic trypomastigotesIn Trypanosoma brucei, metacyclic trypomastigotes become ________ _______.bloodstream trypomastigotesIn Acute T. brucei rhodesiense, Trypomastigotes are located in the _______ and _______.blood and lymphIn Chronic T. brucei gambiense,Trypomastigotes are located in the _______.CNSIn Trypanosoma brucei, the bite of tsetse fly ingest ________ ________.bloodstream trypomastigotesIn Trypanosoma brucei, trypomastigotes become __________ __________ in midgut.procyclic trypomastigotesIn Trypanosoma brucei, trypomastigotes leave midgut and
become ___________.epimastigotesIn Trypanosoma brucei, epimastigotes multiply (binary fission) in salivary glands and become _________ __________.metacyclic trypomastigotesDescribe the pathology of trypanosomiasis
T. b. gambiense and T. b. rhodesiense.*Chancre*
- Sore at bite site for 1-2 weeks
*Winterbottom sign*
- Swelling of posterior cervical lymph nodes in patients with African sleeping sickness
- Neck, groin, legs
*Cyclic feverish episodes*
- Increased parasite numbers and swelling
- Pain, weakness, headache, cramps
*Fevers last for up to a week*
*Asymptomatic episodes last for several weeks*
- A. Trypanosomal chancre on shoulder of patient with lymphangitis toward axilla
- B. Trypanosomal chancre on throat of patient
*Early (multiplication in lymph and blood)*
- Headaches, fever, weakness, pain in the joints, and stiffness* WHO AM I?* - typical sleeping sickness
- Apathy, mental dullness, lack of coordination
- Paralysis, convulsions
- Increasing sleepiness
- Coma, deathT. b. gambiense (chronic form)Rapid weight loss and death in a few months are associated with _________?T. b. rhodesiense (acute form)When diagnosing Trypanosoma brucei, you will often find tryopomastigotes in what places?Blood
Lymph
Cerebrospinal fluid (CSF)
Any body fluidWhen treating Trypanosoma brucei, what do you use for the early stage of *T.b. gambiense?*PentamidineWhen treating Trypanosoma brucei, what do you use for the early stage of *T.b. rhodesiense?*SuraminWhen treating Trypanosoma brucei, what do you use for the advanced stage of *T.b. gambiense and T.b. rhodesiense*MelarsoprolWhen treating Trypanosoma brucei, what is the only treatment available for the late stage of *T.b. rhodesiense?*MelarsoprolWhen treating Trypanosoma brucei, what is only used for treating advanced stage of the *T.b. gambiense* and not in treating *T.b rhodesiense (because it's ineffective)?*EflornithineWhat is the first line treatment for advanced stage *T. b. gambiense?*Combination of eflornithine and nifurtimoxCauses slow onset *chronic* trypanosomiasis in humans. Most common in *central and western Africa*, where *humans* are thought to be the *primary reservoir*
*WHO AM I?*T. brucei gambienseCauses fast onset *acute* trypanosomiasis in humans. Most common in *southern and eastern Africa*, where *game animals and livestock* are thought to be the *primary reservoir*
*WHO AM I?*T. brucei rhodesienseCauses animal *African trypanosomiasis*, along with several other species of trypanosoma. T. b. brucei is not human infective due to its susceptibility to lysis by human apolipoprotein L1
*WHO AM I?*T. brucei brucei*WHO AM I?*
- Thin blood film containing Trypomastigote stage:
- *"S" shape*
- Have small Kinetoplast near blunted, posterior end .
- Conspicuous undulating membrane with flagellum.
- One nucleus
- This is Dividing stage in definitive host.Trypanosoma b.gambiense & T.b. rhodesiense*WHO AM I?*
- Thin blood film containing Trypomastigote stage:
- Size range: 12-35 um long by 2-4 um wide.
- Shape: "C" or "U" in stained blood films.
- *Appearance: Long and slender*
- Nucleus: One, located anterior to the kinetoplast.
- Large Kinetoplast near the pointed posterior end.
- Inconspicuous undulating membrane.Trypanosoma cruziDescribe the signs of early stage of *Chagoma*Small red nodule at inoculation site with swelling of local lymph nodes
Usually on face or trunk
Several centimeters in diameter
Painful
Subsides in 2 - 3 months
*Contains tryposmastigotes*Describe Romana's sign- Edema of eyelid and conjunctiva
- Swelling of preauricular lymph nodes, usually unilateral
- Swollen lymph nodes in 3 days, contain amastigotesDescribe the symptoms of *late Pseudocysts*anemia, weakness, nervous disorders, chills, muscle / bone pain, heart failure, feverWhat happens due to chronic Pseudocysts?- Nervous system dysfunction leading to loss of muscle tone (cardiac, smooth)
- Heart failure - Cardiomyopathy, congestive heart failure - Enlarged, flabby heart
- Abnormal heart rhythm, shortness of breath, exercise intolerance
- Megaesophagus/megacolon
- Enlarged, flabby gastrointestinal tract
- Constipation, painWhat are Pseudocysts?Cyst-like pockets of amastigotes in muscle tissueWhat happens with rupturing pseudocysts?- Destruction of host cells
- Local inflammation
- Parasitemia
- Invasion of more host cellsELISA is a serologic tests used to diagnose chronic stages. What does it stand for?(enzyme-linked immunosorbent assay)IFAT is a serologic tests used to diagnose chronic stages. What does it stand for?(immunofluorescence antibody test)XenodiagnosisAllow parasite free vectors to feed on patient, look for trypomastigotes in vectorPhlebotomus spp. is found in the (old/new) world.oldLutzomyia spp. is found in the (old/new) world.newWhat are definitive hosts for Leishmaniasis?Humans
Dogs
RodentsWhat is the vector for Leishmaniasis?female sand fliesNagleria fowler is a free living amoeba which can__________?establish an infection in human host brainAll or part of the life cycle must be a parasitic relationship with a hostObligate parasiteNormal host is a different speciesIncidental (exotic) parasiteA definitive host does what?harbors sexual (mature) stages of parasite; if parasite undergoes sexual reproduction, it will occur in this hostHost that is required in life cycle of parasite; parasite undergoes some development in this host.Intermediate hostOrganisms that transmit parasites to a vertebrate host are called ________?vectorsBiological vectors are ____________?
Parasite must undergo some of its life cycle development in this vectorEssential to the life cycle completion of the parasiteWhat is the Sylvan cycle?a parasite cycles through its life cycle among wild animals normally
(man gets into the cycle accidently, usually)Infectious agent (parasite) that can be transmitted from animals to man is called _________?ZOONOSISWhat is the Urban cycle?A parasite cycles among domestic animals (and rats).
- Easy for man to get included in this cycle.What is a niche?Tissue site in host to which a parasite will locateWhat is host susceptibility?parasite can establish infection before host can eliminate itWhat is host resistance?host eliminates before parasite can establish infectionWhat is the ultimate goal of host-parasite relationship?survival of both host and parasite
-development of accommodation and tolerance between parasite and host which is co-evoulutionWhat is co-evolution?host and parasite have long, shared evolutionary history
-parasite benefits but does not usually kill the host
-- both host and parasite defense mechanisms are involved
--each is putting selective pressure on the otherWhen the host has low level of parasite infection (may be clinically undetectable)
-protects against challenge infectionpremunitionThe cause of a disease (can involve infectious agents, genetic factors, &/environment)EtiologyThe processes involved in the development of the diseasepathogenesisStructural alterations induced in the cells and organs of the bodymorphological changesCell proliferation caused by accelerating cell division (cell growth responds to normal cell growth controls).HyperplasiaIncrease in cell size (organ size) without an increase in cell numbersHypertrophyThe conversion of one type of tissue into another (is reversible)MetaplasiaTissue starts to grow abnormally. It is not an inflammatory response, is not required for tissue repair and does not respond to normal cell growth controls.NeoplasiaMalignant neoplasm is....?invasive and/or metastaticBenign neoplasm.....?remains localized with no invasion of adjacent tissuesWhat are lesions?"any pathological change in tissue"________ and _________ are not considered to be pathological changes in tissue.Hyperplasia; hypertrophyCan metaplasia result in a pathological change?YESIs neoplasia is a pathological change?YESAn _________ is multiplication of organisms inhabiting the body.infection__________ is characterized by presence of clinical signs/symptoms.diseaseIf something does not cause disease in host, it is....?non-pathogenicCan a non-pathogen still infect you?Yes, but it doesn't cause any harm, it just multipliesAre commensal organisms non-pathogenic?YESWhere can you find *Leishmania tropica* ?old world (Eastern Hemisphere)Where can you find *Leishmania major*old world (Eastern Hemisphere)Where can you find *Leishmania mexicana*new world (Western Hemisphere)How do *L. tropica and L. major* differ?Locality
Reservoir & intermediate hosts
LesionsA _________ boil is a cutaneous ulcer associated with L. tropica and L. major.JerichoWhat are some symptoms of Cutaneous Leishmaniasis
L. tropica and L. major?-Papule at bite site
-Develops into ulcers and sores
-Painless
-Ulcers heal in 2-12 months
-Leaves scar
-Secondary infectionWhere is *L. tropica* distributed?-Asia, Africa, Mediterranean, Russia
-Densely populated areasWhat is the definitive host for *L. tropica*?humansWhat is the vector for *L. tropica*?Phlebotomus sand fliesWhat are the reservoir hosts for *L. tropica*?-Dogs
-Foxes
-RodentsThe ulcer in *L. tropica* contains ________ amastigotes.manyThe ulcer in *L. major* contains ________ amastigotes.fewWhere is *L. major* distributed?Middle East, Russia, *Brazil*
Rural areasWhat is the definitive host for *L. major*?humansWhat is the vector for *L. major*?Phlebotomus sand fliesWhat are the reservoir hosts for *L. major*?RodentsWhere is *L. mexicana* distributed?Central and South America; North AmericaWhat is the definitive host for *L. mexicana*?Humans
Especially agricultural workersWhat is the vector for *L. mexicana*?Lutzomyia sand fliesWhat are the reservoir hosts for *L. mexicana*?Donkeys
Sloths
RodentsWhat kind of sore/ulcer is associated with *L. mexicana*?-Chiclero ulcer
-Bay sore
-Ear ulcersWhat is used to treat Cutaneous Leishmaniasis?-Antimonial compounds
-Paromomycin ointmentsWhen diagnosing Cutaneous Leishmaniasis, what are the differentials? What will you see after doing a Giemsa or Wright's stain of an ulcer sample?-Leprosy
-Tuberculosis
Amastigotes will be presentWhat is *Leishmania braziliensis* also known as?Espundia or UtaWhat is the definitive host of *Leishmania braziliensis*?humansWhat is the vector of *Leishmania braziliensis*?Lutzomyia sand fliesWhat is the reservoir host of *Leishmania braziliensis*?-Sloths
-AnteatersAlthough *Leishmania braziliensis* is difficult to treat, what is used to help control it?Antimonial compounds (made of the element antimony - toxic)
Pentamidine (anti-protozoal medicine)
(Amphotericin B)
(Topical paromomycin and imiquimod)When diagnosing *Leishmania braziliensis*, there will be a presence of __________ in the tissues.amastigotes*Leishmania donovani* is also known as?Dum-Dum fever and kala-azarWhat is the definitive host of *Leishmania donovani*?humansWhat are the spp. of *Leishmania donovani*?L. d. donovani
L. d. infantum
L. d. chagasiWhat are the reservoir hosts of *L. d. infant and L. d. donovani*?
Who is mostly affected?-Canids
-Porcupines
Children are affectedWhat are the reservoir hosts of *L. d. chagasi*?
Who is mostly affected?-Canids
-Felids
Children are affectedWhat is the vector of *Leishmania donovani*?-Phlebotomus spp
-Lutzomyia spp.Where are amastigotes found in *Leishmania donovani*?Macrophages, spleen, liver, lymph nodes, intestine, bone marrow (throughout body)For slower onset of *Leishmania donovani*, you will have....?Fever, malaise
Progressive wasting and anemia
Enlarged liver and spleen = protrusion of abdomen
Death (if untreated) in 2-3 yearsFor faster onset of *Leishmania donovani*, you will have....?Fever, chills, vomiting
Edema of face, bleeding of mucous membranes
Difficulty breathing, diarrhea
Death in 6-12 monthsIn *Leishmania donovani*, what are the blood producing organs and why do they produce?-Spleen
-Bone marrow
Produce macrophages to replace destroyed onesIn *Leishmania donovani*, what decreases resulting in Anemia and enlarged spleen and liver?RBC productionWhat is used in treatment of *Leishmania donovani*?-Antimony compounds
-MiltefosineTo diagnose *Leishmania donovani*, there would have to be ___________ present in the blood.amastigotes________ ________ has emerged as important opportunistic infection associated with HIVVisceral leishmaniasisIs the most common flagellate of human GI tract....*Giardia intestinalis**Giardia intestinalis* is also known as....?G. lamblia & G. duodenalisWho discovered *Giardia intestinalis*?Anton van LeeuwenhoekWhat are the 5 species of *Giardia intestinalis*?-G. duodenalis
-G. muris
-G. ardeae
-G. psittacii
-G. agilisWhat species of *Giardia intestinalis* is associated with mammals?G. duodenalis
G. murisWhat species of *Giardia intestinalis* is associated with birds?G. ardeae
G. psittaciiWhat species of *Giardia intestinalis* is associated with amphibians?G. agilisIn the evolution of *Giardia intestinalis*, it is considered to be the missing link between ________ and ________.prokaryotes and eukaryotesThe distribution of *Giardia intestinalis* is....?widespreadWhat are the routes of infection for *Giardia intestinalis*?oral(ingest cysts)
hands
fecal-oral
inanimate objects*This happens in Giardia...what is it called?*
Resorption of locomotor organelles
Adverse environmental conditions
-Low food
-Desiccation, low O2,pH
-Temperature change
-Osmotic change
Mechanisms
-Secretion of cyst wall
-Storage of food, e.g., glycogen, starch
-One or more nuclear divisions occurEncystment*This happens in Giardia...what is it called?*
Reactivation of metabolic pathways
Internal reorganization of organelles
Stimulated by a return to favorable environmental conditions
Re-form vegetative cell
Mechanisms
-Absorption of water
-Cyst swelling
-Secretion of enzymes by protozoan
-Action of digestive enzymes on cyst wallExcystmentIn *Giardia intestinalis*, ________ are found in feces at the diagnostic stage. They are responsible for transmission of giardiasis. This is an ineffective/resting stage.cystsCysts are infectious when passes...?in stool or shortly afterwardDuring excitation in *Giardia intestinalis*, each cyst produces how many trophozoites?2In *Giardia*, ________ are found in feces at the diagnostic stage. This is their active feeding stage.
*They multiply by binary fission* and remain in lumen of proximal small bowel (free or attached to the mucosa by a ventral sucking disk)
*Encystation occurs as parasites transit toward the colon*trophozoites*Giardia intestinalis* has what kind of life cycle?directWhat are the definitive hosts of *Giardia intestinalis*?mammalsWhat are the reservoir hosts of *Giardia intestinalis*?Beavers, dogs, cats, horses, humans, cattle, and birdsDescribe the morphology of trophozoites-Pyriform (pear shaped)
-2 nuclei with karyosomes
-8 flagella - 4 pairs
-2 median bodies
-Adhesive disc on ventral surfaceDescribe the morphology of cysts-8-12 μm long
-4 nuclei
-4 median bodies
-6 flagella (in mature cysts)The pathology of *Giardia intestinalis* includes...?-Enteritis
-Mechanical damage to intestinal villi
-Malabsorption
-Foul-smelling, clay-colored diarrhea, flatulence, abdominal cramps
-Increased mucous production
-Dehydration, weight loss
-Steatorrhea (malabsorption) with fatty stools
-Copious, light-colored, fatty
-Vitamin deficiencies
* Bloody stool, vomiting, fever ARE NOT SYMPTOMS!*When diagnosing Giardiasis, there will be ______ or ______ present.
__________ shed intermittently - must take several samples over a period of days.trophozoites or cysts
CystsWhat is used in treatment of *Giardiasis*?-Atabrine
-Metronidazole (Flagyl): Less toxic to childrenHOW MANY FLAGELLA FOR EACH TRICHOMONAD?
1. tritrichomonas
2. trichomonads
3. pentatrichomonas3
4
5Trichomonads have an ________ membrane. They also have an __________, which is a median tube-like organelle.Undulating; AxostyleWhat is the definitive host for *Trichomonas vaginalis*?human reproductive tracts
Females - vagina, urethra
Males - prostate, seminal vesicles, urethraTrichomonas vaginalis has a ______ life cycle.directTrichomonas vaginalis is primarily transmitted ___________, but can also be transmitted possible by artificial insemination or congenitally.
.sexuallyTrichomonas vaginalis is *extracellular* and has *NO __________ stage*.cystMost strains of *Trichomonas vaginalis* are (symptomatic/asymptomatic)asymptomaticWhat is used in treating *Trichomonas vaginalis*?Metronidazole (Flagyl)*Tritrichomonas foetus* life cycle is very similar to ________ ________.Trichomonas vaginalis*Tritrichomonas foetus* is distributed among the U.S. and ________.europeThe definitive hosts of *Tritrichomonas foetus* are...?-Cattle, horses, other large mammals
-CatsDescribe the morphology of *Tritrichomonas foetus*.-3 anterior flagella
-Undulating membrane
-Nucleus
-AxostyleWhen diagnosing *Tritrichomonas foetus*, there will be a presence of....?parasitesEntamoebidae includes...?Entamoeba
Edolimax
IodamoebaEntamoeba histolytica is of the Entamoeba species and has a __________ nucleus and small endosome near center.VesicularEntamoeba histolytica causes the disease __________.AmoebiasisEntamoeba histolytica evolved from eukaryotes and therefore has both flagellate & __________ stagesameboidEntamoeba histolytica is distributed worldwide especially in the....?tropical regionsMain route of transmission for Entamoeba histolytica is...?Mature cysts ingested in food, water, hands contaminated with fecesWhat are the reservoir hosts for Entamoeba histolytica?infected peopleWith the noninvasive infection of the Entamoeba histolytica life cycle, trophozoites...?remain confined to intestinal lumenWith the Intestinal disease of the Entamoeba histolytica life cycle, trophozoites...?invade intestinal mucosaWith the Extraintestinal disease of the Entamoeba histolytica life cycle, trophozoites...?Throughout the bloodstream
Liver, brain, and lungsE. histolytica and E. disbar are morphologically indistinguishable. So how can you tell the difference?erythrophagocytosis is observed.
That is, E. histolytica with ingested red blood cellsIn Entamoeba histolytica excystation, each cyst releases _____ trophozoites.4In Entamoeba histolytica, where do cysts migrate to?large intestineIn Entamoeba histolytica, cysts are passed by________.fecesIn Entamoeba histolytica, trophozoites are passed by________.fecesIn Entamoeba histolytica, trophozoites are found in _________ __________.diarrheal stoolIn Entamoeba histolytica, trophozoites multiply by _________ _________ and produce _________.binary fission; cysts(Asymptomatic/Symptomatic) carriers of Entamoeba histolytica shed cysts infective to others/remain in lumenasymptomatic(Asymptomatic/Symptomatic) carriers of Entamoeba histolytica get Colitis, Diarrhea, abdominal cramps, nausea, fatiguesymptomaticWhat are Amebomas and what are they associated with?Granulomas containing trophozoites
-Associated with Entamoeba histolytica dysenteryThe pathology of Extraintestinal amoebiasis include what?
Try to be specific..-Amoeba digest intestinal wall, enter circulation
-Hepatic (liver)
◦More common
◦Abdominal tenderness, enlargement
◦Abscesses (may rupture)
Usually one in right lobe
-Extensive
-Copious purulent exudate
◦Fever, weight loss, severe continuous pain
◦Liver abscess (gross pathology)What is used in the treatment of Entamoeba histolytica?Metronidazole (Flagyl)What are at least eight amoebas live in human intestinal lumen?E. histolytica
E. dispar
E. moshkovskii
E. coli
E. hartmanni
E. polecki
Iodamoeba bütschlii
Endolimax nanaWho Am I?
-Also known as N. aerobia
-Primary Amoebic Meningoencephalitis (PAM)
-Free-living amoeboflagellateNaegleria fowleriWho is at risk for Naegleria fowleri?Young, active peopleWhen diagnosing Naegleria fowleri, there are signs of acute meningoencephalitis as well as trophozoites that are found in...?cerebrospinal fluid (CSF) and brain tissueWhat is used in treating EARLY Naegleria fowleri?Amphotericin B
Fluconazole
RifampicinIodamoeba buetschlii affects who?people, pigs, monkeysBalamuthia mandrillaris is a ________ parasite and moves by means of ____________.facultative;pseudopodsBalamuthia mandrillaris causes what diseases?PAM and Granulomatous amebic encephalitis (GAE)Balantidium coli is an example of a...?ciliateDescribe Balantidium coli morphology, etc.Morphology - largest protozoan parasite of humans
-Trophozoites are oblong, spheroid, or more slender, 30 μm to 150 μm long by 25 μm to120 μm wide
-Lives in the cecum and colon of humans, pigs, guinea pigs, rats, and many other mammals
-Not readily transmissible from one species of host to another
-Trophozoites multiply by transverse fission
Encystment caused by dehydration of feces
Parasite is very similar to Entamoeba histolyticaElaborate on the pathogenesis of Balantidium coli.-Ingests particles through a vestibulum and cytostome
-Produce proteolytic enzymes that digest away a host's intestinal epithelium
-Ulcers:flask shaped, like amebic ulcers
-Produce necrosis and sloughing of the overlying mucosa
-Urogenital organs are sometimes attacked
vaginal
Uterine
bladderWhat is used in the treatment of Balantidium coli?Carbarson
Diiodohydroxyquin
TetracyclineApicomplexa:
1.____________
2.___________
3.___________Apical complex
All are parasitic
No cilia or flagella (except for some flagellated microgametes)What are the 2 classes of Apicomplexa?Conoidasida and Aconoidasida.Conoidasida contain...?Sporozoites that have conoidsAconoidasida generally lack conoids but have...?-Malaria parasites
-Piroplasms_____________ parasitize invertebrates
-Primarily annelids and arthropods
-CryptosporidiumgregarinesCoccidia includes ___________, ____________, and ____________.Isospora
Sarcocystis
ToxoplasmaList 4 Plasmodium spp.Plasmodium vivax
Plasmodium ovale
Plasmodium falciparum
Plasmodium malariaeCryptosporidium parvum is a major problem for who?immunocompromised individuals, e.g., AIDS, cancerBriefly explain the life cycle ofCryptosporidium parvum-Prepatent period
-Oocysts (thin or thick-walled)
-Thin-walled oocysts can sporulate and excyst in host intestinal lumen
*Autoinfection*
-Thick-walled oocysts
Ingested
Sporulated
Released in feces
No sporocysts
4 sporozoites
-Oocysts are swallowed
Excyst in intestine
Sporozoites infect epithelial cells
Intestines
Respiratory
-Merogony
-Meronts produce 8 merozoites
-2 generations of merogony - cell death
-Microgamonts:Produce 16 microgametes
-Gametogony
-ZygoteRoute infection for Cryptosporidium parvum?fecal-oralHost range for Cryptosporidium parvum?humans/other animalsCryptosporidium parvum oocysts are....?Sporulated
Released in feces
No sporocysts
4 sporozoitesCryptosporidium parvum diagnosis will have...?parasites presentIsospora
Toxoplasma
Sarcocystis
Are examples of...?coccidiaCoccidian Oocysts contain ___________ and are produced by sexual reproduction.sporocystsSporocysts contain ________. They are involved wth transmission to the host. Their infective stage is housed n the oocyst,sporozoitesMerozoites are produced by __________ reproduction (______________/_______________) and are
Housed in (______________/______________).asexual; merogony/schizogony
-meronts/schizontsInfected people shed _______________ Cyclospora cayetanensis oocysts in their stool.
Immature oocysts usually require at least one week under favorable laboratory conditions to sporulate (become infective).unsporulated (non-infective; immature)Cystoisopora belli has a _________ life cycle. Briefly explain it.Direct;
-Ingest sporulated oocysts
-sporozoites enter intestinal cells
-Undergo merogony (make merozoites)
-Undergo gametogeny (make big and small gametes)
-Fertilization - (zygote/oocyst forms)
-Oocyst passed in feces (unsporulated)What is the definitive host of Cystoisopora belli?humans; small intestinal cellsCystoisopora belli is an _________ parasite and its Oocysts has
___ sporocysts with ___ sporozoites each.intracellular; 2, 4What is used when treating Cystoisopora belli?Trimethoprim/ sulfamethoxazoleCystoisosporiasis (formerly known as isosporiasis)
Instestinal disease of humans. What is its etiologic agent?
What does this Oocyst look like?Cystoisospora belli
Oocyst has two mature sporocysts containing sporozoitesWhat are the definitive hosts of Toxoplasma gondii?Felids (domestic and wild) CATS!
-Ingest bradyzoites in tissue: most common
Ingest oocystsWhat are the intermediate hosts of Toxoplasma gondii?Humans, mammals, birds
Wild and domestic animals
-Ingest oocysts
Ingest bradyzoites in meat
Transplacental/transmammary transfer of tachyzoitesTransplacental host of Toxoplasma gondiiMother infected; recovered before becoming pregnant
No transmission to fetus
Infection in first trimester
More pathology
Infection in third trimester
Higher transmission rateWhat are the transmission routes of Toxoplasma gondii and what do they transmit?fecal-oral: ingestion of oocysts
predation: bradyzoites
transplacental: tachyzoites
transmammary: tachyzoitesDescribe the stages of acute tachyzoite in Toxoplasma gondii.-Rapidly dividing tissue stages found in all vertebrate hosts
-Invade & multiply asexually within cytoplasm of any nucleated cell
-Can become systemic
-Transmammary
-Transplacental
-Can be found throughout body
-Blood, peritoneum, milk
CNS, skeletal and cardiac muscle
Liver, lungs
Fetus, placentaDescribe the stages of chronic bradyzoite in Toxoplasma gondii.-Slowly dividing, encysted tissue stages found in all warm-blooded vertebrate hosts
-Dormant encysted stage (not an oocyst)
-Can be found in eye, brain, muscle, liver, retina- form tissue cystWho is at risk of getting Toxoplasma gondii?-Baby by way of pregnant woman
-Butchers
-People who eat undercooked meat - esp. pork and lamb, but also beef
-Gardeners
-Immunocompromised people (AIDS, cancer)Acute Toxoplasma gondii infection in humans includes...?Tachyzoites spread to other sites
Prefer: nervous cells (CNS, eyes) and muscle cells (skeletal, smooth)
Fever, headache, muscle pain, anemiaToxoplasma gondii chronic Infection usually happens in an _______ host.intermediateWhat happens in Toxoplasma gondii chronic Infection? Do people know they're infected? What are the signs/what do the depend on?-Immune system slows the proliferation of tachyzoites
-Tachyzoites encyst as bradyzoites (tissue cysts)
-Tissue cysts can persist for years and have no clinical signs
-People don't know they are infected
-Signs depend on site of tissue cyst
CNS - encephalitis
Retina - blindness
Liver - hepatitis
Heart - myocarditis
Uterus/fetus - range of signsToxoplasma gondii Congenital Infection: Mother has acute infection. What does this mean?
What does it result in?Tachyzoites in blood at the time of conception or during pregnancy
-Passed through placenta
-Form tissue cysts, especially in brain/retina
Results stilbirth, Hydrocephalus
Intracerebral calcification
Retinochoroiditis
Retina damage
Inflammation of retina and choroid (vascular layer)
Mental retardation
*Most congenital infections are asymptomatic*What is used in treating Toxoplasma gondii?Combo of pyrimethamine and sulfonamides
SpiramycinWhat are the definitive host of Sarcocystis cruzi?dogs/carnivoresWhat are the intermediate host of Sarcocystis cruzi?herbivoresThe oocysts of Sarcocystis cruzi are (thin/thick) walled? And produce how many sporocysts with how many sporozoites?thin
2;4Briefly describe the life cycle of Sarcocystis cruzi in carnivores.-Dogs eat sarcocysts in IH
-Bradyzoites released
-NO merogony
-Gametogony and fertilization in small intestines
-Thin-walled oocysts sporulate in small intestine
-Oocyst wall breaks down
-See sporocysts in fecesBriefly describe the life cycle of Sarcocystis cruzi in herbivores.-Cattle ingests sporocysts
-Sporozoites released, infect endothelial cells of various organs - usually blood vessels (extraintestinal)
-4 generations of merogony, produce merozoites
-Stage 4 merozoites enter muscle (cardiac, skeletal), become metrocytes ("mother cells")
-Metrocytes divide asexually - form sarcocyst
-Eventually form bradyzoites within sarcocysts
-Cysts mature in 2-3 monthsBriefly describe the life cycle of Neospora caninum.Transplacental -Tachyzoites, from mother to fetus
-Oocysts shed by definitive hosts
-Canids eat tissues of intermediate hosts with bradyzoites
Activated in gut
Produces oocysts
Excretion in feces
-Cattle ingest oocysts (feed or pastures)Briefly describe the pathology of NeosporosisProliferation of tachyzoites within tissues
Leads to inflammation, granulomata formation, and necrosis
Tachyzoites present within many tissuesThe life cycle of plasmodium is (direct/indirect)?indirectWhat is the definitive host (sexual reproduction) of plasmodium? Give an example.invertebrate animals
-spp Anopheles spp. (mosquito)What is the intermediate (asexual reproduction) of plasmodium?vertebrate animalsPlasmodium _________ and P. _______
Dormant stage (_________) may persist in liver
-Causes relapses by invading bloodstream weeks, or even years latervivax;ovale;hypnozoites__________ are a sudden attack or increase of symptoms of a disease (such as pain, coughing, shaking, etc.) that often occurs again and again.Paroxysms__________ is an early symptom (or set of symptoms) that might indicate the start of a disease before specific symptoms occur.ProdromeCaused by destruction of infected and uninfected RBC
Inability to use iron in hemozoin
*Lack of erythropoietic response*
Coagulopathy - affect clotting ability - uncontrolled bleedingAnemiaDescribe the Cold Phase in plasmodium.Cold Phase (chills)
Feeling of intense cold
Rapid rise in body temp (104-106 F)
Teeth chatter, bed rattles from shivering
Nausea and vomiting
Pale skinDescribe the Hot Phase in plasmodium.Hot Phase (fever)
Begins 30-60 minutes after cold phase
Intense headache
Feeling of intense heat
Flushed skin
Mild delirium
Copious perspiration - signals end of episode (normal temp 2-3 hours later)Describe the Relapse stage in plasmodiumHypnozoites (dormant schizonts) in liver cells remain dormant for years; can release merozoites months or years laterWhat are the 3 types of malaria?*Benign tertian (P vivax and P oval)* with a fever every 2nd day (e.g., Monday; fever, Tuesday; no fever, Wednesday; fever)
*Benign quartan (P malaria)* with a fever every 3rd day (e.g., Monday; fever, Tuesday; no fever, Wednesday; no fever, Thursday; fever)
*Malignant tertian* (P falciparum), in which the cold stage is less pronounced and the fever stage is more prolonged and intensified (if the fever is recurring it occurs every 2nd day)____________- the infection recurs from persistent blood stages of the malaria parasite.
Higher levels of parasitemia than other speciesRecrudescencesPlasmodium falciparum Acute malaria. What happens?Trophozoites produce certain proteins
Cause deformations of RBC membrane called knobs
Knobs cause RBCs to adhere to vein endothelium
Result
Only see ring stages or gametocytes in blood (gametocytes produce no knobs)
May prevent clearance of infected RBCs by spleen
Infected RBCs form rosettes
Infected RBCs may bind to uninfected RBCs
Clog venues
Recrudescences
Small populations of parasites remain in RBCs
JaundicePlasmodium falciparum Severe malaria. What happens?Cerebral Malaria
Gradual or rapid onset
Headache followed by coma
Uncontrollable rise in body temp (108 F and above)
Psychotic symptoms
Convulsions
*Death*
*Severe anemia*
Shock
Impaired consciousness
Respiratory distress
Mechanism
Spleen removes infected and uninfected RBCs'
Body cannot use iron in hemozoin
Bones cannot keep up with RBC production - inadequate erythropoietic response
*ErythropoietinWhat are some complications of Plasmodium falciparum?*Algid Malaria* - a form of falciparum malaria chiefly involving the gut and other abdominal viscera; gastric algid malaria is characterised by persistent vomiting; dysenteric algid malaria is characterised by bloody diarrheic stools in which enormous numbers of infected red blood cells are found.
Shock = low blood pressure
Circulatory system collapse
Constricted veins
Cold and clammy skin
Pulmonary edema
Blackwater FeverMost common cause of malaria
Found in subtropical and temperate areas of the worldP vivaxCause relapsing malariaP vivax and P ovaleFound in tropical regions
Causes most severe and fatal diseaseP falciparumLimited entirely to subtropical regions
Less common than P falciparum or P vivaxP malariaeLeast common malarial species
Endemic in AfricaP ovale_________________ - Any of the fine, round, uniformly red or red-yellow staining dots occurring in red blood cells infected withPlasmodium vivax or P. ovale. Also called Schüffner's granule.Schuffner's dots______________- a disposal product formed from the digestion of blood by some blood-feeding parasites, e.g., hematophagous organisms such as Malaria parasites (Plasmodium spp. )Hemozoin____________- Exoerythrocytic schizozoite of Plasmodium vivax or P. ovale in the human liver, characterized by delayed primary development; thought to be responsible for *malarial relapse*.HypnozoitesWhat is used in treating P. vivax and P. ovalePrimiquine
ChloroquineWhat is used in treating P. malariae?ChloroquineWhat is used in treating P. falciparum?ArtemisininWhat prophylactic treatments are used on Plasmodium spp.?-Artemisinin
-MefloquinePrimaquine is used to treat_______ and is effective against all forms and species of Plasmodium.hypnozoites___________ is effective for Chloroquine resistant strains.
Neurotoxic at high doses and prolonged exposureArtemisinin___________- A state of existing resistance of a host to infection or reinfection with a parasite; used especially in malaria epidemiology.Premunition(Recrudescence/Relaspse)???
P. ovale
P. vivax
P. falciparum
P. malariaerelapse
relapse
recrudescence
recrudescenceCaused by single amino acid mutation (valine instead of glutamate at the 6th position) in beta chain of hemoglobin geneSickle cell geneSickle cell diseaseInheritance of mutated gene from both parentsHaemoproteus columbae and Leucocytozoon spp. are examples of...?AVIAN MALARIADefinitive host of Haemoproteus columbae?
Intermediate host of Haemoproteus columbae?Hippoboscidae spp. (Flies)
PigeonsDefinitive host of Leucocytozoon spp.?
Intermediate host of Leucocytozoon spp.?Simuliidae (Black Flies)
Many birdsBabesia microti - Life cycle:
Talk to me...Definitive host: *Tick (Ixodes)*
-Life cycle involves 2 hosts, rodent (primarily white-footed mouse, Peromyscus leucopus)
-During blood meal, Babesia-infected tick introduces sporozoites into mouse host
-Sporozoites enter RBCs; undergo asexual reproduction (budding)
-Once ingested by tick , gametes unite and undergo sporogonic cycle resulting in sporozoites
-Transovarial transmission
-Humans enter cycle when bitten by infected ticks
-During blood meal, a Babesia-infected tick introduces sporozoites into human host
-Sporozoites enter RBCs; undergo asexual replication (budding)
-Multiplication of blood-stage parasites responsible for clinical manifestations of disease
-Humans usually dead-end hosts
-Human-to-human transmission well recognized via contaminated blood transfusionsBabesia bigemina - Texas Cattle fever:
Definitive host?
Intermediate host?Definitive host: Boophilus annulatus tick (Ixodes spp)
Intermediate host:
Ruminants
Primarily cattle
Deer, water buffalo
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