Parasitology Quiz 1

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Parasite

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An organism that LIVES IN OR ON ANOTHER ORGANISM of a different species (host). It is metabolically dependent on the host during part or all of its life, and is usually harmful to the host.

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Parsitism

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A kind of SYMBIOTIC relationship between TWO DIFFERENT SPECIES of organisms in which one, THE PARASITE, IS METABOLICALLY DEPENDENT ON THE OTHER, the host, and lives at the expense of the host. There are degrees of parasitism: essentially harmless (= commensalism) to highly virulent.

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Facultative parasite

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An organism that is capable of living either a FREE OR PARASITIC EXISTENCE (e.g., the threadworm Strongyloides stercoralis in dogs or humans).

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Endoparasite

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A parasite that LIVES MAINLY INSIDE THE BODY of its host (e.g., hookworms).

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Ectoparasite

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A parasite that LIVES MAINLY ON THE SURFACE OF its host (e.g., fleas, ticks and lice).

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Helminths

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Roundworms or nematodes (e.g., ascarids) and flatworms (e.g., tapeworms or cestodes) and flukes or trematodes.

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Protozoans

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Single-celled, eukaryotic organisms (e.g., amoebae).

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Arthropods

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Organisms with exoskeletons (made of chitin) and JOINTED APPENDAGES (e.g., insects, arachnids, mites).

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Pseudoparasite

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An object (e.g., pollen) or nonparasitic organism (e.g., grain mite) that is mistaken for a “true” parasite.

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Host

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Living organism (e.g., animal, human) in or on which a parasite subsists, develops and/or reproduces.

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Definitive host

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An obligatory host in which a parasite develops to SEXUAL MATURITY.

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Intermediate host:

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An obligatory host in the life cycle of a parasite in which IMMATURE OR ASEXUAL STAGES UNDERGO ESSENTIAL DEVELOPMENT and/or proliferation before transmission to the definitive host (e.g., mosquito).

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Mechanical vector

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A nonessential host which passively carries infective parasite stages on its body; source of parasite contamination (e.g., boot, syringe).

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Biological vector

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Usually an arthropod (e.g., face fly); may be an intermediate host or a mechanical vector.

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Paratenic (or Transport) host

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A nonessential host, (e.g., rodents, roach), in the life cycle of a parasite capable of harboring and maintaining immature stages; PARASITES UNDERGO NO DEVELOPMENT OR PROLIFERATION WITHIN THESE HOSTS BUT ARE MERELY CARRIED WITHIN THE BODY UNTIL CONSUMED BY THE PROPER DEFINITIVE HOST.

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Reservoir host

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A population of infected hosts which serve as a potential source of infection for other species of susceptible domestic animals or humans (e.g., wild [feral] animals).

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Infective stage (Life Cycle)

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Developmental stage of the parasite capable of initiating a new infection within another host (e.g., eggs, oocysts, larvae).

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Direct life cycle

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Transmission of parasitic infection from one host to another WITHOUT THE REQUIREMENT OF AN INTERMEDIATE HOST; one-host life cycle.

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Indirect life cycle

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Transmission of parasitic infection from one host animal to another THROUGH ONE OR MORE ESSENTIAL INTERMEDIATE HOSTS; multi-host life cycle.

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Pre-patent period (Life Cycle)

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The time between ingestion and invasions of infective stages of a helminth parasite in its definitive host until eggs or larvae are first produced (e.g., the time between ingestion of infective L3 nematode larvae until the appearance of eggs in the feces).

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Patent period (Life Cycle)

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The life-span of the adult parasite in the host.

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Infection

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Establishment of a parasite within a host, with or without development of clinical signs; generally, ENDOPARASITES INFECT THEIR HOSTS (e.g., nematodes, cestodes and flukes).

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Infestation

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Establishment of a parasite on the surface of their host, with or without development of clinical signs. ECTOPARASITES INFEST THEIR HOSTS (e.g., insects and arachnids).

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Disease

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Clinical manifestations of infection or infestation.

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Acute disease

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Clinical infection by parasites characterized by rapid onset, large parasite numbers and usually dramatic clinical signs (e.g., anemia, death).

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Chronic disease

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Clinical infection by parasites characterized by slow debilitation, small to moderate parasite numbers, and clinical signs are usually slow in developing.

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Subclinical infection

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Parasite infection in which no clinical signs are manifested, however, evidence of parasitism may be detected by decreased growth, loss of production, etc. Many herd health parasitic problems are related to subclinical infections.

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How do parasites injure their hosts?

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They feed on blood, lymph, exudate or solid tissues; compete with the host for nutrition; they cause mechanical obstruction; they may produce pressue atrophy; destroy host cells by growing in them; they may produce toxic substances; they may produce host allergic reactions; they may promote the neoplastic transformation of cells; they may be biological vectors or intermediate hosts; contribute to decreasing the host’s immune system.

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Arthropods

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insects and arachnids

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Helminths

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roundworms and flatworms

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Protozoa

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protozoans

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Trophozoites (Protozoa)

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motile, feeding form; very fragile; MAY BE FREE-LIVING OR INFECTIVE STAGE (DEPENDS ON THE PROTOZOAN).

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Cyst (Protozoa)

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RESISTANT, RESTING, BUT INFECTIVE STAGE; may be multinuclear.

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Modes of feeding (Protozoa)

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Protozoan nutrition may be obtained from endogenous or exogenous sources.

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What are Protozoa classified by?

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THE ORGANELLES OF LOCOMOTION ARE THE BASIS OF CLASSIFICATION OF THE PROTOZOAN.

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Protozoa with flagella are the?
Cilia is what?

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flagellates (e.g., trichomonads, Giardia, etc.).
Cilia are simply small flagella that move in an oar-like manner (e.g., Balantidium coli).

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Protozoa with an undulating membrane are?

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trypanosomes, trichomonads

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Pseudopods

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"false feet" - they are temporary extensions of the cytoplasm (e.g., amoebae).

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Subpellicular microtubules

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cause movement by flexing and gliding (e.g., apicomplexans).

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Protozoan modes of asexual reproduction are? define? (3)

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1. BINARY FISSION - may be longitudinal or transverse.
2. MULTIPLE FISSION OR SCHIZOGONY - nuclear division precedes cytokinesis; cytokinesis results in the formation of many new organisms.
3. BUDDING - new organisms bud from the external surface of an existing parent organism.

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Protozoan modes of sexual reproduction are? Define? (2)

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1. CONJUGATION - temporary fusion of cells with nuclear exchange; newly formed organisms then divide by binary fission (e.g., Balantidium coli).
2. SYNGAMY - the union or fusion of sexually distinct gametes to form a ZYGOTE (OR OOCYST); (e.g., apicomplexans; macro & microgametocytes).

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Direct mode of transmission

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single host; NO INTERMEDIATE HOST REQUIRED.

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Indirect mode of transmission

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obligatory, multi-host; INTERMEDIATE HOST or (BIOLOGICAL VECTOR REQUIRED).

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Transport host mode of transmission

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NON-obligatory, multi-host

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Paratenic host

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active carriers

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Mechanical vectors

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passive carriers

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TRITRICHOMONAS foetus (Bovine Trichomoniasis, "Silent Calf Thief") is considered a protozoal parasite of? It is classified as?

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It is a protozoa of the REPRODUCTIVE TRACT. TRICHOMONADS ARE FLAGELLATES. Bovine Trichomoniasis is a reportable disease, with economic loss due to impairment of reproductive function.

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Trichomonad morphology

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CELL BODY IS USUALLY PYRIFORM

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Trichomonad Biology and Life Cycle

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The parasite LIVES IN THE PREPUTIAL CAVITY OF THE BULL. It has also been found in the urethra, testes, epididymis and seminal vesicle.
It LIVES IN THE VAGINA, UTERUS AND OVIDUCTS OF THE COW. Division is by longitudinal binary fission.
It is TRANSMITTED BY COITUS (DIRECT, SEXUAL).
THERE IS NO (RESISTANT) CYST STAGE.

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Clinical Features of Bovine Genital Trichomoniasis in the COW

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early abortion (3- 4 months of gestation)

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Clinical Features of Bovine Genital Trichomoniasis in the BULL

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The disease is usually asymptomatic in the bull. Occasional swelling of the prepuce accompanied by a mucopurulent discharge. INFECTED BULLS SHOULD NOT BE USED AS BREEDING ANIMALS. The prognosis for therapeutically clearing the chronically infected bull is GUARDED. Check with state authorities regarding importation/exportation regulations.

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Bovine Genital Trichomoniasis diagnosis

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Gel PCR assay and real-time PCR (false-positive results). It is recommended that a combination of culture and the gel PCR assay performed on 3 sequential scrapings (or washings) was the best method for identifying bulls that were carriers for T. foetus during an outbreak

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Bovine Genital Trichomoniasis Treatment/Control

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Artificial insemination for at least 2 years. Sexual rest (of cow) for 2 to 6 mo. if artificial insemination is not possible. Avoid the commingled grazing of infected w/ healthy (uninfected) herds. Cull bulls 3+yo. ALCIDE (lactic acid & chlorine dioxide) treatment is very labor intensive and difficult.

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Can you treat Bovine Genital Trichomoniasis with Metronidazole?

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No! THE EXTRALABEL USE OF IMIDAZOLE DERIVATIVES (I.E., METRONIDAZOLE) IN FOOD-PRODUCING ANIMALS IS STRICTLY FORBIDDEN.

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TRICHOMONAS gallinae (Avian Trichomoniasis; "Cankor" in doves/pigeons or "Frounce" in raptors) is considered a protozoal parasite of?

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PROTOZOA OF THE GASTROINTESTINAL TRACT

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Trichomonas gallinae Morphology & Life Cycle

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4 anterior flagella, NO CYST STAGE.

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Trichomonas gallinae mode of transmission?

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DIRECT TRANSMISSION; T. GALLINAE IS TRANSMITTED FROM ADULTS TO SQUABS IN PIGEON MILK PRODUCED IN THE CROP. IN OTHER BIRDS, T. GALLINAE IS TRANSMITTED BY FECAL-ORAL CONTAMINATION. The parasite may survive in contaminated water, food and bedding. During courtship, doves and pigeons have direct “bill to bill” contact during cross feeding and “billing” (touching of bills). Birds of prey contract an infection by consuming infected doves or pigeons.

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Clinical disease from Trichomonas gallinae?

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The disease usually affects YOUNG BIRDS; may be mild or rapidly fatal; weight loss, ruffled feathers and difficulty in breathing, mucoid nasal exudate; CASEOUS NECROTIC MASSES in upper digestive tract

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Trichomonas gallinae diagnosis?

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History, clinical signs, the location of the lesions and finding organisms in these lesions. Trichomonad organisms can be found in the saliva or in smears of the cheese-like necrotic lesions in the upper digestive tract. These samples must be collected within 48 hours of the bird’s death to be viable.

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Trichomonas gallinae treatment?

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Dimetridazole, enheptin, copper sulfate, carnidazole and metronidazole (Flagyl). SOME OF THESE MEDICATIONS ARE UNDER REVIEW AND SOME CAN BE SPECIFICALLY USED ONLY ON NON-FOOD BIRDS (METRONIDAZOLE). TREATMENT of wild birds is difficult because of the availability of natural food and water sources.

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HISTOMONAS meleagridis (HISTOMONIASIS; "BLACKHEAD DISEASE") is considered a protozoal parasite of? Classified as? Infects?

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PROTOZOA OF THE GASTROINTESTINAL TRACT. It is a flagellate parasite of turkeys, chickens and other gallinaceous birds. Economically important problem with range birds.

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Morphology of Histomonas?

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Histomonas is PLEOMORPHIC.
The AMOEBOID FORM IS FOUND IN THE INTESTINAL LUMEN.
In the TISSUES, it is found singly or in clusters and FLAGELLUM IS ABSENT.
TRANSITIONAL FORMS may be present in the lumen; enclosed in a dense membrane; both lumen and tissue forms die rapidly when exposed to outside temperatures.
There is NO EVIDENCE OF A CYST STAGE. A cyst stage has been produced experimentally in tissue culture (in vitro), with unknown infectivity.

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Histomonas meleagridis Life Cycle?

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DIRECT, BUT UNIQUE. INFECTION OCCURS VIA EGGS OF THE NEMATODE PARASITE, HETERAKIS GALLINARUM (CECAL WORM). Eggs of Heterakis containing Histomonas are passed in the vertebrate host's feces. Eggs develop on the ground to the L2 infective stage. The Heterakis egg is ingested, hatches in cecum where the histomonads are liberated.
Flagellated forms of Histomonas are in the cecal lumen. Heterakis nematodes ingest Histomonas, which may pass into eggs of the nematode. Flagellated forms lose their flagella, penetrate the cecal wall and pass to the liver.

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Histomonas meleagridis Clinical Disease?

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Virulence factors have been associated with clinical signs. The disease is most severe in turkeys; chickens are apparently less susceptible. Yellow droppings are characteristic of histomoniasis. Ruffled feathers, hanging wings and tail. The skin on the head may turn black ("BLACKHEAD") which is ASSOCIATED WITH SECONDARY BACTERIAL INFECTIONS (i.e., E. coli & C. novyi).

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Histomonas meleagridis pathology?

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The principle lesions are in the CECUM AND LIVER

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Histomonas meleagridis diagnosis and treatment?

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Diagnosis of histomoniasis is based on clinical signs, and on the presence of liver and cecal lesions.
Nitarsone (Histostat®-50), fenbendazole and metronidazole (non-food producing birds). Turkeys are treated during the early growth period (1st eight weeks). Chickens are usually not treated prophylactically except in areas where periodic outbreaks occur. Young birds should be reared above the ground on wire to control Heterakis. Piperazine or phenothiazine will eliminate Heterakis from infected birds. Separate chickens and turkeys.

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GIARDIA lamblia [syn = intestinalis, duodenalis] is a protozoal parasite of?

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PROTOZOA OF THE GASTROINTESTINAL TRACT. Most commonly diagnosed human intestinal parasite in public health labs in the U.S. (2-7%); 40% prevalence (developing countries). The geographic distribution is worldwide.

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Giardia lamblia hosts?

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Many mammals (rodents, ruminants, pigs, dogs, cats, beavers), INCLUDING HUMANS and birds. Reportable in 43 states [HUMANS ONLY]. People usually get Giardia from other people.

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Which Giardia lamblia assemblages are zoonotic?

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A1, A3, & B ARE ALL ZOONOTIC.

*A1 in humans, ruminants, cats, dogs, sheep
*A3 in wild hoofed animals, humans and cats
*B In humans, monkeys, guinea pig, rabbit and dogs
***A2, C, D, E, F, & G are NOT zoonotic assemblages***

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Giardia lamblia morphology? (2)

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TROPHOZOITE: fragile, motile feeding stage, pyriform-shaped, binucleate. Ventral adhesive disk; 2 MEDIAN BODIES; 4 pairs of flagella, and axonemes. Usually trophs are found in diarrhea (feces). This is the NON-INFECTIVE STAGE.

CYST: dormant, resistant stage MAINLY RESPONSIBLE FOR TRANSMISSION. Contains two “potential” trophozoites. Axonemes, 4 nuclei and fragments of the ventral disks can be seen. Cysts are usually found in formed feces.

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Giardia lamblia life cycle?

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The life cycle of Giardia is DIRECT, fecal-oral. NO INTERMEDIATE HOST. When a cyst is ingested, two trophozoites excyst in the duodenum and attach via their adhesive disks to the microvillus surfaces of epithelial cells of the duodenum, jejunum & ileum. Encystment occurs in the lower intestinal tract. FRESHLY PASSED CYSTS ARE INFECTIVE. Distribution in the intestinal tract varies according to the host and diet. Trophozoites divide by longitudinal binary fission every 12 hours. PPP is 6-8 days.

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Giardia lamblia clinical disease?

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The majority of infections are without clinical signs. There are no signs that distinguish giardiasis from other enteropathies. DIARRHEA IS COMMON DURING CLINICAL DISEASE. Feces are usually pale, greasy and mixed with mucus. The trophozoite damages the surface of the microvillus and causes crypt atrophy. “Sulphur” smelling feces and belching. The gallbladder may be affected. Weight loss, dry skin, and poor quality of hair coats, growth retardation, and borborygmi (abdominal sounds) upon abdominal auscultation. Diarrhea and chronic wasting has been reported in calves, lambs and goats.

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Giardia lamblia diagnosis?

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RECOVERY OF CYSTS (zinc sulfate flotation followed by iodine staining).
*DIRECT SMEAR (saline mount): Trophozoites can also be stained with trichrome or iron-hematoxylin.
*ENDOSCOPIC DUODENAL ASPIRATION
*ELISA & IFAT - cats & dogs

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Giardia lamblia prevention/control?

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Chemical treatment and filtration (4 µm or less filter); boiling water; good hygiene, wash fruits and vegetables before eating.

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Giardia lamblia treatment?

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TREAT ALL ANIMALS SIMULTANEOUSLY; BATHE AND MOVE THEM TO A CLEAN ENVIRONMENT (DOGS & CATS); REMOVE FECES PROMPTLY.

DOGS & CATS- Fenbendazole (Panacur), Metronidazole (Flagyl), Drontal-Plus, GiardiaVax, Nitroimidazole drugs like Tinidazole is 99% effective with a single dose; [Albendazole is not labeled for dogs and cats due to toxicity issues]

RUMINANTS - fenbendazole; [Remember metronidazole has been BANNED for use in ruminants!]

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ENTAMOEBA (Amebiasis; amoebic dysentery; E. histolytica) are protozoal parasites of?

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PROTOZOA OF THE GASTROINTESTINAL TRACT. Believed to affect ~ 1 billion people; 110,000 deaths/year. Important pathogens of humans, nonhuman primates and reptiles.

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Entamoeba histolytica affects which species?

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It is ZOONOTIC; affects various mammals including HUMANS (& NONHUMAN PRIMATES).

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Entamoeba invadens affects which species?

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It causes SEVERE DISEASE AND DEATH IN CAPTIVE REPTILES. More pathogenic in snakes and carnivourous lizards; usually nonpathogenic in herbivorous chelonians. Located in the intestine; sometimes in the stomach, liver, spleen, kidneys, and lungs.

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Morphology of Entamoeba histolytica trophozoites?

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10-60 µm; single nucleus with a distinct CENTRAL ENDOSOME; FOOD VACUOLES WHICH CONTAIN RBC'S IN THE PROCESS OF DIGESTION.

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Morphology of Entamoeba invadens trophozoites?

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9-39 µm; nucleus with CENTRAL ENDOSOME.

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Morphology of Entamoeba histolytica cysts?

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4 NUCLEI (CENTRALLY- LOCATED ENDOSOME); 5-20 µm in diameter. The cyst is the INFECTIVE STAGE; smaller than the trophozoite.

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Morphology of Entamoeba invadens cysts?

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9-24 µm; one to 4 nuclei with CENTRALLY-LOCATED ENDOSOME. The cyst is the INFECTIVE STAGE; smaller than the trophozoite.

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Entamoeba life cycle?

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DIRECT BY FECAL-ORAL CONTAMINATION. (PRECYST -> CYST -> METACYST -> METACYSTIC TROPHAZOITE)
- Ingestion of the cyst, cyst wall is digested in the small intestine releasing 4 motile, amoeboid trophozoites.
- E. histolytica resides in the crypts of the large intestine. Trophozoites divide by binary fission in the the crypts of the cecum and colon. Establishment of intestinal infection may be followed by invasion of other organs including liver, lung, and brain.

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Entamoeba clinical disease?

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E. histolytica and other amoebae appear to cause little if any harm to domestic animals. Trophozoites and cysts very frequently appear in fresh fecal smears of asymptomatic, healthy cattle, sheep, goats, horses, and swine. In the dog, E. histolytica localizes in the cecum. Occasionally invades the tissues and produces clinical signs of acute or chronic amoebiasis.

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Pathology and Pathogenicity of Entamoeba histolytica?

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In humans & nonhuman primates, lesions occur when trophozoites invade the cecal, colonic, or rectal mucosa. Ulcers are FLASK-SHAPED. Liver disease: ABSCESSES, contents are purulent & necrotic or sterile (no bacteria) and odorless. Life-threatening: pulmonary and CNS involvement.

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Diagnosis of Amoebiasis (Entamoeba)?

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- CYSTS ARE USUALLY SEEN IN FORMED STOOLS (zinc sulfate flotation/iodine stain) - not very sensitive technique. TROPHOZOITES ARE USUALLY SEEN IN DIARRHEIC STOOLS - not very sensitive.
- ELISA, IFAT, hemagglutination test, PCR & DNA probes; ELISA & IFAT (diagnosis of amoebic liver abscess and hepatitis).

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Treatment of Amoebiasis (Entamoeba)?

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Very little is known about the treatment of canine amoebiasis (metronidazole, 50 mg/kg for 5 days). Humans & nonhuman primates: metronidazole (Flagyl™). Cysts are resistant to water chlorination, but are rapidly destroyed by drying or deep-freezing. Cysts are rendered noninfectious by heating to 50 C for 5 minutes. Tetracycline, Tinidazole, and Fenbendazole are other treatment options.