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Parasitology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Parasitism is literally defined as

A

Two organisms traveling together

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2
Q

Commensalism

A

The “host” is neither harmed or helped

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3
Q

Parasitism

A

Metabolic dependency of one organism (parasite) upon a second organism (host); sustenance (nutrition), survival, maturation, and reproduction

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4
Q

Parasite - shelter requirement

A

Stable environment & protection from competition & predation by other organisms

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5
Q

Do parasites live at the measurable expense of the host?

A

Yes; hematocrit, fecundity, BCS (lack of feed), feed efficiency, and time to conception

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6
Q

Is disease resulting from this association? Primary or secondary?

A

Secondary; parasites exist to perpetuate the species in space & time

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7
Q

Subject to all constraints (fitness) of evolutionary biology

A

Parasites that kill their host MUST fine a way (ADAPT) to be successful & overcome the “fitness cost”

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8
Q

How is fitness characterized by a parasite’s ability?

A
  • Colonize/become established in host
    -Ability to resist environmental stresses; drug resistance & seasonal climatic extremes
    -Survive host defenses; immunomodulation & immune avoidance
    -Reproduce & disseminate its progeny
    -May incur “fitness cost”
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9
Q

Do parasites have the ability to alter their biologic functions?

A

Yes, in order to enhance the odds for survival & reproduction

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10
Q

What are two parasite populations?

A

Plastic & dynamic`

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11
Q

Capacity to respond to a variety of conditions & stimuli (selection pressures) by permanent alterations of their genetic composition - what are the 3 alterations?

A

-Hypobiosis (arrested development)
-Vertical transmission of developmental stages
-Shorter or abbreviated lifecycle development

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12
Q

Are parasite populations drug resistance?

A

Yes; survive drug selection pressures

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13
Q

Are parasite populations have the ability to colonize new hosts?

A

Yes; new hosts/sites within hosts

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14
Q

Is parasitism common in wildlife and domestic animals?

A

Yes
-Most animals will develop some degree of acquired immunity to parasitic infections
-Mechanisms to mitigate (minimize) associated disease

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15
Q

Is parasitism common in natural settings and host populations?

A

It is RARE, its occurrence in domestic livestock & companion animal populations is generally a consequence of management

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16
Q

Are parasitic disease related to the numbers of parasites infecting the host?

A

Yes usually
-Hyper-contamination of living/grazing environment
-Hyper-infection leads to host death by depletion of host resources
-Function of the relative susceptibility of the host
-Acquisition of large numbers of parasites in the absence of acquired immunity
-Loss or reduction of immunity (parasite or host suppression)
-Increases susceptibility to other agents of mortality

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17
Q

What happens when there is a disrupt transmission between parasites & their host population?

A

-Breaking the life cycle of infection & reinfection
-Rarely achieved by pharmaceutical intervention alone

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18
Q

What are development (enhancement) of host immunity?

A

-Vaccination
-Low levels of exposure (premunition)

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19
Q

What are changes in management/modification of environment?

A

-Protected environment for neonates
-Reducing environmental contamination w/ infective stages
-Selective breeding
-Better nutrition

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20
Q

What is the 1st way parasites cause disease?

A

-Suck blood (mosquitoes, hookworms), lymph (midges), or exudates (lungworms)

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21
Q

What is the 2nd way parasites cause disease?

A

Feed on solid tissues directly (giant kidney worms, liver flukes) or after liquefying them (chiggers, amoebas)

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22
Q

What is the 3rd way parasites cause disease?

A

Compete with the host for ingested food; ingesting intestinal contents (ascarids) and absorbing them through the body wall (tapeworms)

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23
Q

What is the 4th way parasites cause disease?

A

Traumatic injury by mechanical obstructions:
- Intestine (ascarids), bile ducts (ascarids, fringed tapeworm)
- Blood vessels (dog heartworm), lymph channels (filariids), bronchi (lungworms), or other body channels
-Pressure atrophy of hydatid cysts against body organs

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24
Q

What is the 5th way parasites cause disease?

A

Destroy host cells by growing in them (coccidia, malaria)

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25
Q

What is the 6th way parasites cause disease?

A

Production of various toxic substances that aid in their ability to enter host tissues, feed, or reproduce; hemolysins, histolysins, anticoagulants

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26
Q

What is the 7th way parasites cause disease?

A

Cause various host reactions such as allergic, inflammatory, hypertrophy, hyperplasia, & nodule formation

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27
Q

What is the 8th way parasites cause disease?

A

Stimulate the development of cancerous cell growth (Spirocerca lupi)

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28
Q

What is the 9th way parasites cause disease?

A

Carry (vector) additional diseases (parasites, viruses, bacteria)
-Malaria (mosquitos), swine influenza (lungworms), salmon poisoning (flukes), & heartworms (mosquitoes)

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29
Q

What is the 10th way parasites cause disease?

A

Reduce host resistance to other diseases & parasites

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30
Q

What are parasitic associations?

A

Obligatory parasite & facultative parasite

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31
Q

What is the obligatory parasite?

A

-Can’t complete its lifecycle w/o spending part or all its time on or within a host
-May have free-living stages
-May use a successive series of different hosts
-May spend entire lifecycle within or upon a host

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32
Q

What is a facultative parasite?

A

-Not normally parasitic, but become so when eaten or OPPORTUNISTICALLY enter a host through & orifice or wound
-Naegleria fowleri causative agent of Primary Amoebic Meningoencephalitis (PAM) “brain eating amoebae”
-Halicephalobus a causative agent of encephalitis in horses

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33
Q

Endoparasite

A

Organisms living within a host environment

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34
Q

Ectoparasite

A

Organisms living on host (external environment); fleas/ticks

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35
Q

Aberrant parasite

A

-Organisms found in locations where they do NOT normally occur; generally do NOT mature or facilitate transmission and often result in disease state
-“Ectopic infections”; Toxocara larvae in the eye of its host, Dirofilaria immitis in the brain of a tiger, & Paragonimus in the liver (lung parasite)

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36
Q

What are the 3 parasitic associations?

A

-Accidental/incidental parasite
-Pseudoparasite
-Hyperparasite

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37
Q

Explain accidental/incidental parasite

A

-Parasitic organisms that enter or attach to host species that are different from the one(s) with which they are normally associated
-May not be able to survive in the host or often elicits a major pathological response from the host
-Repeated successful colonization of an accidental host can become the basis of “host switching” & development of a new host association

38
Q

Explain Pseudoparasite

A

-Not really a parasite
-Diagnostic parasite stages or other artifacts (plant pollen, fungi, arthropods) that superficially resemble protozoan cysts or helminth eggs in the feces, blood, or urine of an examined animal
-Misnomer because “pseudo-parasite products” are not associated with a true host-parasite association
-Eimeria (rabbit poop) oocysts passed in dog feces, various pollen mistakenly attributed to parasitic species infecting a host

39
Q

Explain Hyperparasite

A

-When a parasitic organism is host to another parasite species
-Mosquito that is host to Plasmodium sp. or Dirofilaria immitis
-Flea that is host to Dipylidium caninum

40
Q

Explain definitive host

A

-Adult parasite lives
-Where a parasite attains reproductive maturity
-Evidenced by the circulation or passage (in feces or other host tissues) of progeny capable of colonizing additional host species

41
Q

Explain intermediate host

A

-Larvae
-In which a larval or intermediate stage parasite must undergo development to become infective for the “definitive” or final host
-Often an obligate or required developmental stage for completion of the life cycle

42
Q

Explain Paratenic host

A

-Opportunistic
-A facultative host used by a larval or intermediate stage parasite to facilitate transmission to the “definitive or final host”
-Parasites that infect a paratenic host do NOT undergo any development
-This is an important distinguishing difference between paratenic (birds) & intermediate hosts (snails/slugs)
-This facultative relationship (convenience & opportunity) often bridges an ecological gap between passage of infective stages & successful transmission & establishment in a new host for completion of a lifecycle & perpetuation of the parasite population

43
Q

Explain Reservoid host(s)

A

-Maintain a parasite in the population at sufficient levels to facilitate its transmission between susceptible hosts
-Population parameter rather than individual parameter
-For zoonotic parasites & infectious diseases, the reservoir hosts are animals; lyme disease: deer, white-footed mice
-Coyotes, & stray & unprotected canines are reservoir hosts for potential infection w/ Dirofilaria immitis; stray/wild canine vs. companion (pet) canine
-May be definitive (adult parasites), intermediate (obligate developmental stages), or paratentic (facultative developmental stages)
-Emphasis on population rather than individual

44
Q

Explain vectors

A

-Organisms that facilitate transmission of infective parasite stages between different individuals of a host population

45
Q

Explain biological vectors

A

-Assume the existence of an obligate relationship for successful transmission & maintenance of the parasite species in the host populations; often also play role as intermediate/paratenic hosts

46
Q

Explain mechanical vectors

A

-Do not have an obligate role
-Flying syringe, transport on feet, ect..

47
Q

Explain direct lifecycle

A

-Parasites infect host directly
-Stages passed from host in feces/other tissues
-Infective to another “definitive host” (dog to dog)
-May require period of development to infective stage; larval development w/ in eggs, free living larval stages in environment

48
Q

Explain indirect lifecycle

A

-Obligate
-Require intervention of an intermediate host
-Stages passed from host in feces/other tissues
-Infective to the “intermediate host”
-Obligate requirement for development to infective stage
-Indirect transmission to “definitive host”
-May involve paratenic host; “bridge the ecologic gap”

49
Q

Explain indirect lifecycle

A

-Facultative
-Indirect transmission to “definitive host”
-Optional intervention of an intermediate or paratenic host
-Stages passed from host in feces/other tissues
-Infective to definitive host or the “optional host”
-“bridge the ecologic gap”

50
Q

Principles of Transmission: Horizontal

A

-Parasites colonize susceptible individuals by usual routes
-Infection across different generations of host population not required

51
Q

Principles of Transmission: Vertical

A

-Transmission of parasites from mother to offspring by transplacental or lactogenic routes
-Trans-generational requirement
-Prenatal or perinatal

52
Q

Principles of Transmission: Host Specificity

A

-High specificity (monospecific)
-Limited number of hosts capable of completing lifecycle
-Pinworms in primate hosts

-Low specificity (heterospecific)
-Wide variety of species capable of hosting parasite
-Typical of intermediate & paratenic hosts
-Toxoplama gondii, Baylisacaris procyonis

53
Q

Principles of Transmission: Zoonotic

A

-Animal to human

54
Q

Principles of Transmission: Anthroponotic

A

-Human to animal

55
Q

Endemic (enzootic)

A

-The normal or usual distribution of parasites in a host population or geographic area
-Eimera sp. is endemic in Tennessee cattle

56
Q

Epidemic (epizootic)

A

-An excess number of parasite cases, far exceeding the normal or usual distribution in a host population
-Temporal & spatial characteristics
-50% of the last years kid crop were aborted in an epizootic of toxoplasmosis

57
Q

Prevalence

A

-The occurrence of a parasite in a population defined by time & space

58
Q

Incidence

A

-The rate at which new cases are added to a host population defined by time & space

59
Q

Nematode parasite - General features

A

-Numerous & ubiquitous
-Over 25,000 species described
-Free-living environment dwelling
-Over 50% are parasitic in plants & animals; recall @ least 4 times independently
-Parasitologists study the species in animals & humans b/c of veterinary & medical significance

60
Q

Nematode Parasites - Classification

A

-Morphological
-Molecular
-By host species; companion animal & livestock

61
Q

Nematode Parasites - Nomenclature

A

-Scientific names
-Family relationships between species
-Genus
-Species
-Person who 1st named the worm
-Other person who studied it & reclassified it

62
Q

Morphological characteristics - Roundworms

A

-Bilaterally symmetrical
-Cylindrical & elongate
-Body size range from very small to huge
-Trichostrongylid species in cattle, sheep, & goats
-Ascarid species in dogs & cats

63
Q

What type of parasite has -Worm-like bodies covered w/ cuticle; collagenous tissue resist fluid loss & dehydration & support as flexible exoseleton?

A

Roundworm

64
Q

What type of parasite is longitudinal muscles only, somatic musculature part of body wall & divided into contractile & non-contractile portions (different morphology has diagnostic significance in cross-section)

A

Roundworm

65
Q

What type of parasite has a primitive nervous system?

A

Roundworm

66
Q

What type of parasite has dioecious (in two houses)? Explain it.

A

-Roundworm

-Sexes separate
-Females are larger
-Males w/ elaborate apparatus; copulatory bursa, spicules, & reproductive functions & important taxonomic characteristics

67
Q

What type of parasite has pseudo-coelomate? Explain it.

A

-Roundworm

-Cross-sectional view “tube within tube” body design
-Fluid filled body cavity under hydrostatic pressure
-Female reproductive tract; variable ovary morphology (monodelphic, didelphic)
-Complete digestive system; defined oral opening (buccal capsule or lips), esophagus, gut, & excretory outlet

68
Q

Explain nematode lifecycle

A

-All rational control efforts are based on understanding of life history of parasite & host
-May be direct or indirect lifecycle
-MOST involve 3 larval stages
-Pre-patent period; time to reproductive maturity, also known as “egg reappearance period” following treatment
-Biological variation in life history; some species undergo tracheal migration enroute to final infection site, some species undergo hypobiosis (arrested development), & most species induce “age associated immunity”
-Transmission from infected to susceptible; fecal-oral (horizontal transmission), vertical transmission, & vector borne

69
Q

Hookworm History

A

-Recognized as a causative agent of anemia in humans by late 19th century
-Joseph Leidy observed worms 1886, from necropsy of an anemic cat
-Suggested previously unrecognized cause of pernicious anemia
-Potential zoonotic association

70
Q

Hookworm Scientific Names

A

-Ancylostoma caninum
-A. tubaforme
-A. braziliense
-Uncinaria stenocephala

71
Q

General Morphology - Hookworms

A

-Small, stout worms ranging from 10 to 16mm
-Dioecious, sexually dimorphic, females are larger
-Males w/ copulatory bursa (diagnostic significance)
-Anterior end curved dorsoventrally giving appearance of hooked head
-Buccal cavity w/ teeth or cutting plates
-Esophagus club-shaped, very muscular functional as very powerful pump; VORACIOUS BLOOD SUCKERS

72
Q

Biology - Hookworms

A

-Development to infective stage in environment (outside of the host)
-Generally, occupy small intestine of vertebrate hosts; humans, dogs, cats, livestock, reptiles, species in elephants found in the bile ducts

73
Q

Morphology - Ancylostoma caninum

A

-Canine hookworm

-Small worms; males (10-12 mm), females always larger (14-16 mm), large buccal capsule (3 pairs large teeth), males w/ copulatory bursa
-Club-shaped, muscular esophagus
-Functional at very powerful pump (voracious blood suckers)
-Cause disease

74
Q

Biology - Ancylostoma caninum (canine hookworms)

A

-Direct lifecycle; eggs passed & larvae develop in environment (7 to 14 days)
-Host infection by skin penetration & oral ingestion
-Tracheal migration through somatic tissues; arrested development of larvae
-Adults in small intestine; 17 to 21 days following infection (lifespan 12 to 18 months in absence of reinfection)

75
Q

Oral Infection - Ancylostoma caninum (canine hookworms)

A

-2 modes of transmission

-Direct ingestion of infective larvae; environmental sources/fecal contamination, paratenic hosts, & older animals, >12-15 weeks

-Arrested larvae passed by lactogenic route most important
-Nursing puppies infected by larvae sequestered in mother’s tissues

76
Q

Lactogenic route in Ancylostoma caninum (canine hookworms)

A

-Larvae do not appear to migrate
-Mature directly in the small intestine following attachment
-Clinical signs of anemia in about 8 days post-infection
-Peak blood loss between the 15th to 18th day post infection
-Nursing puppies may pass eggs as early as 10-12 days after birth

77
Q

Sources of infective larvae (L3 stage) for oral infection in Ancylostoma caninum (canine hookworms)

A

-Environmental sources; pet parks, hyper-contaminated backyards & exercise runs
-Paratenic hosts; no development of larvae, “bridge the ecologic gap”, opportunity for infective larvae to “warehouse” (suitable host for transmission & refuge from inhospitable environmental conditions)

-Some penetrate inside of mouth & migrate while other’s proceed directly to GI

-Sequestered larvae can be an important source for subsequent lactogenic transmission

78
Q

Distrubtion of Ancylostoma caninum (canine hookworms) based on positive fecal exams collected by CAPC 2022

A

-A majority of south states have highest proportion of cases; statewide prevalence >4%, approx. x2 the avg. national prevalence
-TN: 4.10% –> Claiborne 16.67%
-Bell Co, KY; dogs 3.85% & shelter dogs 57.4%

79
Q

Pathogenesis for Hookworms

A

-Can cause disease because they are voracious blood suckers
-Adult female worms estimated to ingest approx. 0.1ml of blood per worm per day; 10ml/100 worms
-Severity of disease depends on:
intensity of infection, age of host, nutritional status, degree of iron reserves, & presence of acquired immunity

80
Q

Peracute as seen in neonatal puppies types of clinical disease

A

-Significant blood loss; rapid progression to a microcytic, hypochromic anemia within hours or days as worms begin feeding voraciously at 8 days post infection, pales mucous membranes (almost white), diarrhea w/ black tarry stools, partially digested blood leaking from lesions produced by feeding worms
-Acquisition of large numbers of worms in very short period of time; 50-100 worms are sufficient clinical burden to cause severe disease in neonatal puppies
-Naive immune status
-Deficient nutrition (all energy acquired through nursing is allocated to early growth so few excess reserves available), insufficient iron reserves, insufficient iron in milk

81
Q

Explain acute clinical disease

A

-Acute = exposure of older puppies & even adults to large numbers of infective larvae
-Worm burdens acquired from environmental exposure over short period of time
-Hyper-contaminated kennel/dog run/yard or experimental treatments
-Animals exhibit a normochromic, normocytic anemia that becomes hypochromic, microytic
-Cumulative process w/ prolonged exposure & progressive acquisition of additional worms

82
Q

Chronic compensated disease

A

-Presence of infection without overt clinical signs
-Measurable reductions in PCV, Erythrocyte count, low end of normal or slightly below
-Blood loss may be compensated for by rapid erythropoietic response in animals w/ adequate iron reserves

83
Q

Secondary decompensated disease

A

-Older dogs w/ other (primary) health issues; metabolic or metastatic etiologies
-Malnourished/emaciated animals, hookworm as a secondary causative effect - pushes the animal over the brink

84
Q

Diagnosis - Clinical presentation

A

-Peracute disease
-Neonatal puppies showing profound anemia (significant blood loss in the 8th to 15th day of life)
-Pale mucous membranes
-Hematocrit or PCV <20%
-Marked weakness, listless, anorexia, ADR
-Bloody diarrhea
-Fecal examination may be negative (significant blood loss from immature worms)

85
Q

Acute disease - routine physical exam

A

-Older animals (>3 or 4 months thru adults)
-Noticeable clinical signs
-PCV <25%
Listless w/ pale mucous membranes
-Diarrhea w/ black-tarry stools
-Low BCS, emaciation
-Poor hair coat
-Dermatitis on feet/lower extremities
-Appearance of eggs on fecal exam (thin shelled & in morula stage, avg. 60 x 40 um)

86
Q

Chronic disease - routine physical exam

A

-Older animals (>3 or 4 months thru adults)
-W/o noticeable clinical signs, may even be BAR but PCV on low end & perhaps below normal (~27 to <30%), low weight for age/low BCS, poor hair coat, dermatitis on feet/lower extremities
-Appearance of eggs on fecal exam; thin shelled & in morula stage, avg. 60 x 40um

87
Q

Secondary De-Compensated Disease - routine physical exam

A

-Older animals (>3 or 4 months through adults
-Variable clinical signs, generall ADR; PCV below normal (<27), emaciated appearance w/low BCS
-Poor hair coat
-Dermatitis on feet/lower extremities
-Appearance of eggs on fecal exam
-Parasitic disease is 2nd to underlying metabolic or metastatic disease; chemotherapy & immunosuppression

88
Q

Peracute Disease - Treatment of Clinically Ill Animals

A

-Generally have poor prognosis
-Immediate anthelmintic treatment (single dose Pyrantel pamoate, suspension 10mg/kg)
-Complete assessment based on age, clinical presentation, hematocrit, clinical chemistry
-Supportive care important to keep the patient alive long enough for the treatment to be effective; fluids, electrolytes, iron supplementation, blood transfusion
-Pyrantel is the drug of choice: fast acting, peak serum levels in 3-6 hours, wide margin of safety LD50 is approx. 138x the labeled dose (poor absorbed in the GI tract & passed out in the feces within 24 hours, unchanged, makes it safe for use in young & severely debilitated animals

89
Q

Treatment of Infected Animals W/O signs

A

-Therapeutic target is removal of egg laying adult worms from the small intestines. Single female worm capable of producing on avg. 16000 eggs/day (hazardous contamination of dog runs, backyards, residential environment
-Available drugs: pyrantel pamoate, fenbendazole, heartworm prophylaxis regimens purge deworm GI parasites at monthly intervals (Advantage, HeartGard, Interceptor, Sentinel), adequate for control but not prevention of infections, protocol allows infection to occur but worms are removed monthly prior to the accumulation of clinical significant worm burden, ~21 day pre-patent period allows adult worms to mature; eggs passed from the host to the environment (contaminate)

90
Q
A

Parasitology (14 decks)

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