Veterinary Parasitology Final Exam

Front 1

co-evolution

Back 1

shared history between parasite and hosts

Front 2

host switching

Back 2

when a parasite switches from one host lineage to another

Front 3

co-speciation

Back 3

speciation of host is accompanied by speciation of parasite

Front 4

co-adaptation

Back 4

eveolution of adaptations in the host in response to selection imposed by parasite, followed by evolution of adaptations in parasite in response to reciprocal selection imposed by host - evolutionary arms race

Front 5

PARASITE
-virulence
-infectivity
-pathogenicity

Back 5

-parasite induced decrease in host fitness
-capability of a parasite to enter host
-capability of a parastie to produce clinical disease

Front 6

HOST
-resistance
-infectibiility
-susceptibility

Back 6

-host induced decrease in parasite fitness
-propensity for host to be infected
-propensity for host to exhibit clinical disease

Front 7

evolution of virulence

Back 7

parasite evolves to increase their fitness - may result in a decreased virulence of increased virulence :)

Front 8

Specialist and generalist parasites:
host range

Back 8

the number of host spp used by each stage of a parasite spp in its life cycle

Front 9

Specialist and generalist parasites:
host specificity
two types of?

Back 9

to which host species are utilized at each stage of a parasite spp in its LC - how frequently diff host spp are infected
-specialist parasites have a high host spec. generalist low
-host spec can differ b/w closely related parasites and b/w LC stages of same parasite
e.g. Trypanosoma vertical vs vector (tsetse) transmission

Front 10

Specialist and generalist parasites:
determinants of host specificity
1. encounter filter
2. compatibility filter

Back 10

1. excludes all hosts the parasite cannot meet for eco or bahavioural reasons

2. excludes all host spp in which the parasite cannot survive and develop for morph, physiological or immunological reasons

Front 11

Specialist and generalist parasites:
Consequences of specialization?

percent generalist vs specialist in both human and domestic spp?

Back 11

-specialist parasites are well adapted to their host but usually cannot exploit others
-geneeralists may be outcompeteed by specialists but can exploit alternative hosts
- 60% human/80% domestic spp parasites are generalists

Front 12

Parasite Ecology:
Microparasites

Back 12

sm. reprocude w/i DH, short generation time, short infection time, often invoke persistent immunity
1. viruses, bacteria, many protozoans
2. host pop. can be divided into susceptible, infected and immune classes
3. driving force is rate of gains and losses of host from diff classes

Front 13

Parasite Ecology:
Macroparasites

Back 13

lrg. do NOT repro w/i DH, long generation time, provoke weak and transient immunity
-arthropods and helminthes
1. host pop can be divided into host harbouring diff #'s of parasites
2. driving force is survival and repro of indv parasites - diff in abundance amoung hosts is a key feature
3. often overdispersed or aggregated - due to heterogenity in host exp. or host resistance (genetic variation etc)

Front 14

Parasite Ecology:
Heirarchical nature of parasite populations
1. infrapopulations
2. component populations
3. suprapopulations

Back 14

1. all member of a parasite spp in an ind host at a particular time
2. all members of a parasite spp in all members of a particular host spp at a particular place and time
3. all members of a parasite spp and the env, at a particular time and place

Front 15

Parasite Ecology:
Measure of parasite distribution and abundance
1. prevalence
2. incidence
3. intensity
4. abundance (give ex)

Back 15

1. # of hosts infected w/ a particular parasite spp at a particular time
2.# of new hosts infected 1/ a particular spp. during a specified time interval
3. mean # of parasite of a particular spp per infected host
4. mean of parasites of a particular spp per host (inf and uninf) ie. bird shistosomes, dirofilaria in humans (VLM)

Front 16

HELMINTHE LC
transmission:
1. direct/indirect?
2. infective stage?
3. How is host infected?
- Mode of transmission

Back 16

See chart

Front 17

HELMINTHE LC:
W/i the Host:
1. migratory or non-migratory?
multiplication by asexual repro?
what stage leaves the host

Back 17

See chart

Front 18

HELMINTHE LC:
1. DH
2. IH
3. PH
4. Vector
5. Resevoir host
6. Accidental host

Back 18

1. host in which sexual maturity is attained
2. additional obligatory host in LC
3. additional non-obligatory host in LC
arthropod carrier of infective stages from one host to another
5. alt. host. usually one which does not suffer cl. dz. but can act as a source of infection for other hosts
6. host which does not norm. harbour parasite - parasite cannot complete LC

Front 19

Modes of transmission:
1. Horizontal: give ex
2. Vertical: give ex

Back 19

1. injestion, inhalation, skin penetration, wound invasion, sexual transmission, injection
ex.
2. transovarian, transplacental, transmammary
ex.

Front 20

LC in the host:
1. pre-patent period
2. incubation period
3. latent period

Back 20

1. time from 1st infection of DH until 1st appearance of eggs or juveniles (diagnostic stages)
2. time from 1st infection of host until onset of clinical symptoms
3. time from 1st infection of host until host is able to transmit infection

Front 21

Why is transmission key to survival?

Back 21

a) At each new transmission stage the probability of finding a new host is sm
b) Adaptations to aid transmission
i) ↑ number and survival of infective stages
ii) Maximize spatial and temporal overlap w/ new host
iii) ↑ number of hosts
iv) Chg bhr of existing host

Front 22

Importance of understanding LC?

Back 22

1) Knowledge of migration patters w/i host aids Dx of parasitic disease and enables prediction of pathogenesis
2) Knowledge of transmission pattern aids dev of effective control prog

Front 23

What is a successful parasite

Back 23

- those which have reached a state of balanced pathogenicity or a stable host-parasite rel

Front 24

Why is it not in the best interest for a parasite to kill its host
give examples

Back 24

may limit opportunities for repro and transmission but
a) Eimeria can repro and rel infective stages b4 death of the host
b) Echinococcus may kill/impair performance of host ↑ chance of predation
c) Dirofilaria- usually achieves repro aims b4 it causes symptoms

Front 25

Stress factors and host parasite relationship?

Back 25

nutrition, climate, competition, concurrent infections

Front 26

Importance of nutrition in H/P relationship?
ex?

Back 26

a) Hosts w/ poor to severe nutrition may never overcome parasitic infections
b) Host will give priority to the reversal of pathophysiological consequences of parasitism over other body fxns
c) Improved nutrition often provides improved resistance  hwr fxns of gth, preg and lactation take priority over expression of immunity  ↑ nutrition may affect the ° of expression during these phases
d) Some parasites enter a dormant phase as a result of immune pressure  toxoplasma

Front 27

relationship between allergy, parasites and the hygiene hypothesis?

Back 27

1) - suggested that frequent exchg of infections may have a protective effect
a) Exposure to infections like Toxoplasma gondii ↓ allergies by >60%
b) Perhaps the lack of infections in industrialized countries owing to improved hygiene, vaccination, and use of antibiotics may alter the human immune system such that it responds inappropriately to innocuous substances
c) The observation that the repeated stimulation of the immune system by pathogens is central to the development of a balanced regulatory system also highlights the need to identify molecular patterns on parasites and to study their immunomodulatory potential

Front 28

Why is the H/P relationship described as an evolutionary arms race?

Back 28

Most parasites have co-evolved w/ their hosts over a long period of time
1) Selection acts on parasite host genotypes to maximize reproductive success in the short term - both virulence and resistance may ↑ or ↓

Front 29

How Parasites Damage their Host:

Back 29

• Entry via skin/mucosa
• Growth and development- migration, pressure effects (SOL), intracellular
• Adults may cause blockage of various organs
• Vacating stages
• Host reactions (hypersensitivity)

Front 30

How Parasites Damage their Host:
Obstruction:
give ex

Back 30

i) Ascaris, toxocara- lg parasites loads may cause intestinal obstruction
ii) Dirofilaria- lg vascular load may lead to chronic heart disease
iii) Oslerus- possible blockage of the trachea
iv) Fasciola- obstruction of the bile ducts
v) Plasmodium (human)/babesia (cattle)- indirect=  cause RBCs to become sticky
• Mechanisms used b/w the two are v similar and host response is the same
• Asymptomatic/mild/severe disease  severe may lead to cardiac arrest, stroke and death

Front 31

Damage to Host:
Interfere w/ fxn

Back 31

i) Giardia- ↓ absorptive surface area via interference of absorptive channels (not sure how)  may also induce allergy (asthma)
ii) Gasterophilus- build up of bots in the stomach interferes w/ fxn
iii) Ostertagia- gth of parasite causes pressure necrosis in the glands of the abomasum
iv) Draschia- nodules can interfere w/ stomach fxn
v) Anoplocephala- lg parasite load may impede SI absorption or cause bile duct blockage
vi) Diphyllobothrium- competes w/ host for Vit B12  pernicious anemia
vii) Trypanosome cruzi- reproduction in tissues (Cam/SmM) and cellular rupture interferes w/ heart and gut fxn
viii) Lungworms- induce overprod of mucous and may initiate 2° infection

Front 32

Damage to Host:
Growth

Back 32

a) Pressure necrosis any protozoa undergoing marogony cause cell disruption/bursting
i) Echinococcus- dev of lg cysts
ii) Ostertagia- dev in the glands of the stomach of cows (sheep – teledorsagia)
• Ingested larvae (L3) may become dormant - gth of L4 may cause damage and induce hyperplasia of damaged periacinar cells - ↑ acid prod in stomach (host response exacerbates situation)

Front 33

Damage to host:
Tissues and Cell Disruption

Back 33

a) Migrating Larvae causing Local hemorrhage and Necrosis  2° bacterial infection is a problem w/ many of these
i) Ascaris, Toxocara
• If infection via eggs (L3), larvae migrate through liver/lungs (L4) most migrate up the trachea to the SI (adults); some suspend in tissues

Front 34

Examples of tissue and cell disruption in host

Back 34

i) Ancyclostoma (Hookworm)
• Infection by ingestion or skin penetration by L3 (tracheal migration to SI)
• Some suspend dev in the tissues, reactivate and migrate to mammary glands
ii) Fasciola- Cysts encyst in gut, yg flukes penetrate gut wall and migrate to liver (6wks)  bile duct to mature (4wks)
iii) Strongylus vulgaris- L4s migrate in the mesenteric artery
iv) Strongyloides- dept on host immune competency
• Ingestion or skin penetration of L3 larvae  blood lungs  trachea  esophagus  SI mucosa
v) Taenia hydatigena- Ingestion of infective eggs  GIT  mesenteries/peritoneal cavity  Liver (cysticercus)
vi) Blowfly larvae- Larvae secrete enzymes which digest tissues which they feed on  flank and other soiled areas (sheep)

Front 35

Damage to host:
intracellular

Back 35

i) Coccidia- Developing multiplying stages in schizonogy
ii) Babesia
iii) Plasmodium
iv) leishmania
V) T.cruzi

Front 36

Damage to host by Ingestion of Host Cells

Back 36

a) Plug feeders- parasites w/ a lg mouth which take out plugs of tissue
i) Fasciola (liver), Paramphistomes, Strongylus, Chabertia, Blowfly larvae, Biting lice
•Decrocilium- smaller, EU/NA, ↓ abrasion (no spines), no invasive phase (do not migrate in the liver)

Front 37

Damage to host through blood sucking

Back 37

loss of protein and Fe:
a) Ticks, Fleas (wasteful feeders), Lice
b) Biting flies- Tabanids
c) Ancyclostoma, Haemonchus
d) Fasciola, Leeches

Front 38

Damage to host:
Direct Food Utilization

Back 38

a) Cestodes- like having an everted gut - tries to absorb nutrients b4 you do
b) Enteric protozoa- contributor to failure to thrive and nutritional deprivation (not sure how)
c) Lg nematodes- Ascaris- feed on gut contents
d) Fasciola- consumes bile and blood
e) Paramphistomes, ‘Bot’ larvae (Gastrophilus)- browse on gut contents
f) Estrus ovis- feeds on mucous in the nose (sheep)

Front 39

Damage to Host:
Affect Gut Physiology

Back 39

a) Villous Atrophy (consequence of host inflammatory rxn)  Malabsorption and anorexia- Trichostrongylus, Cooperia, Nematodirus
b) Stomach fxn due to host response and physical damage to glands- Ostertagia
c) Cestodes
i) Hymenolepis diminuta (Rat)  ↓pH and ↑ CO2, impair fluid and glucose transport  does not appear to clinically affect host
•Hymenolepis nana (Human)- contributes to failure to thrive
•If host is on a deprived plane of nutrition, effects of parasites may be more severe than usual
ii) Dyphyllobothrium- competes w/ the host for Vit B12
d) Protozoa
i) Giardia- malabsorption, toxin prod?, allergy

Front 40

Damage to host:
Predisposition to Neoplasia

Back 40

a) Spirocerca lupi (esophagus)- presence is assoc w/ the dev of fibrosarcomas in that region
b) Clonochis sinensis (Chinese Liver Fluke), Taenia taeniaeforis (Rodents), and Echinococcus spp (Hydatid)- long lived nature seems to induce cancers  liver sarcoma

Front 41

Damage to host:
Transportation of other pathogens

Back 41

a) Heterakis  Histomonas  blackhead in turkeys
b) Metastrongylus  Swine influenza
c) Ticks  Babesia
d) Mosquitoes  Plasmodium and Dirofilaria
e) Tsetse flies  Trypanosoma
f) Strongyle larvae  Pathogenic bacteria into gut as dev in feces
g) Nanophyetus (fluke) Salmon poisoning in dogs (Rickettsia)

Front 42

Damage to Host:
Produce toxins

Back 42

a) Ixodes holocyclus (tick)- tick paralysis in dogs
b) Tissue parasites - necrosis
c) Enzymes to aid penetration - may be toxic
d) Cellular substances- kinins, etc

Front 43

Damage to host:
Hypersensitivity

Back 43

a) Immediate- Mosquito, Tick
b) Delayed- cellular responses around tissue parasites (more serious)
i) Fleas
ii) Culicoides (Horses)
iii) Intestinal nematodes  villous atrophy due to CMI response, IL, IgE
iv) Schistasoma- systemic response (esp in liver) to eggs (covered in histolytic enzymes which migrate to the GIT or liver - CMI resp)
v) Dictyocaulus- inflammatory response to nematodes in respiratory passages

Front 44

Damage to Host:
Irritation and Annoyance

Back 44

1) economic importance in livestock
a) Lice, Mites, Ticks, Flies
b) Enterobius (Human pinworm), Oxyuris (Horse)- inhabit LI and cause irritation via sticky eggs in perianal area
c) Dipylidium (Dog)- proglottids move around perianal area

Front 45

Parasite Survival
what is required or needs to be avoided?
Methods of?

Back 45

- to survive a parasite must avoid provoking an immune response or avoid the effects of the immune response
Cysts
Antigenic variation
Host Ag acquisition/mimicry
Premunition

Front 46

Parasite survival:
cysts

Back 46

a) Encapsulation- host response against parasite
b) Encystment- parasite
c) Encapsulation and encystment- e.g. hydatid cyst

Front 47

Parasite survival:
Antigenic Variation

Back 47

1) the ability of an org to vary the configuration of certain Ag genetically
a) Each chg is assoc w/ the expression of a particular Ag-determining gene - chg specific to circumscribe chgs induced by host

Front 48

Parasite survival:
Premunition

Back 48

1) protection against reinfection as a result of an existing infection  prod of memory cells req living parasite present
a) Immunity is related to a prev infection
b) Schistosomiasis- dilemma as Tx of patients with relatively little clinical signs puts them at risk for reinfection due to the loss of premonition, as a result subsequent infection might be more severe than initial

Front 49

Parasite survival:
Host Ag Acquisition/mimicry

Back 49

1) uptake or prod of host-type Ag by the parasite
a) Seems to be largely confined to helminths
i) Most work done on schistosomes and toxocara

Front 50

Diagnosis:
DNA based techniques

Back 50

A) DNA-based Tecniques
1) Most are PCR-based  direct characterization of parasite stages in feces and env samples
2) Determination of molecular characteristics- types, strain determination, sequencing

Front 51

Prophylaxis

Back 51

A) Clinically effective responses to 1° infections, such as occur in many bacterial and viral disease, are rarely seen in parasitic infections, hwr, there is abundant evidence that animal parasites are immunogenic and do sensitize the host’s conventional immune effector pathways often resulting in immunity to challenge
1) Complete clinical cure due to immune response is rare
2) Parasites have evolved means of evading the potentially lethal consequences of immunity

Front 52

Parasite Control:
Different types?
Considerations?

Back 52

-Chemotherapy - $, resistance
-vector control - $
-public health issues - usually can do no more than keep disease w/i tolerable limits ,usually an adjunct to other control measures
-vaccines (discussed on another card)

Front 53

Parasite control:
vaccines

Back 53

A single approach to any parasite control is unlikely
b) Parasitic Antigens- may be:
i) Stage specific - which stage do you want to dev a response against
ii) Common to other parasites
iii) Common to Ag of the host
iv) May be- secretions and metabolic prod, E used for feeding/tissues penetration, excretory prod, moulting substances, structural components, prod of repro - get an immune response to each of these
• Somatic Ag bound to tissues of the parasite
• Attempts to vaccinate against these turned out to be largely unsuccessful
-Relevant, protective Ag need to be ID, isolated and purified
-Homogenates are a crude/complex mixture -exposing host to 100’s of diff Ag (may confuse immune sys)
-Relevant, protective Ag are metabolic substances which are actively excreted/secreted
• Metabolic Ag- Ag released during gth, dev and penetration
In some cases, metabolic Ag can be prod in vitro and easily harvested -may not be practical on a routine basis w/ other parasites

Front 54

Current Strategies for Prod of Protective and useful Parasite Ag

Back 54

a) ID and isolate protective Ag using monoclonal Ab
b) Purify Ag using preparative biochem methods e.g. chromatography
c) Prod of Ag by recombinant DNA techniques (cloned Ag)

Front 55

Other approaches to Parasites Vaccines:
Attenuation

Back 55

i) Irradiation
ii) Passage
iii) Aim- to prod an infection by the norm route so that dev of the infection is prematurely terminated and pathogenicity ↓
• Such prod of a norm infection of controlled duration ensures that the fxnl Ag is delivered to the strategic sites by the parasite itself  using parasite extracts, it does not ensure the arrival of the Ag at the strategic site
iv) Limitations
• Short shelf life
• Genetic trait for attenuation may not be stable
• Possible contamination w/ other pathogens
• Low profitability – cannot readily be patented
• Hidden Ag
• Parasite pro not normally seen by the host  should be of fxnl significance
E.g. gut assoc Ag in blood feeding parasites
• Cattle Tick Vaccine

Front 56

Parasite control:
Maternal Immunity

Back 56

a) Maternal Immunity- take advantage of the transfer of maternal Ab to their yg (in utero or via colostrum)
i) Eimeria, cryptosporidium, toxoplasma
ii) Advantages- only need to vaccinate mothers, yg protected immediately

Front 57

Parasite control:
Malaria Vaccines CARD 1 of 3
-obstacles
-vaccine for ind/community

Back 57

a) Obstacles- antigenic variation, the need for an appropriate adjuvant, the req for a subunit vaccine
b) Vaccines for communities- prevents morbidity and mortality w/o preventing infection
c) Vaccines for individuals- prevents morbidity and mortality by preventing infection
i) Residents of endemic areas
ii) Tourists, business/army personnel, aid workers

Front 58

Parasite control:
Malaria Vaccines CARD 1 of 3
-problems with?

Back 58

There are several immune responses that restrict parasites gth  but eh parasite persists
The parasite benefits from immune responses if they lead to chronic infection  enhance transmission to the mosquito
None of the immune responses identified in humans accurately predicts protection from infection or disease
Do not know which branches of the immune sys will succeed in eradicating the parasite
Diff stages of the parasite express diff Ag each assoc w/ diff immune responses
Many parasite pro exhibit polymorphism  5-6,000 pro
Humans exhibit great heterogeneity int heir immune response, and protective genetic traits

Front 59

Parasite control:
Malaria Vaccines CARD 1 of 3

-current approaches?

Back 59

Pre-erythrocytic- anti-infection vaccine
• Against sporozoites and/or liver stages
• Prevent blood stage infection
• Avoid all manifestations of disease
Erythrocytic- anti-morbidity/mortality vaccine
• Against asexual blood stages
• Reduce clinical severity
Mosquito stages- transmission blocking vaccines
• Against mosquito stages
• Prevent dev in mosquito

Front 60

Chemotherapy and Resistance:
Chemotherapy

Back 60

A) Tx of parasitic disease w/ a chem of known constitution
1) Implies we know some semblance of the details of the parasite as well as the nature of the chemical

Front 61

Chemotherapy and Resistance:
Parasiticide:
-major categories (list)

Back 61

drug that is effective in killing parasites
-anti-protozoals
-anthelmintics
-insecticides

Front 62

Chemotherapy and Resistance
-Anti-protozoals
-give examples of protozoan target

Back 62

diverse gp of chem w/ rel narrow spectrum for use
a) Sulphonamides e.g. sulphanitron – Eimeria
b) Nitroimadazoles e.g. metronidazole – Giardia, Entamoeba
c) Carbamides e.g. suramin – Trypanosoma
d) Aminoquinolines e.g. chloroquine – Plasmodium
e) Macrolides e.g. clindamycin – Babesia, Toxoplasma
f) Imidocarb dipropionates e.g. imizol - Babesia

Front 63

Chemotherapy and Resistance
Anthelmintics:
give ex of parasite target

Back 63

1) (Flukes, cestodes, nematodes, flatworms)- used in humans and all domestic spp – lg market sheep/cattle

a) Piperazines e.g. diethylcarbamazine- nematodes
b) Imidazothiazoles e.g. levamisol- nematodes
c) Benzimidazoles e.g. mebendazole– nem/ces (protozoans)
d) Salicylanilides e.g. closantel – flukes, cestodes, Haemonchus
a) Macrocyclic lactones e.g. ivermectin – nematodes (arthropods)

Front 64

Chemotherapy and Resistance
Insecticides with examples

Back 64

1) (insects) and Ascarides (ticks/mites)- lg market, esp 4 livestock and companion animals and env control for people

a) Organochlorides e.g. DDT, lindane - general
b) Organophosphates e.g. diazinon - general
c) Synthetic pyrethroids e.g. permethrin - general
d) Carbamates e.g. carbaryl - general
e) Macrocyclic lactones- general
f) Formamidines e.g. amitraz – Demodex
g) Fripols e.g. fiprinol – fleas
h) Insect gth regulators e.g. lefenuron - fleas

Front 65

Chemotherapy and Resistance:
The ideal parasiticide?

Back 65

.

Front 66

Chemotherapy and Resistance:
Use of parasiticides?

Back 66

1) Therapeutic- to Tx existing infections
2) Prophylactic- timing based on knowledge of epidemiology
3) Concentration w/ time profile- determined by rate of absorption and rate of elimination which are in turn affected by drug, host and parasite properties

Front 67

Chemotherapy and Resistance:
Administration of parasiticides

Back 67

1) Determined by location of the parasite, ease of application and acceptability
2) Injection- SC, IM
3) Orally- drenches, pastes, pills, salt licks, boluses
4) Skin- pour-on, spot-ons, dusts, sprays, washes, tags and collars

Front 68

Chemotherapy and Resistance:
Major problems associated with chemotherapeutics?

Back 68

1) Resistance- a genetic chg in the parasitic pop in resp to selection by an anti-parasitic drug  may lead to avoidance of the drug, detox, ↓ target site sensitivity or ↓ penetration)
a) Rate of dev of resistance is determined by genetic, ecological and operational factors
b) Resistance management programs air to ↓ the discrimination by parasiticides b/w susceptible and resistant parasite genotypes, either by enhancing the survival of susceptible genotypes or by overpowering resistant genotypes

Front 69

Epidemiology and Control
Epidemiology -principles of?

Back 69

the study of distribution and causation of disease frequency in populations -deals w/ pop not indv (pop at risk)
1) Diagnostic- determining the causes of disease in a population
2) Directed action- implementing procedures to prevent or control disease in a population

Front 70

Epidemiology and Control
Determine the problem - how?

Back 70

1) Understanding the LC and transmission of the parasite
2) Identifying the temporal pattern of disease occurrence (sporadic, endemic, or epidemic)
a) Sporadic disease- occurs infrequently and irregularly w/i a pop
i) Parasite is exotic and brought in occasionally
ii) There is a subclinical occurrence and an env chg causes a burst of infection
iii) Switching host and reservoirs
b) Endemic disease- occurs regularly and predictably w/i a pop
i) Hyper-endemic- high prevalence
ii) Hypo-endemic- low prevalence
c) Epidemic (epizootic) disease- occurs in excess of expected frequency in a population
-Disease patterns and parasite ecology- patterns of disease occurrence determined by the parasite’s reproductive rate

Front 71

Epidemiology and Control:
Determine the aim - 3 options

Back 71

1) Prevent the occurrence of parasitic disease where it doesn’t already occur
2) Prevent parasitic disease from ↑ in freq, where it already occurs
3) Eradicating parasitic disease
-To do this we usually need to drive the repro ratio of the parasitic pop to <1

Front 72

Epidemiology and Control
Reproductive rate (R)

Back 72

measure of the lifetime reproductive success of the parasite (repro rate usually higher for microparasites)

Front 73

Epidemiology and Control
R for microparasites

Back 73

Microparasites- R is the mean number of 2° infections generated b one 1° infection introduced into a host pop
i) Factors influencing R

• Infection of susceptible host (β)
• Recovery of infected host (v)
• Death of infected host (α)

ii) Transmission parameter R=β/α + v
iii) Key factors (target control)- R is inversely proportional to the rate of env contamination by infective stages, the rate of entry of new infective stages and the rate of transmission of infective stages to susceptible hosts

Front 74

Epidemiology and Control
R for macroparasites

Back 74

Macroparasite- R is the mean number of female offspring produced throughout the lifetime of a mature F or the ratio of number of adult parasites in the next generation (number of adult parasites in this generation)

Front 75

Factors effecting reproductive rate (R)

Back 75

Factors affecting R

Establishment in susceptible host (β)
Env contamination by infective stages (λ1)
New infective stages (λ2)
Death of hosts (a)
Death of parasites (b)
Death of infective stages (µ)

Transmission parameter R=βλ1λ2/(a+b) + µ
Key factors (target control)- R is inversely proportional to the death rate of infective stages (the parasite death rate) and the death rate of infected hosts

Front 76

R values of parasitic population

Back 76

i) R<1pop cannot persist (disease sporadic)
ii) R=1 pop persists, but does not ↑ (disease endemic)
iii) R>1 pop ↑ (disease epidemic)

Front 77

Key factors of R

Back 77

Rate of env contamination

Biotic pot’l of the parasite- # of infective stages
Suspended dev- hypobiosis
Host density- ↑ # hosts, ↑ # of infective stages
Immune status of the host- esp imp for macroparasites

Death rate of infective stages
Microclimate- temp and moisture (humidity)
Rate of entry of new infective stages

Infected definitive hosts/IH/parentenic hosts coming into the pop
Effluent
Rate of transmission of infective stages to susceptible hosts

Intrinsic (genetic) diff in susceptibility
Acquired immunity
Diet- ↑ resistance w/ ↑ plane of nutrition
Preg and lactation
Multiple (concurrent) infections
Age

Front 78

IDENTIFY PARASITE CONTROL OPTIONS

Back 78

1) Most parasitic disease outbreaks occur for one of 4 basic reasons: ↑ in # of infective stages, ↑ in host susceptibility, intro of susceptible hosts or intro of infection. control options need to prevent the build up of infective stages, limit contact and prevent spread

Front 79

Control Programs

Back 79

a) Prevent, eradicate or control parasitic disease
i) Prevention- maintain sporadic disease
ii) Eradication- epidemic  endemic  sporadic (can never fully eliminate)
iii) Control- epidemic - endemic / hyperendemic - hypoendemic
b) Drive R to ≤ 1

Front 80

Control Strategies

Back 80

Prevent build-up of infective stages by ↓ env contamination and ↓ survival of infective stages
Antiparasitic drugs
Tactical use- Tx disease
Strategic use- ↓ env contamination (prophylactic)
Host density and Health status- ↓ env contaminants
Hygiene and Biological control- ↓ survival of infective stages
Prevent spread of infective stages

Control of vectors
Quarantine
Slaughter

Limit contact b/w susceptible hosts and infective stages by ↓ number of susceptible hosts and isolating susceptible hosts
Vaccination- ↓ number of susceptible hosts
Genetic improvement b/w and w/i pop/breeds (breed for resistance or heritability)- ↓ number of susceptible hosts
Host mvmt- remove from source of infection isolate susceptible hosts)
Pasture management- rotational grazing, alternate grazing (rotate diff spp) and sequential grazing (rotate diff classes of host, i.e. susceptible (yg) animals w/ older more resistant hosts)

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Things to be aware of when implementing control strategies?

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will they lead to ↑ clinical disease, drug resistance or virulence?
i) Management of resistance
• 3 approaches
• Combination- use drugs w/ diff MOA
• ↓ Tx
• ↑ strength/dosage- enough to kill heterozygotes and leave homozygous resistant (few) who will mate w/ homo recessive
b) Appropriate options
i) What we target is dept on our aim and lifecycle (macro (ltd contact b/w infective stages and susceptible hosts is rel more imp) vs. micro (prevent build up of infective stages is usually more imp))

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EVALUATION OF CONTROL PROGRAMS

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1) Cost/benefit comparison at indv level (farm) or state/national level
a) Evaluation of indv control prog- based on a partial budget and net returns
b) Evaluation of a state control program- based on benefit cost analysis
2) Provides a basis for logical decision making
3) Monetary value used as a unit of economic measurement of costs and benefits
4) Problems with evaluation
a) Lack of data on which to base est of benefits and costs
b) Items diff to measure w/ monetary value

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IMPLEMENTATION AND MONITORING of CONTROL PROGRAMS

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Once the control options have been considered an a control prog evaluated, the prog can be implemented, and its success monitored  how this is done is dept on the aim of the prog
a) CS of parasitic disease
b) Presence of parasites
i) Fecal/blood samples for int parasites
ii) Direct examination for ectoparasites

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Parasites in Ecosystems
Ecosystem health

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the condition, performance or functioning of an ecosystem as defined in terms of some desired (healthy) endpt
-Ecosystem fxn- the flow of energy through an ecosystem

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Parasites in Ecosystems
PARASITES REGULATE HOST POPULATIONS - how?

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- determine biomass
1) Measured by ecosys stocks (e.g. animal biomass) and ecosys flows (e.g. organic carbon flux)
Parasites cause pathology in all multicellular organisms and may provide density dept regulation of host pop through effectors on host mortality and fecundity rates
a) Host spp ↑ - parasite pop ↑ - build-up - ↑ mortality and eventually a pop crash

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Parasites in Ecosystems
How do parasites mediate interactions b/w hosts?

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competitive
1) Parasitic infection can affect the outcome of competitive and predatory interactions (i.e. which host indv are killed by predators)
a) Native spp have more parasites than exotic as well as > spp richness - exotic seem competitively superior

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Parasites in Ecosystems
How do parasites act as ecosystem engineers?

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1) chg the biotic/abiotic env to affect the availability of resources to other spp in the ecosys
a) Parasites may alter the phenotype of their hosts to create new resources
i) E.g. Beaver – dams chg env to create a new niche
ii) Cockles- infected ones do not burrow as deeply into the sand -provide a larger attachment area for other critters (rather than sea anemones) to attach

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Parasites in Ecosystems
Emerging parasitic disease

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1) parasitic diseases that have newly appeared or have existed but are rapidly ↑ in incidence or geographic range
2) Emerging parasitic disease of ppl, domestic animals and wildlife are often assoc w/ human-induced env chg
a) Env chgs ↑ survival/transmission of infective stages, ↑ susceptibility of hosts to infective stages, ↑ contact b/w hosts and infective stages
b) Eutrophication- ↑ nutrition in env - ↑ parasitic pop hwr acid rain generates a loss of habitat - ↓ nutrition in env and ↓ in parasites #’s
i) Chgs in water pH due to dev cause the bk↓ of mucous on fish scales, resulting in lesions

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Parasites and ecosystems: How do parasites act as indicators of environmental stress?

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1) Env chgs may lead to ↓ rates of parasitic infection, esp for those w/ complex, indir life cycles
↓ survival or transmission of infective stages and ↓ contact b/w hosts and infective stages - parasites may serve as bioindicators of env stress

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Control in Practice

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A) Implementation depends on
1) Type of medicine you are practicing
2) Whether you are treating indv or herds/flocks
3) Cost benefit analysis of the control/Tx program- personal and economic situation of the client - need to be advantageous

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Control in Practice
-Steps for successful control and Tx of parasitic disease

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1) Defining the problem and/or need
a) Dx a parasitic disease  based on CS or the results of a diagnostic test
b) Identification of a potential problem based on management, environmental factors, breed predisposition etc.

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Control in Practice:
Define the aim of the control/treatment program

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a) Eliminate/reduce clinical disease?  to treat or not to treat?
b) Prevent the occurrence of disease or prevent transmission and spread (prevent infection)
c) Eliminate clinical disease AND prevent re-occurrence (re-infection)

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Control in Practice
Identify “tools” available to you as a veterinarian

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a) Drugs
b) Vaccines
c) Insecticides
d) Management factors
e) Other

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Control in Practice
Implement and Evaluate Program

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a) After implementing the control program, you must follow up with the client to ensure the program is working effectively (clinical signs eliminated? Parasite levels decreased? Compliance? Is the program practical?)

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Control in Practice
control and Tx of parasites requires knowledge of?

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1) Parasite

a) Life Cycle and Transmission
b) Pathogenesis and Pathophysiology
c) Clinical Signs
d) Epidemiology
e) Diagnosis

2) Host

a) Immunology and Immunopathology
b) Physiology
c) Behaviour and Management

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Flea spp?

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a) **Ctenocephalides felis- most common  found on cat and dog
b) Ctenocephalides canis
c) Echidnophaga gallinacea- common in poultry farm  also dogs/cats/humans
d) Pulex irritans- human flea  likes to breed in pig stys
e) Xenopsylla cheopis- rat  mj vector of plague (yersinia pestis)
f) Tunga Penetrans- burrows into the feet of ppl in Latin America

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LC of Fleas


EXAM*

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a) Adults feed and mate on host - F 15µl/feeding 15x/d - eggs stick to pelage and when dry fall off w/ flea feces (undigested blood)- larva req nutrients in that blood to survive -2 moults (3 instars) - temp and humidity imp in survival pupate - (spin silken cocoon) - adult in cocoon is highly resistant to desiccation - emerge when host nearby

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Control of fleas

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a) Aim
i) Prevention of disease - pot’l infestation
ii) Tx and Prevention - current infestation
b) Fundamentals- successful control prog involves:
i) Eliminating the resident pop on the animal (adults)
ii) Eliminate the env pop that can re-infest the animal
iii) Protest the animal from exposure from an outside source

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Flea demographics

Back 99

a) - for every adult there will be a lg number of eggs which may act to re-infest the host - 1 adult=99 juveniles

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Drugs for flea control

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a) Animal- adulticides - rapidly kill adults on host
i) Fipronil- Frountline
ii) Imidacloprid- Advantage
iii) Selemectin- Revolution
iv) Nyenpyram- Capstar
v) Lufenuron- Program and Sentinel  NOT an adulticide - insect gth regulator

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other tools to control fleas?

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a) Env
i) Mechanical
• Vacuum- house and vehicle, pet’s bedding
• Landscaping
ii) Chemical
• Insect gth regulators (Methoprene)  must have residual activity (larvae deep in carpets)  do both high traffic and rest areas  professional pest control if needed
b) Preventing reinfestation
i) Flea preventatives- good prod  Have diff modes of action - pot’l resistant -rotate?
ii) Prevent pets from accessing infested areas and potentially infested animals

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Gastrointestinal Parasites
Protozoa:
-Clinical signs
-Diagnosis

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1) diarrhea, abdominal discomfort, melena  tend to be non-specific
2) Diagnosis- is imp as control and Tx is tailored to the parasite
a) ELISA based kits
b) Fecal smear- quick/easy, positive are valid, delicate forms are observed  poor sensitivity
c) Fecal floatation- concentrates and clarifies, ↑ sensitivity, time consuming, destroys delicate forms
d) ↑ watery diarrhea, see ↑ trophozoites and ↓ cysts, opp for more formed feces

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Giardia duodenalis/lamblia
-LC
-Pathophysiology
-Clinical signs
-Dx
-Control
-Tools

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1) Life cycle- direct- cysts in env ingested by host - excysts in duodenum and rel trophozoites -adhere to epithelial surface and reside (non-invasive) encyst and pass out in feces
2) Pathophysiology- gen diffuse shortening of the microvilli (irrespective of adherence)  malabsorption, ↑ intestinal motility
a) Infections disrupt the epithelial barrier -cause ↑ permeability and diffusion of macromolc across mucosa - may stim immune effector cells e.g. mast cells - histamine
3) Clinical signs- **asymptomatic, diarrhea, steatorrhea (fat in feces), urticaria
4) Dx- observation of cysts in feces (Zn sulphate  collapsed cysts)
5) Control
a) Define the aim
i) Eliminate/↓ clinical disease
ii) Prevention- dev of disease, transmission/spread
iii) Tx and prevention
b) Tools
i) Chemotherapy- Fenbendazole (Febantel)- approved for cats
-Hygiene- bath dog after Tx
-Vaccine- giardia vax – dogs
-Implement- follow up

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Coccidiosis
-2 Genera

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Eimeria, Cystoisospora (Isospora)

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Coccidiosis
-LC
-Clinical SIgns

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a) Life cycle- oocyst req time in env to sporulates  ingested  sporozoites rel  invade epithelial cells (location spp dept)  asexual repro (schizogony)  rupture from cell  invade another epithelial cell  asexual repro (# of cycles is spp dept)  macro/microgametes  oocyst in feces
i) ***Dose of oocyst ingest is directly proportional to the # of sexual cells which dev
b) Need to differentiate the presence of coccidian from the disease of coccidiosis (assoc w/ confinement, yg animals and stress)
i) Common in commercial poultry operations, feedlots, pet shops  high risk env
c) CS- severity proportional to # of oocysts ingested, diarrhea, anemia, poor wt gain, emaciation

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Coccidiosis
-diagnosis
-control
-treatment

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1) Diagnosis- CS + oocyst excretion, intestinal lesions at necropsy
2) Control
a) Aim- eliminate/↓ clin disease, prevention (dev/transmission), Tx and prevention
b) Tools
i) Drugs- numerous used (host specific) all prophylactic  Poultry- ~95% are on ionophores
ii) Vaccines- poultry only  prob w/ administration
c) Prevention is key  prophylactic use of drugs, ↓ stress, ↓ exposure to oocysts (don’t house diff ages together, ↓ stocking rate, management)
d) Controlling Outbreaks- isolate those w/ CS -admin anticoccidials to those w/o -CS -supportive therapy and fluid replacement for clinical
i) Drugs will not work on those w/ the disease, may help w/ 2° infection of bacteria
e) Implement and evaluate- outbreaks? Resistance? Practicality?

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GI Nematodes in Ruminants
LC
Clinical Signs

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A) Life cycle- eggs passed in feces  contain morula which dev in the env  1st stage larvae hatch out of egg, stay in fecal pat and moult to 2nd stage  feed on bacteria  moult to 3rd stage larva  migrate out of fecal pat  on pasture  L3 ingested while grazing
B) CS- most severe in yg animals, severity of disease is proportional to infectious dose which is proportional w/ pasture contamination

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Haemonchus
clinical signs

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1) Clinical signs
a) Hyperacute- massive dose (>20,000 worms), bleed to death, sudden death, anemia, melena
b) Acute- 2,000-20,000 worms in abomasums, anemia, hypoproteinemia, submandibular edema, black feces, lethargy, no milk prod, high fecal egg count
c) Chronic- most common, no anemia/edema, low fecal egg count (for hemonchus)

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Trichostrongylus and Cooperia
clinical signs

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1) Usually asymptomatic, lg burdens  debilitating watery diarrhea ‘black scours’

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Ostertagia/Teledorsagia-
important stuff

Back 110

more imp in cattle
1) Invade gastric glands in abomasums, L4 can enter hypobiosis for several mths

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types
clinical sx

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a) Type 1- yg cattle, heavy infection, many lava mature to adult stage, late winter spring (Aug-Oct)
b) Type 2- due to hypobiotic larva resuming dev, occurs in yearlings grazed prev spring, occurs late summer/autumn (Feb-May)
c) CS- diarrhea, unkempt coat, submandibular edema, nodules in abomasums ‘Moroccan leather appearance’

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Ostertagiasis:
cause of disease (including host and enviro factors)

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i) Parasite factors
• Direct- gth and dev (↑ 10x in size w/i gastric gland), release of immature, adult migration in abomasums  loss of parietal/chief cells and replaced w/ undifferentiated cells w/ no secretory fxn
• Indirect- excretory/secretory products prod by parasite which damage parietal cells
ii) Host factors- inflammatory resp inhibits parietal cells  ↑ pH, ↑ bacterial pop, and ↓ pro utilization, recruits N° and E°
iii) Env factors- build of infectious larva, stress

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Ostertagiasis:
Outcome of disease and Tx and control

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i) Severe watery diarrhea- bac in gut, osmotically active
ii) Lower feed intake- gastrin, distention, inappetance
iii) Edema- hypoproteinemia
b) Control and Tx- separate animals from source of outbreak, Tx w/ anthelmintic (resistance)  right drench right time
i) Subclinical production loss of great economic significance
ii) Worm management- integrated approach is vital  anthelmintic use, pasture management, genetics
• Manage REFRUGIA- targeted selection (not whole gp)
• Pasture management- cross spp grazing, spelling (10wks), rotational grazing
• Genetics- breed nematode resistant sheep

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Systemic parasites

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Toxoplasma, neospora, ancyclostoma, toxascaris

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Toxoplasma and Neospora

LC

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1) T Lifecycle- parasite enters tissues and repro as a tachyzoite  encyst in tissue (CNS or SmM/SkM) and repro bradyzoite - oocyst excreted - req time in env to sporulate
2) N Lifecycle
a) Cattle are susceptible to tachyzoite infection  abortion (midterm) and repro failure, may transmit parasite in subsequent pregnancies  sometimes sheep
b) No known human infections
3) Apicomplexan parasites- apical complex- which have E/pro used to invade host cell

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Toxoplasma and Neospora:

Pathogenesis, clinical signs and Dx

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1) Pathogenesis- Tachyzoite invades cells  asexual repro  cell rupture  tachyzoites are rel and invade other cells  host immune response destroys free tachyzoites  tachyzoites in cells encyst  bradyzoites
2) Dx- fecal exam  oocytes look similar  can’t distinguish
3) Clinical disease
a) CS- reflect organ sys infected (eye, CNS), severity rel to timing of infection (preg- worse if infected early), and immune status of host
i) N- hindlimb paralysis and atrophy, skin lesions
ii) Abortion- tachyzoites can invade and multiply in maternal and fetal placental cells  inflammatory resp ensues  cytokine profile chgs
• Host has to choose b/w parasite immunity and abortion of the fetus
iii) Detection of parasite using biopsy, histology, PCR, serology

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Toxoplasma and Neospora:

Tx Aim and education

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a) Define the aim- Tx clinical cases if possible -**prevent clinical disease**  routes of transmission- oocyst (soil, water), tissue cyst (undercooked meat), tachyzoite (vertical transmission)
i) Human infection- cook meat thoroughly (esp pork, wild game), wash hands after handling raw meat and soil, empty litter box daily, drink pasteurized milk
b) Education and awareness
i) Expectant mothers and immunosuppressed
ii) Livestock- prevent cats from contaminating feed and water, cull affected cows (N)
iii) Feline- curtail hunting activity and do not feed undercooked meat/viscera
iv) Canine- do not let eat dead things, do not breed from mamas w/ affected pups (infect subsequent litters)

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Ancylostoma caninum

Disease
-acute
-chronic

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A) (hookworm)
1) Peracute disease- lactational transmission  puppies deteriorate rapidly in 2nd week (pale mucosa, dark, soft feces)  req anthelmintic Tx and supportive therapy
2) Acute disease- sudden exposure to larva, many eggs found in feces, CS may precede eggs
3) Chronic (compensated) disease- usually asymptomatic, eggs in feces  usually older dogs w/ prev ailments  profound anemia, malnutrition

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Toxascaris:
Clinical signs
Tx/prevention

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1) Heavy infections cause severe abdominal discomfort  death due to int obstruction/rupture
2) Worming
a) Puppies ever 2/4/6/8/12 wks and monthly until 6 mths - Tx nursing mama concurrently
b) Kittens- 3/5/7/9 wks - Tx nursing queen concurrently
c) Adults- consider patent infections, geographic location, contact w/ reservoirs (paratenic hosts) - parasites encyst in tissues
3) Implementation- compliance, resistance - VLM in humans

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Zoonoses CARD 1 of 2

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Trichinella spiralis
Giardia
Echinococcus multiocularis (hytadid disease)
Toxoplamsosis
Leishmania
Trypanosoma

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Describe the above zoonotic diseases CARD 2 of 2

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Trichinella spiralis- direct zoonoses  eating raw or poorly cooked meat (pork and wild game- bear, horse, bison)
Low host specificity and req only 1spp of carnivorous/omnivorous vertebrates to perpetuate LC
Giardia- pot’l for transmission is high, hwr doesn’t occur all that often (in domestic household settings)
Echinococcus multiocularis (hydatid disease)- foxes in Europe, chgs in land use
Toxoplasmosis- human infections are usually rapidly controlled by the immune sys, on of the commonest infections but rarest diseases
Cat only DH- only problematic w/ pregnancy, or in ppl w/ compromised immune sys
Found in relatively everything- kangaroos  otters
Leishmania infantom- hunting dogs in US
Trypanosoma (Chagas disease)
Sterconia- triatoma bug feces vs. Salivaria- tsetse fly transmissiion
Incredible host range- any mammal in the area

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awareness of the range of exotic parasites in order to effectively prevent their establishment in Australia, dept on?

Back 122

1) Introduction and rel into the env in an infective state
2) Conditions supportive of transmission, incl the presence of suitable IH
3) Presence of susceptible adequate definitive host reservoirs

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Effective biosecurity and exotic parasites

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A) dept on surveillance and the ability to respond
1) Threats- animals/animal prod, immigrants, visitors/tourists
2) Consequences- babesiosis, echinococcus, toxoplasmosis, sarcoptic mange in wombats
3) Successful elimination- malaria, filariasis (Wucheria bancrofti)
4) Recent new disease- babesia gibsoni (dog), and spinose ear ticks (horses), varroa mite in bees (Nth A)
Mj threats to livestock- screw worm fly (chrysoma bezziana), surra (trypanosome evansi), trichenellosis
A) Leishmaniasis- vector capacity of Australian sandflies?  found in Kangaroos, dogs imported from other countries
B) Surra (T. evani)- high mortality in horses and native animals, pigs highly susceptible to infection, chronic disease in livestock  transmitted by march flies  though to be an immediate threat b/c of its proximity to Indonesia, Papua new guinea

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Humans as a source of exotic parasite

Name some

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A) returning Australian travellers, migrants, refugees
1) Malaria- malaria- most frequently-reported parasitic infection imported into Australia
2) Schistosoma- mj env chgs could enhance local transmission
3) Tenia solinum- life cycle unlikely to become established in Australia
4) Neurocysticercosis- avg time of presentation after leaving endemic area  11yrs
a) Limitations to detection- uncommon, lack of understanding and post-graduate training, long incubation period, diagnostic and Tx delays

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Parasites in Zoo Medicine
practiced medicine

Back 125

A) Practiced Medicine
1) Preventative medicine- fecal screening, heartworm
2) Quarantine/biosecurity
3) Clinical manifestations- demodex in dibblers
4) Disease surveillance- sarcoptic mange in wombats
5) Zoonotic risk- giardia, entamoeba histolytica, echinococcus
6) Exotic parasites
7) Research- emerging disease, and novel org

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Zoo Medicine:

Diagnostic testing

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1) Fecal conc
2) Direct we mount- reptiles and primates  mobile protozoa
3) Others- fecal culture and larval ID, haematology, skin scrapes, path, PM

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ZOo med:
-complexities and problems

Back 127

1) Samples prob- elephant vs. frog
2) Feces consistency
3) Bhr- (tortoises burrowing underground)
4) Social vs. solitary
5) Seasonal chgs- python (may take 9mth b4 poo), reptiles (ectotherms)
6) Access to samples- husbandry carnivores
a) Enclosure design- wetlands
b) Management
7) Health and safety

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Zoo med:
Tx and administration

Back 128

1) What is normal? Just b/c you find a parasite doesn’t mean you have to Tx it  may not be the 1° etiological agent (often 2°)  often husbandry related
2) Risks- therapeutic drug doses for various spp, adverse affects/CI, where avoiding Tx use env management
3) Administration- oral/parenteral/topical
4) The great unknown- if you look you will find - new parasites, Tx, etc.

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Role of parasites in wildlife health and conservation

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1) Pop management- fecundity, survivorship, cyclicity
2) Host/parasite bal- may be disturbed by anthropogenic factors  disease does not occur in isolation  big pic
3) Evolution- host/parasite bal
Parasite conservation