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Parasitology > Mid-Semester Exam > Flashcards

Mid-Semester Exam Flashcards

1
Q

What is a parasite?

A

An organism that lives off another organism (hosts) for feeding and reproduction

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2
Q

What are 3 groups of parasites?

A

Protozoa
Helminths
Arthropods

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3
Q

What are 2 zoonotic parasites?

A

Ascaris and hookworm

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4
Q

Of the endemic diseases that affect livestock in Aus, which have the largest impact on farm productivity?

A

Parasites

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5
Q

What were the 3 spikes in the word parasite in history?

A

Both world wars and the vietnam war

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6
Q

What are 2 benefits of parasites?

A

Maggots - heal amputations

Hookworms can help to control allergies

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7
Q

Define endoparasite

A

Parasites that live inside internal organs of the host

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8
Q

Define ectoparasite

A

Parasites that lives on the external parts of the host

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9
Q

Define obligatory parasites

A

Parasite that cannot live without host

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10
Q

Define facultative parasite

A

Parasites that can live free in the environment until they find a host

Most of these will die outside the host

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11
Q

What is a definitive host?

A

Host affected by the adult stage of the larvae

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12
Q

Define intermediate host

A

Infected by larval stages of parasite

Larvae develop further (L1-L2-L3-L4) feeding from the host, meaning it is pathogenic causing damage to host

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13
Q

Define paratenic host

A

Larvae that do not develop in host

Alive but inactive inside host

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14
Q

Define direct life cycle

A

eggs picked up from the ground to definitive host for example
- Disease happens quick

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15
Q

Define indirect life cycle

A

different hosts included like an intermediate

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16
Q

Define migratory life cycle

A

Host infected with parasite, migrates from system it was first in to a new system - eg digestive system to brain

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17
Q

Define non-migratory life cycle

A

pick up parasite and it stays there (inhale = goes to lung and stays there

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18
Q

What are 6 routes of infection

A 
Oral ingestion - Eimeria
Inhalation 
Through the skin (injection by mosquito) - Plasmodium
Sexually - tritrichomonas
Transplacental - toxocara canis
Transmammary - toxocara canis
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19
Q

Define prepatent period

A

Period between infection with a parasite and the production of eggs by a female

The interval between infection and the first ability to detect from that host a diagnostic stage of the organism

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20
Q

Define infective stage

A

one in which the parasite is capable of entering its host and continue its development within the host

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21
Q

Define free living stage

A

parasites survive outside the host in this period until they find a new host

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22
Q

What is the latin name for strongyles?

A

Trichostrongylus sp.

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23
Q

What life cycle does strongyles have?

A

Direct and non-migratory with no intermediate host and all stages in host GIT

Stronglyes -> nematode -> helminth -> metazoan

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24
Q

What is the latin name for liver fluke?

A

Fasciola hepatica

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25
Q

How do we write latin names?

A

Genus and species
Genus capital letter
Species lowercase
always in italics

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26
Q

What are 6 host factors affecting infection, parasitism and pathogenicity?

A 
Age and exposure
Quantum of infection 
Genetics -> some animals more resistant
Periods of stress
Pregnancy/lactation
Management factors
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27
Q

what are 6 parasite factors affecting parasitism?

A
  1. Parasite life cycle and climate
  2. Survival of free living stage in environment
  3. Parasite fecundity
  4. Virulence of parasite
  5. Availability of IH or vectors and their ecology
  6. Impacts on host behaviour
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28
Q

What is the latin name for hookworm?

A

Andylostoma duodenale

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29
Q

How does hookworm causes haemorrhage?

A

Grabs intestinal tissue and sucks blood

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30
Q

Which parasite can cause thrombus formation?

A

Strongylus vulgaris -> larval stages can cause thickening of arterial wall and thrombus formation

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31
Q

Name 6 problems caused by parasites

A
  1. Necrosis
  2. Haemorrhage
  3. Thrombus formation
  4. Prevent nutrient absorption
  5. Digest tissue
  6. Allergy and inflammation
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32
Q

What are 3 groups of protozoans?

A

Apicomplexa
Sarcomastigophora (giardia, trypanosoma)
Ciliophora

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33
Q

What are 2 groups of metazoans?

A

Helminths and arthropods

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34
Q

How can protozoa be described?

A

Motile unicellular, eukaryotic microorganisms

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35
Q

Contrast extracellular and intracellular protozoa characteristics

A

Extracellular -> live external to cells, eg in intestinal tract or blood and are antigen masking

Intracellular -> invasive, penetrate host cells and invade cell of immune system, live in parasitophorus vacuole in enterocytes

Protozoa are endoparasites

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36
Q

What are 2 groups of sarcomastigophora?

A

Sarcodina (amoeba) and zoomastigophora (flagellates)

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37
Q

How do amoeba replicate?

A

Binary fission - nucleus and body divided into 2

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38
Q

How do flagellates move?

A

Whip like motion

Undulating cell membrane

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39
Q

How do flagellates reproduce?

A

Binary fission

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40
Q

What 3 groups of flagellates (zoomastigophora) are there?

A

Diplomonadida (giardia)
Trichomonadida (tritrichomonas)
Kinetoplastida (trypanosoma and leishmania)

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41
Q

What is the latin name for giardia?

A

Giardia intestinalis

part of diplomonadidia -> zoomastigphora -> protozoa

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42
Q

What is the host range of giardia?

A

Diverse mammal host range

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43
Q

Where does giardia live during free living stage?

A

Soil, food and water

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44
Q

Describe the structure of giardia in the host and in free living stage

A

host -> 2 nuclei, flagella, median bodies, adhesive disc to attach to intestinal tissue - cover large SA decreasing nutrient absorption

Free living -> 2 giardia encapsulated in each cyst

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45
Q

Describe the lifecycle of giardia

A
  1. Dog infected from cysts in environment
  2. Cysts goes to stomach and small intestine
  3. Establishes in right environment and become trophozoites
  4. Reproduces by binary fission
  5. Make cysts to be shed in faeces
  6. Cysts picked up by next host

Direct lifecycle, internal endoparasites

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46
Q

Name 3 routes of infection for giardia

A
  1. Family member with it
  2. contaminated water, food
  3. direct person to person
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47
Q

Clinical signs of giardia

A

fatty diarrhoea, cramps, weight loss, dehydration, blood, bile function affected

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48
Q

How do we diagnose giardia?

A

Faecal sample to look for cysts and live parasites (trophozoit)

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49
Q

How do we treat giardia? how do we prevent it?

A

Medication for pain and symptoms

If no symptoms -> no treatment

Handwashing, hygiene, wash vegetables

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50
Q

How do we

A
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51
Q

Explain the structure of tritrichomonas foetus

A

Pear shaped, 3 anterior flagella, undulating membrane

Trichomonadida -> zoomastigophora -> protozoa

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52
Q

How does tritrichomonas replicate?

A

Binary fission

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53
Q

Where is tritrichomonas found?

A

Bull penis and prepuce, membranes inside sheath, not normally in semen

Vagina, uterus and oviduct

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54
Q

Tritrichomonas lifecycle

A

Veneral pathogen, infected bull -> passes trophozoites to cow -> lives in reproductive tract

No cysts form as no free living stage

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55
Q

Symptoms of tritrichomonas in cows and bulls

A

Vaginitis, placentitis, abortion 1-16 weeks after service, uterine discharge, irregular oestrus cycles

Bulls -> pain on micturation, dont want to serve, mucopurulent discharge, signs disappear in 1-2 weeks, permanent asymptomatic carrier

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56
Q

How do we diagnose tritrichomonas?

A

Bulls -> 2 weeks of sexual rest followed by testing, smegma samples

vaginal mucous or saline washings of preputial or fetal tissues cultured at 37 degrees for 4-7d, microscope exam, isolate trophozoites

Can also PCR test

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57
Q

what are 2 kinetoplastida

A

leishmania and trypanosoma

Part of zoomastigophora -> protozoa

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58
Q

What is an amastigote and promastigote?

A

Amastigote - Form of parasite with no external flagella

Promastigote - flagella comes from front of body

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59
Q

what is an epimastigote and trypomastigote?

A

Epimastigote - flagella comes from posterior part of body but not past the nucleus

Trypomastigote - completely posterior flagella

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60
Q

What variations of flagella does leishmania have?
Where does it live?
What does it cause?
What are the hosts?

A

Kinetoplastida -> zoomatigophora -> protozoa

Amastigote (in wbc) and promastigote (in fly)
Immune system and targets macrophages
Causes fever, anaemia, lethargy
host sandfly and vertebrates

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61
Q

Leishmania lifecycle

A

Binary fission in wbc as amastigotes -> wbc burst and picked up by other macrophages

Picked up by sandfly (IH) -> turns into promastigote -> replicates in midgut -> migrates to proboscis -> female injects promastigotes in definitive host -> phagocytosed by macrophage -> back into amastigote

Indirect, migratory

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62
Q

How do we diagnose leishmania?

A

Blood smear to detect amastigote in white blood cells

Cutaneous leishmania - sample these areas

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63
Q

Leishmania treatment

A

Liquid nitrogen to skin lesions - freeze lesion killing tissue causing lesion healing

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64
Q

Is trypanosoma intracellular or extracellular and what does it cause?

A

Kinetoplastida (like leishmania) -> zoomastigophora -> protozoa

Extracellular -> swims between rbc and exposed to antibodies and other defence systems
Clinical signs -> vessels blocked, anaemia, emaciation

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65
Q

Trypanosoma lifecycle

A

Initially macrophage increase to combat but then parasite sheds membrane

Vector is tsetse fly -> injects trypomastigotes during blood meal -> binary fission in body fluids + blood -> fly has blood meal and ingests -> multiply by binary fission in fly midgut -> leave midgut and transform to epimastigotes -> multiply in salivary gland and go back to trypomastigotes -> injects trypomastigotes into person

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66
Q

In livestock what is the zoonotic type of trypanosoma? how is it diagnosed and treated and what are symptoms in humans? How do we control it?

A

T. Brucei -> Fever, muscle aches, enlarged lymph nodes, rash, neurologic problems

Cattle - blood sample to detect trypomastigote
human - body fluid or tissue microscopy

Treatment - Metamidium

Prevention -> minimise contact with tsetse flies, traps, chemical control

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67
Q

How are apicomplexa described? What are the developmental stages?

A

Intracellular
Most have indirect lifecycles
Has an apical complex which penetrates the cell (only seen on electron microscope)

Merogony (sexual reproduction), gametogony (sexual reproduction), sporogony (asexual and usually outside the host)

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68
Q

What are 2 types of apicomplexa?

A

Eimeria (coccidia) and piroplasms (malaria)

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69
Q

Route of infection of Eimeria and clinical signs

A

Oral to intestine - uses apicomplex structure to go into enterocytes

causes diarrhoea, dehydration and lethargy

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70
Q

Lifecycle of Eimeria

A

Chickens ingest from moist litter with sporozoites -> enter enterocytes -> merogony to produce meront (pack of offspring in original apicomplexa) -> releases merozoites (new offspring) into lumen that attach to new enterocyte -> this happens for 4-5 generations

Then sexual differentiation happens in the lumen -> female macrogamet goes into enterocyte -> male microgamet releases elongated offspring that go into female to become a zygote then an oocyst with membrane around it -> exits in faeces -> oocyst gets 4 sporocysts inside with 2 sporozoites in each (sporulated oocyst) -> this is infective stage

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71
Q

Diagnosis of eimeria, control + prevention

A 
farm history
Clinical exam
Post-mortem exam
Microscopic exam
Scraping of intestinal wall shows meronts

Vaccinate in first week - avoid overstocking and faeces - treat with sulphonamides

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72
Q

Control/treatment and prevention of Eimeria

A

Vaccinate chickens in first week -> prevent overstocking and contamination of litter
Use anticoxidials

Treat infection with sulphonamides, monensin

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73
Q

What sort of parasite is toxoplasma gondii? What are the hosts? What are the effects?

A

Apicomplexa, intracellular, zoonotic
Definitive -> cats (gametogony)
Intermediate -> beetles and humans

Abortion in humans

Causes behavioural changes in intermediate hosts

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74
Q

Lifecycle of toxoplasma gondii

A

similar to eimeria
But instead of 4 sporocysts with 2 sporozoites in each, it is 2 sporocysts with 4 sporozoites in each

Sporulated oocyst in felid faeces ingested by intermediate host -> vertical or meat transmission -> cyst ingested by final host again (cat) -> bradyzoite (AKA sporozoites) invades enterocytes -> 4-5 gens merogony -> merozoites burst enterocytes -> gametogony -> macro+micro gametes form zygote -> unsporulated oocyst in faeces -> sporulated oocyst with 2 sporocytes and 4 sporozoites in each sporocyst

Moves to brain and causes behaviour change in intermediate host

Asexual reproduction in intermediate hosts, asexual + sexual reproduction in cat intestine

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75
Q

Human toxoplasmosis

A

congenital -> foetal damage
Acute, postnatal -> tachyzoites (AKA trophozoites) invade blood and tissues causing neurological damage, fever

Chronic -> persistance of acute symtpoms up to several years

Latent -> bradyzoites remain in tissues and maintains immunity

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76
Q

Diagnosis of toxoplasma gondii

A

Find oocysts in cat faeces

Humans -> serology for specific IgG and IgM antibodies, symptoms

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77
Q

Cryptosporidium -> where is it, hosts

A

Apicomplexa found in blood, one group found in tissue

C Parvum -> found in cattle intestine, zoonotic, waterborne transmission

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78
Q

Cryptosporidium lifecycle

A

TRACHEA AND INTESTINE - thick walled and thin walled oocysts

Sporulated oocyst comes out -> sporozoite goes into epithelial cell in trachea/intestine to undergo merogony -> bursts cell -> merozoite released -> repeat for few generations

Some become microgamete and macrogamete -> micro find macros and a zygote is formed -> oocyst forms with no sporocysts at all -> only one oocyst with 4 sporozoites (naked oocyst)

Thick walled oocysts leave the host, thin walled stay in and reinfect

Route of infection - inhalation

Direct, non-migratory lifecycle

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79
Q

Clinical signs and diagnosis of cryptosporidium

A

Clinical signs -> asymptomatic, young immunocomprimised animals, villous atrophy, malabsorption

Diagnosis -> visualise oocysts in faeces, immunofluorescence, RAT, PCR

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80
Q

Plasmodium spp. 4 species infecting humans

Type of parasite

A

P. Malariae
P. Ovale
P. Vivax
P. Falciparum

Apicomplexa

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81
Q

Malaria transmission

A

Caused by bites of infected anopheles mosquito vectors - only females

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82
Q

Plasmodium lifecycle

A

Indirect, migratory
Prepatent period -> when sporozoite goes into person to when we do blood test
Definitive host -> mosquito

Mosquito bites -> from blood infects liver with sporozoite where mergony happens in hepatocytes -> 4-5 gen merogony -> merozoites penetrate rbc and replicate to engagement ring shape -> micro and macrogametes form -> rbc bursts and releases gametes -> loss of rbc and toxin response (shivering) -> gametocytes form and taken up by pregnant mosquito -> go to stomach -> female and male combine to produce zygote called ookinete then oocyst in gut wall -> produces sporozoite (no sporocyst) -> oocyst ruptures and releases sporozoites -> sporozoites find saliva -> new host

Forms proteins on rbc that stick to vessels to avoid going to spleen

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83
Q

Symptoms and diagnosis of plasmodium

A

Symptoms -> 3 day cycle fever for malaria, 2 day cycle for p. vivax
fever, shiver, okay, repeat
Anaemia, splenic enlargement, involvement of brain, liver, kidneys, rbc block vessels

Diagnosis -> microscopy - ring, trophozoite, schizont, gametocyte, make blood smear and look for young trophozoites (ring shape)
PCR, patient antibodies

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84
Q

Prevention and control of plasmodium

A

Anti-malarial drugs, insecticides

  • resistance to both of these
  • chemical repellents, bed nets
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85
Q

Describe babesia spp. -> distribution, definitive host, name of disease

A

Parasite of rbc - B bovis inside 1 in 5000 ticks, B bigemina 1 in 500 ticks
Definitive host cattle
Disease called babesiosis or tick fever
Northern aus or east coast

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86
Q

Lifecycle of babesia

A

Zoonotic

Tick takes blood meal introducing sporozoites into host -> sporozoites enter rbc and undergo generations of mergony -> merozoites then form gametes -> tick ingests gametes -> Microgamete ruptures and finds macrogemete for fertilisation in midgut -> ookinete enters salivary gland -> sporogony in salivary glands to sporozoites -> restart

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87
Q

Clinical signs, control and animal susceptibility of babesia

A

clinical signs - fever over 40, loss of appetite, depression, weakness, anaemia, diarrhoea, abortion in cows, head pressing, convulsions

Control -> eliminate the ticks

Susceptibility -> british and euro breeds, bos indicus resistant, maternal antibody passed down in utero, endemic stability possible where clinical signs absent

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88
Q

Describe Theilieria spp.

A

Apicomplexa - involves ticks and cattle
parasite of lymphocytes -> when it gets heavy it may also be of rbc

Lifecycle is unknown
Vectors -> lice and tabanid flies

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89
Q

Diagnosis, pathology and clinical signs of Theileria spp.

A

Diagnosis -> blood sample in EDTA anticoagulant, PCR for species identification

Clinical signs -> severe anaemia, lethargy, lack of appetite, exercise intolerance, pale mucous membranes, abortion and stillbirth

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90
Q

Name 4 types of helminths

A

Platyhelminths
Nematodes
Acanthocephala
Annelida

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91
Q

Characteristics of platyhelminths

A

No body cavity, incomplete to no digestive system, hermaphrodites

Classified as:

  • Turbellaria (free living)
  • Monogenea
  • Trematoda
  • cestodes
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92
Q

Describe fasciola species - 2 types, distribution, hosts

A

Parasites of sheep, horse, cattle, wildlife and humans

Lost production, stock death, found on every continent but few infections in aus

A fasciola hepatica - temperate liver fluke >29mm
B fasciola gigantica - not present in aus, higher pathogenicity, >52mm

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93
Q

Fasciola hepatica lifecycle

A 
Prepatent period -> consumption of metacercaria until we can detect them in faeces
Definitive host -> mammals
Intermediate host -> snail
Indirect, migratory
Infective stage -> metacercariae

Adult parasite lives in bile duct of sheep - hermaphrodite + produces eggs -> eggs go to bile duct, duodenum + intestine -> environment -> egg has operculum that opens to release miracidium in water -> babies (miracidium) have cilia to swim -> find snail -> becomes sporocyst inside containing germinal cells to produce more sporocyst -> rediae -> cercariae -> cercariae leave snail + encyst on water plants -> become metacercariae ingested by humans, sheep or cattle -> encysts in duodenum, travels to liver to become adult in bile ducts

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94
Q

Fasciola hepatica location

A

south east QLD, coastal and tableland NSW, all victoria, eastern tas

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95
Q

Fascioliasis - acute vs chronic

A

acute -> blood loss, anaemia, inflammation, swollen liver, tracts in liver, death

Chronic -> damage to bile duct, liver atrophy, anaemia, weight loss, progressive weakness, submandibular edema

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96
Q

Diagnosis of fasciola hepatica

A

behaviour of sheep
faecal sample for eggs -> sedimentation, presence or absence
Blood test for enzymes associated with liver damage (glutamate dehydrogenase)
Blood test for serum antibodies

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97
Q

Prevention and control of fasciola hepatica

A

Drench
Cook watercress
Pasture management for draining/fencing off swampy areas
Quarantine new sheep

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98
Q

Fasciola hepatica immunity and resistance

A

Cattle -> resistance to re-infection after 7 weeks of a primary infection. Immunity transferred with lymphoid cells rather than serum

Sheep -> immunity less clear than with cattle, little immunity is generated during natural infections due to worm burdens

99
Q

Describe the size of paramphistomes and what they are known as

A

Stomach flukes
<1cm
orange/red as adults

trematode -> platyhelminth -> helminth -> metazoa

100
Q

Stomach flukes lifecycle

A

Ruminants ingest metacercariae on vegetation -> goes to stomach to become adult then to beginning of intestine -> causes damage and exits through lumen -> some back back up tract to stomach again -> eggs are produced and go into aquatic environment that have operculum that opens to release miracidium -> miracidium have cilia to swim -> picked up by planorbid snail in 24 hours -> miracidium become sporocysts and then cercariae -> then exit snail and encyst and become metacercariae on vegetation

Intermediate host -> planorbid snail
Definitive host -> ruminant
Indirect and nonmigratory

101
Q

Paramphistomes (stomach fluke) distribution

A

Mainly in coastal NSW
Light infection -> southern and central tablelands, slopes and coastal areas

Serious outbreaks -> heavy infections with immature flukes - new england tablelands

102
Q

Stomach fluke clinical signs

A

Immature flukes in the intestine -> strong suckers, destroy intestine lining - most damage caused by this stage

Heavy infection with developing flukes -> ulceration, haemorrhage, weight loss, enteritis diarrhoea, death

Moderate infections with the immature fluke -> reduced weight gain, reduced milk production

103
Q

Immunity towards stomach fluke

A

Resistance occurs after exposure

Weaner cattle and lambs are the most susceptible

104
Q

Diagnosis and control of stomach fluke

A

Diagnosis -> post-mortem, history of the outbreak, clinical signs, examination with magnifier of the small intestine

Dx -> roundworm, liver fluke, poisonings

Why not faecal egg count? If clinical signs are not present this wont be used

105
Q

Control of stomach fluke

A

Draining, fencing off wet areas, alternative water sources and drenching (no drenches registered in nsw)

106
Q

Describe blood flukes - size, where they live, where the adults are

A

> 25mm
Parasites of blood vessels - like different vessels in different hosts
Adults in ruminants, birds and humans - the blood flukes we have in aus do not infect cattle

Birds -> nasal vessles of ducks and portal vessels of seagulls

Snails are intermediate host

107
Q

Blood fluke lifecycle

A
  1. Eggs are passed in faeces, hatch and release miracidia via operculum under optimal conditions
  2. Miracidia swim and develop in snail - two generations of sporocysts then production of cercariae
  3. Infective Cercariae exit snail and penetrate skin of definitive host (eg duck or human) and migrate through tissues to vessels where they become adult schistosomes (in humans mesenteric veins)
  4. Eggs made by females move to intestinal lumen and passed in faeces
108
Q

How do blood flukes hurt the host?

A

Interfere with normal blood flow
Parasite products form host response and inflammatory granulomas “egg granulomas”
Immunity is hard to generate

109
Q

How do we diagnose blood fluke?

A

Eggs in faeces

Antibodies or antigens in blood or urine samples

110
Q

What schistosoma spp (blood flukes) are found in humans?

A

S. mansoni
S. hematobium
S. japonicum

111
Q

What schistosoma spp (blood flukes) are found in humans?

A

S. mansoni
S. hematobium
S. japonicum

112
Q

Schistosoma lifecycle in humans

A

Adults produce eggs passed in urine or faeces -> eggs hatch in water releasing miracidia that penetrate snail tissue -> generations of sporocysts in snail -> cercariae released by snail in water -> swim and penetrate human skin -> cercariae lose tails and become schistosomulae -> circulation -> portal blood in liver -> become adults -> paired adult worms migrate to mesenteric venules of bowel

113
Q

Symptoms of schistosoma in humans

A

dermatitis (swimmers itch), abdominal pain, diarrhoea, bloody stool, mucosal fibrosis due to inflammatory response to eggs, egg granulomas

114
Q

Diagnosis and treatment of schistosoma

A

Histology, eggs in urine or stool, symptoms

Praziquantel
Eliminate snails, dont swim in snail water

115
Q

Benefits of schistosoma to humans

A

Inject antigens to reduce incidence of type I diabetes in mice
Immunotherapy

116
Q

Describe the morphology of cestodes

A

Have rectangular segments (proglottids) - each is hermaphrodite and can reproduce with central pore
From 0.4mm

Head -> scolex sticks to tissue with hooks, suckers and rostellum
Neck -> germinal cells that produce proglottids

70% of segments produce eggs at once

117
Q

3 classes of cestodes

A

Cyclophyllidea, pseudophyllidea and diphyllobothridea

118
Q

Diphyllobothrium latum lifecycle

A

Proglottids release immature eggs in small intestine that exit in faeces into water -> eggs (gravid) embryonate in water -> coracidia released and ingested by crustacean -> become procercoid larvae -> infected crustacean ingested by small freshwater fish -> procercoid larvae released into new host GIT -> develop to plerocercoid (second IH) -> infected fish ingested by human -> become adults and lay eggs in the intestine (definitive host)

119
Q

Where is diphyllobothrium latum found?

A

Scandinavia, russia, japan, north america

120
Q

Clinical signs of diphyllobothrium latum

A

Can last decades - most asymptomatic

Diarrhoea, weight loss, abdominal discomfort, vitamin B12 deficiency, pernicious anaemia, intestinal obstruction

121
Q

Diagnosis of diphyllobothrium latum

A

Operculated eggs, broad proglottids in stool

Check for anaemia with complete blood count

122
Q

Control + prevention of diphyllobothrium latum

A

cook fish
freeze at -10 for 48h
dont feed reservoir animals in endemic areas (dogs and fish)

Treat with praziquantel

Vitamin B12 may be needed

123
Q

Describe characteristics of pseudophylidiae

A 
2 bothria
single, central uterine pore
ciliated, free living larvae
water essential for transmission
Oval eggs
2-3 IH
124
Q

Describe characteristics of cyclophyllidiae

A 
4 suckers +/- hooks
1-2 lateral genital pores
No free-living stages
water not essential for transmission
Eggs round
1 IH
125
Q

Name the species of pseudophyllidean cestode and its lifecycle

A

Spirometra erinacei - zoonotic (can get to brain of people) -> same lifecycle as diphyllobothrium latum but water flea and tadpole for IH not crustacean and fish

Cat, dog, dingo, fox DH

Egg laid and passed into faeces of DH in water -> eggs embryonate at 2 weeks -> coracidia hatch when operculum opens -> eaten by water flea -> turn to procercoid -> eaten by tadpole -> turn to pleurocercoid -> turns to frog -> Eaten by DH (dogs and cats) and become adult in gut wall

126
Q

Moneizia expansa lifecycle

A

Cyclophyllidea

Adults produce eggs in small intestine -> embryonate in environment -> ingested by IH oribatid mite -> hexacanth develops to cysticercoid -> sheep infected by eating mite -> become adult in small intestine

In cattle -> moneizia benedini

Treat with praziquantel

127
Q

Dipylidium caninum lifeycle

A

Zoonotic
Dog definitive host - human accidental host

Adult worm in dog intestine produces egg -> in faeces -> eggs eaten by flea larvae -> metacestode in adult flea -> back to dog

128
Q

Which taeniid species are zoonotic?

A 
Taenia saginata - DH dog/human and Cattle IH
Taenia solium (pork) - not in australia - humans can be IH and DH + causes neurologic disease (pigs can ingest eggs from human species)

Eggs in environment eaten by IH and then cysts form in muscle - eaten by humans

129
Q

List taeniid species and their IH and DH

A 
T. pisiformis -> rabbit/ dog - liver
T serialis -> Rabbit/ dog - subcut or intramuscular
T. hydatigena -> sheep/ dog - liver
T. ovis -> sheep /dog - muscles
T. taeniaformis -> mouse/cat
130
Q

What is the echinococcus species found in australia?

A

Echinococcus granulosus zoonosis
Causes hydatidosis - found in small intestine of wild dogs
arrived in aus with dogs and sheep

Intermediate stages infect people, livestock and wildlife

East coast

owners must praziquantel dogs within 14d entering Tasmania

70% liver and 20% lungs

131
Q

Diagnosis of echinococcus granulosus in dogs

A

Post-mortem
faecal floatation not useful as all taeniid eggs look alike
Purge with arecoline hydrobromide
PCR using DNA extracted from eggs

Treat with praziquantel 5mg/kg

132
Q

E. granulosus in wildlife

A

Spread when sheep were grazing -> dogs would eat the sheep and leave eggs in environment that macropods would ingest and dogs would eat again

Dogs also susceptible to infection

Cysts found almost exlusively in lungs of wildlife

133
Q

How do we treat tapeworms?

A

Praziquantel 5mg/kg for D. caninum. Echinococcus and taenia spp.

For S. erinacei dogs 35/45mg/kg

For D. caninum flea control should also be considered

134
Q

Describe the structure of nematodes

Males and females

A

Males and females separate
Teeth, cutting plates or leaf crown
Complete digestive system

Males
- caudal papilla, spicules, rays, bursa, testis, vas deferens and seminal vesicles

Females
- vulval flap, one or tubular ovaries containing germinal cells, oviduct, vagina, vulva

135
Q

3 terms to describe the egg laying of nematodes

A

Oviparous -> egg producing (fasciola hepatica)
Ovoviviparous -> eggs have larvae in it when laid (Filaroids osleri)
Viviparous -> give birth to larave, no eggs at all (dirofilaria immitis)

136
Q

4 types of nematodes

A

Ascarids
Strongylids
Spirurida
Enoplida

137
Q

name 2 strongylids of sheep

A

Haemonchus contortus (barbers pole worm)

Trichostrongylus colubriformis (black scour worms)

138
Q

Haemonchus contortus lifecycle

A

Adults in abomasum lay eggs that are shed in faeces (oviparous) -> in right conditions L1 hatch -> L2 -> L3 and migrate from dung to pasture -> L3 infective eaten by sheep -> larvae develop to L4 and L5 in abomasum -> adults

PPP 14-21d

prefers 25-30 degrees

1 week from egg to L3

139
Q

Haemonchus contortus clinical signs

A

Bottle jaw
anaemia
no diarrhoea
death before weight loss due to anaemia

140
Q

Trichostrongylus colubriformis structure and clinical sign

A

Hair like worms tapered at one end
About 6mm for males and females
(females larger than males)
Hard to see at post mortem

Live in first 3m of small intestine + damage gut lining -> scouring

Ruddy brown colour

141
Q

Which nematode demonstrates hypobiosis?

A

Trichostrongylus colubriformis (sheep) - can sit in intestine or abomasum and wait for conditions to be right before becoming adults

Ostertagia ostertagi (type 2)

142
Q

Name 3 nematodes infecting cattle

A

Ostertagia ostertagi
Haemonchus placei (barbers pole worm of cattle)
Trichostrongylus axei

143
Q

Ostertagia ostertagi lifecycle

A

Same lifecycle as haemonchus contortus in sheep

Brown stomach worm
Adult lives in abomasum producing eggs that pass in faeces -> live in dung to L3 -> climb to pasture into water droplet -> ingested by host -> L4 + L5 -> become adults and lay eggs

144
Q

Ostertagia ostertagi symptoms and 2 types of disease

A

Weight loss, scour, hypobiosis, malnutrition (damage to abomasum)

Type I ostertagiasis -> due to ingestion of large L3 over short period occuring in winter/spring. Tablelands where calves weaned in autumn causing watery diarrhoea

Type II ostertagiasis -> larvae ingested and penetrates abomasal wall, staying there for week-months and becoming adults. Damage when they emerge in large numbers

145
Q

Name 3 large strongyles and 1 small strongyles infecting horses

A

Large -> Strongylus vulgaris, S. edentates, S. equinus

Small -> Cyathostomins

146
Q

Strongylus vulgaris lifecycle

A

Bloodworm (horses)

Adult lays eggs in intestine passed in faeces -> develop L1-L3 -> go onto pasture with cuticle -> eaten by horse -> penetrate intestinal wall -> L4 -> migrate to arteries around GIT -> back to LI to become adults

Resistant to freezing but die in hot/dry environment

147
Q

Strongylus vulgaris disease

A

Burrows in the walls of arteries -> blood clots -> disrupts flow to intestine -> larvae move to large intestine lumen to mature

Can cause thrombi

148
Q

Lifecycle of S. edentates and S. equinus

A

Same as strongylus vulgaris but migrate to liver not arteries

149
Q

Cyathostomins lifecycle

A

Horses - in 80-90%
worldwide distribution

Adults in colon and caecum pass ova in faeces -> L1-L3 -> L3 onto pasture ingested -> L4 encyst in wall of colon and become adults

150
Q

Cyathostomins disease mechanism

A

Small strongyles horses
often due to mixed infection with different species of these

Heavy infections have clinical signs
May increase resistance but not become immune

Feed on tissue of intestinal mucosa -> diarrhoea, weight loss

Larvae penetrate gut wall -> cysts disturb normal function + oedema of muscosa

151
Q

Diagnosis of cyathostomins

A

Egg of immature larvae count in faeces

152
Q

Name and describe structure of 1 nematode strongyloid infecting dogs

A

Ancylostoma caninum - hookworms
zoonotic

Large buccal capsule, 3 pairs of marginal teeth and dorsal gutter
Well developed bursa
common in coastal areas

153
Q

Ancylostoma caninum lifecycle and PPP

A

Adults in intestine lay eggs -> hatch and L1-L3 -> L3 can be ingested or climb thorugh skin of dog or person

If ingested - goes to small intestine to become L4 and adult
Percutaneous - blood vessel, lymphatic duct to lungs or trachea or intestine

Can infect pup transmammary

does hypobiosis and PPP 2 weeks

154
Q

Ancylostoma caninum in people

A

Risk factors - bare feet, humidity, dogs
Causes itch
Townsville and north QLD

155
Q

Ancylostoma caninum signs in dogs

A

Black, tarry faeces
pups have reduced haematocrit
microcytic, hypochromic anaemia
Poor coat, loss of appetite, weakness

156
Q

Ancylostoma caninum control

A

treat with all wormers every 3 months
parental iron, vitamin B12 and protein diet
blood transfusion for young pups

remove faeces before hosing, kennel floors clean and dry
beds cleaned daily

157
Q

Name one enoplida, ascarid and spirurida of dogs

A

Enoplida -> Trichuris vulpis
Ascaridida -> toxocara canis
Dirofilaria immitis -> spirurida

158
Q

Toxocara Canis Lifecycle

A

Adults in small intestine lay eggs -> passed in faeces -> L1-L2 in egg -> egg (infective stage) ingested by dog -> goes to SI, blood and lungs -> becomes L3 in lungs -> coughing to mouth -> swallowed to SI -> adults here

Young animals and humans susceptible -> can affect pups in pregnancy

159
Q

Toxocara canis clinical signs and post mortem

A

Heavy infection with lavae -> pulmonary damage, coughing, frothy nasal discharge, larval migration, pneumonia

Heavy infection with adults -> occlusion of gut, enteritis blocked bile duct

Post mortem -> lung focal haemorrhage in puppies, pot belly, worms in intestine and stomach

160
Q

Toxocara canis diagnosis and treatment

A

Faceal egg count
Antibody test
Differentiate T. canis from T. leonina with the structure of alae

Treat with anthelmintics every 3-6 months throughout lives
Hygeinic disposal of dog faeces

161
Q

Trichuris vulpis lifecycle

A

whipworms
zoonotic potential

Adults lay eggs in faeces can survive for years -> L1 infective stage -> eaten -> l1 penetrates gland in ileum and caecum -> undergoes 4 moults -> adults embed anterior end in mucosa

PPP 3 months

most infection light and asymptomatic
Heavy infection - haemorrhagic collitis, anaemia, weight loss, diarrhoea

162
Q

Trichuris vulpis control and diagnosis

A

Whipworm - Enoplida - Nematode
Diagnosis - eggs in faeces

Control - canine all wormer with praziquantel, pyrantel and oxantel every 3 months

163
Q

2 ascardid nematode in horses

A

Parascaris equorum - affects foals and young stock

Oxyuris equi

164
Q

Parascaris equorum lifecycle

A

Adults lay eggs in small intestine -> L1-L2 in faeces in egg -> L2 goes to pasture (infective stage) -> L2 ingested and goes to SI -> liver for a moult -> lungs -> tracheal migration -> SI by coughing and swallowing -> reproduction

165
Q

Parascarid equorum clinical signs

A

Blockage of gut - colic, poor growth, pot belly, rough coat, couhging, damage to lungs and liver

Diagnose with sticky tape in anal area - eggs attach and apply to slide

166
Q

Oxyuris equi lifecycle, pathogenicity and control

A

Ascarid nemaode of horses

Adults in intestine -> eggs laid and stick to perianal area for several days before dropping -> L3 develops within an egg -> ingested -> larvae hatches in intestine -> L4 and adults in colon and caecum

Causes itching around anus, rat tailed, inflammation of intestinal mucosa

Control by sponging to remove eggs and anthelmintics (praziquantel)

167
Q

Describe the lifecycle of tongueworms (Linguatula serrata) and their zoonotic transmission

A

definitive host - carnivores
IH -> herbivores

eggs onto pasture, picked up by herbivores -> goes to mainly lymph nodes, heart, lungs and liver

humans get it by eating infected liver, heart, lung and can infect eyes

Arthropods

168
Q

What family do fleas of vet importance belong to, and what 4 genera are we concerned about?

A

family - pulicidae

Genera -> echidnophaga, ctenocephalides (flea allergy dermatitis), pulex and spilopsyllus

169
Q

What are fleas?

A

Arthropods -> insects -> flea

170
Q

What genera of fleas have both pronotal and genal combs, and just a genal comb?

A

Both -> ctenocephalides

Just genal -> spilopsyllus

171
Q

What genera of fleas have no genal or pronotal combs?

A

Echidnophaga

Pulex

172
Q

Flea lifecycle and ideal conditions

A

Eggs hatch on skin -> larvae feed on organic debris -> pupae 3-4 weeks later -> adults 1 week to 1 year later

Ideal conditions -> 25 degrees and 75% humidity

Die 2-3d without food (host)

173
Q

Facts about fleas jumping

A

About 250x their own height

fleas have protein resilin in leg hinges - elasticity high

174
Q

Flea morphology

A

Head, thorax, 3 pairs of legs and abdeomn
chitinised
3rd pair of legs adapted for jumping
Lateral compression

175
Q

Describe flea allergy dermatitis signs

A

hypersensitivty to saliva - pruritis and scratching = self trauma

Skin thickening, hair loss form middle of back to tail base, down rear legs

176
Q

Diagnosis, treatment and control of fleas

A

Diagnosis -> lesion areas, flea faeces, fleas

Treatment -> oral and topical preventatives

Control -> flea shampoo, collar, powder, spray, oral, daily vacuuming, wash bedding, insecticides, treat other animals in house

177
Q

List diseases fleas can carry in rats, rabbits and dogs

A

Rats -> bubonic plague
Rabbits -> myxomatosis
Dogs -> dipylidium caninum (tapeworm)

178
Q

What are ticks?

A

Arthropods -> arachnids -> ticks

179
Q

Explain the difference between hard and soft ticks

A

Hard -> capitulum visible, dorsal shield, eyes visible, slow feeders, mouth parts anterior, scutum - family Ixodidae, up to 3 host cycles

Soft -> capitulum not visible, rapid feeders, mouthparts underneath, no scutum - family argasidae, multihost cycles (multi-nymph stages)

180
Q

General tick lifecycle (one host)

A

adults drop off host to lay eggs -> 6 leg larvae -> crawl onto host and blood meal -> 8 leg nymph blood meal -> adult

181
Q

2 host tick lifecycle

A

Adults drop off host and females lay eggs in fall -> hatch to 6 leg larvae -> crawl onyo first host to become nymph in spring -> leave first after blood meal and become adults off a host -> attach to new second host for feeding and mating in summer

Becomes nymph->adult OFF the tick

182
Q

3 host tick lifecycle

A

adults drop off host to lay eggs -> 6 leg larvae -> larvae atttach to 1st host and become nymphs -> attach to second host and moult to adults after feeding -> atach to third host for feeding and mating

183
Q

Disease mechanisms of ticks

A

Blood loss - anaemia
reduces growth rate of host
produces toxins when capitulum attaches
hypersensitivity to saliva

184
Q

3 steps for ectoparasite treatment in companion animals

A
  1. Isolation -> of animal to prevent spread to non-infested individuals
  2. Medication -> to kill the parasites
  3. Treatment -> of the animals environment
185
Q

Describe and name the dog tick AKA australian paralysis tick

A

Ixodes holocyclus - hard tick
vectors of infectious agents including babesia
Most medically important

186
Q

Hosts of the australian paralysis tick

A

Natural hosts - bandicoots, possums, kangaroos (immunity protecting against toxins), birds, humans, dogs and cats

spring peak season when develop into adults

187
Q

Australian paralysis tick effects on humans and lifecycle

A

Local itching, hard lump at bump site, to anaphylactic shock

3 host lifecycle -> eggs deposited on ground -> larvae feed on host -> moults to larger nymph -> feed on new host -> adult moves to 3rd host

Bandicoots and possums transmit these ticks and have built up immunity

188
Q

Distribution of ixodes holocyclus

A

Australian paralysis tick
East cost
Dogs infected by walking through long grass

189
Q

Morphology of capitulum of australian paralysis tick

A

Palp -> leg like sensory structures to find things
Chelicera -> pierces the skin
hypostome - anchors tick

190
Q

Pathogenesis of ixodes holocyclus

A 
Anaemia
toxicosis
Inhibits immune processes
Transmit pathogens - babesia
one tick can cause paralysis
change in bark -> wobbly back legs -> paralysis
191
Q

Diagnosis and treatment of ixodes holocyclus

A

IV anti-tick serum
search inside mouth, tongue, lip folds, face, eyes, ears, nostrils, vulva
clip
remove ticks before paralysis signs start
quiet, stress free environment with food and water withheld

192
Q

Describe the southern paralysis tick morphology and distribution

A

Ixodes cornuatus -> similar to I. holocyclus but cornuatus has all legs same brown colour - holo has paler middle legs

Tas, southern vic and nsw

193
Q

Describe hosts of bush tick, distribution and clinical signs - haemophysalis longicornis

A

cattle prefered host
other host - dogs, horses, marsupials and birds

east and west coast of Aus, high rainfall areas of QLD and NSW

Clinical signs -> skin irritation, blood loss, babesiosis in dogs causing anaemia and death

194
Q

Distribution, host lifecycle number and distrinctive characteristic of brown dog tick - Rhipicephalus sanguineus

A

3 host cycle
domestic dogs DH
large eyes distinctive characteristic

Found in tropics and subtropics, mainland aus

195
Q

Pathogenesis of brown dog tick

A 
skin irritation, may also cause paralysis
heavy infestation - anaemia
vector of babesia
can survive off dog for long periods
tick worry at infection site
196
Q

tick removal

A

avoid squeezing body to release more toxin
use fine forceps close to skin to pull

Pyrethroid spray - leave for few mins and spray again to paralyse the tick, it will die and fall off after a few days

197
Q

What is the most important cattle disease in Aus?

What other animals is it found on and where is it found?

A

Rhipicephalus microplus -> asian blue tick
also found on sheep, horses, dogs, pigs, marsupials

found across northern austrlaia and nsw north coast

198
Q

Rhipicephalus microplus lifecycle

A

females and males find each other on skin and breed -> male dies, female drops off lays eggs on ground -> hatch on pasture 2-3 weeks later -> larvae climb onto cow -> larvae engorge -> nymphs engorge -> adults

1 host cycle

199
Q

Rhipicephalus microplus disease, treatment and control

A

Anaemia especially in calves, tick worry, damage to hides

Treatment + control -> insecticides kill all stages on host (spray or plunge dip). Bos indicus are resistant to ticks, rotate cattle on pastures 3-5 month intervals, resistance develops at repeat exposure

200
Q

Name, morphology and distribution for buffalo fly in cattle

A

Haematobia irritans exigua

3-4mm biting fly with silver thorax and dark stripes - only parasitic as adult

Breed in dung

Hot humid regions of NA and north-east NSW to north WA -> need high humidity

201
Q

Lifecycle of buffalo fly

A

7-11d lifecycle

Blood suck on host -> females lay eggs in dung and return to host -> larvae -> pupae -> young adults go to cattle -> adult

202
Q

Clinical signs of buffalo fly

A

Lower weight gain, milk production, severe skin irritation, damage to hides, skin ulcers, allergy
200 flies/animal reduce production

Bulls more infested than cows, aged animals more burden, vector for trypanosoma evansi (flagellate)

Intermediate host for filaroid nematodes

203
Q

Describe sheep lice morphology, scientific name and cost

A

Bovicola ovis - biting lice
flat body, 1.6mm long, bite

cost to treat eith chemicals and for lower quality wool cuts

204
Q

Lifecycle of bovicola ovis

A

adult female lay 2 eggs every 3 days -> eggs attach to wool -> hatch after 10 days -> nymph moults 3 times as it grows (no larvae stage) -> young adults -> adult

all stages on sheep, all stages parasitic,

205
Q

Disease from bovicola ovis
Seasonal pattern
Diagnosis

A

likes 37 degree fleece temperature, no rain
chew skin, hairs sebum, irritation and self trauma
wool ragged

above 45 degrees kills adults
shearing decreases numbers by 90%
declines over summer and high late autumn - winter

10 wool partings

206
Q

Eradication and control of bovicola ovis

A

Same chemicals as flies

Eradicate through short wool treatment with pour on or dip treatment 1-2d after shearing

4-6 weeks after shearing use plunge

207
Q

Management and control of bovicola ovis

A

Shearing, chemical control (dose rate, sufficient time in dip, maintain dip at full strength

Break cycle

208
Q

Name of the australian blowfly
Lifecycle
clinical signs

A

Lucilla cuprina

Female adults lay eggs onto sheep -> become feeding larvae -> drop off sheep to become wandering larvae -> burrow in soil to become pre-pupae over winter -> in spring emerge as pupae -> week later adults

larvae are parasitic not flies - can penetrate skin

Clinical signs -> dark patches in wool, white maggots, septicaemia, fluid loss and death

209
Q

5 forms of flystrike

A

Breech - common due to urine soiling, excess wrinkling, diarrhoea
Body - after prolonged rain
Poll strike - wrinkled merino rams
Pizzle strike - wethers/rams
Wound strike - shearing wounds, mulesing in spring

210
Q

Management of flystrike

A

chemical control - some break lifecycle moulting points but dont kill maggots, others kill maggots

Surgical mulesing with pain relief
Genetic selection

211
Q

Management of flystrike

A

chemical control - some break lifecycle moulting points but dont kill maggots, others kill maggots

Surgical mulesing with pain relief
Genetic selection

212
Q

Morphology of mites

A 
most species free living
<1mm
4 pairs of legs
No eyes (ticks have eyes)
Body has hair - setae
Specialised mouth parts (hypostome) with no teeth
213
Q

Name 4 species of mites

A

Demodex canis
Sarcoptes scabiei
Otodectes cynotis
Canine nasal mites

214
Q

What is the most common form of mange in dogs?

Lifecycle, disease, diagnosis

A

Demodex canis
Host specific dogs
feeds on cells and sebum

Eggs -> larvae 6 legs -> nymph 8 legs -> adult - all stages are in hair follicle

Disease -> demodicosis not contagious to other animals - disease of depressed immune system. Causes hair loss, crusting, itching, blackheads and pustules/papules

Diagnosis -> deep skin scrape with scalpel, biopsy and histology

215
Q

Sarcoptes scabiei lifecycle, clinical signs and hosts

A

Dogs, also cat, fox and human
Legs 3 + 4 dont go further than body margin

Male and female mate on surface of skin –> male dies and female burrows into skin -> lays eggs -> hatch to larvae 6 legs -> back to surface to become 8 leg nymph -> adults

Clinical signs itchiness, crusting, inflammation, destroy epidermis, scabies. Preference for ears, elbows, hocks and ventrum

216
Q

Morphology, lifecycle and clinical signs of otodectes cynotis

A

Ear mitess
Same lifecycle as sarcoptes but all on surface of skin
Causes irritation, thick brown crusts in ears
Suckers on tips of legs

217
Q

Diagnosis and clinical signs of canine nasal mites

A

Diagnosis - endoscopy, CT
Sneezing, nasal discharge, head shaking, epistaxis

No drugs to treat them

218
Q

2 mites of birds

A 
Ornithonyssus
Dermanyssus (poultry)

Feed on blood causing anaemia and reduced egg production

219
Q

Lifecycle of a spirurida in dogs (nematode)

A

Dirofilaria immitis (bloodworm)

Large white-grey worms, females double size of males

Viviparous - lay larvae

Females release microfilariae in right atrium and ventricle -> goes to peripheral vessels -> mosquito takes blood meal and ingests microfilariae -> becomes L3 -> back to dogs blood to become L4 in blood system -> becomes adult and returns to heart

220
Q

Dirofilariae immitis clinical signs

A

Thickened arteries
Thrombi and infarction
Pulmonary artery dilated and increased pressure

221
Q

Dirofilariae immitis diagnosis and preventatives

A

Diagnosis -> antigen kit as antigens released from female reproductive tract. If positive test for microfilariae. Can get false negatives if all males present

Prevent -> oral, topical or injectable medication

222
Q

Human dirofilariosis signs

A

Dying larvae in pulmonary arteries produce granulomas called coin lesions
Cough, chest pain and fever

223
Q

Filaroids osleri type of egg layer, symptoms, treatment

A

Viviparous -> direct lifecycle, DH dog

Causes haemorrhagic or granular wart like nodules in trachea or bronchi >18mm diameter - larvae develop in lung nodules to adults, lay L1 in faeces that are reingested

Spasmodic attacks of hard, dry coughs started by exercise or cold air - more acute in young dogs causing respiratory distress

Treatment -> fenbendazole 50mg/kg 10 days and remove nodules with bronchoscope

224
Q

What is a PCR? 2 advantages and disadvantages

A

Amplification of gene fragments from small amounts of parasite material

A -> Very sensitive and interpreting results is simple

D -> Limited number of genes can be examined and parasite species may not be confirmed

225
Q

What is ELISA, advantages and disadvantages

A

Determines if someone is positive for pathogen using plastic plate with 8x12 matrix of wells 1cm high. First and basic test to test postivity

A -> dont need radioisotopes and quick

D -> substrate enzyme reaction fast so have to read wells ASAP and monoclonal antibodies are harder to find

226
Q

Faecal egg count advantages and disadvantages

A

A -> quick, cheap

D -> large margin for error in diagnosis and hard to find eggs of some species

227
Q

How is a dipstick for heartworm performed, advantages and disadvantages

A

Uses albumin levels in dog urine to detect inflammatory or infectious conditions

A -> Fast, cheap, specific

D -> Doesn’t give diagnosis, breed and species values vary significantly

228
Q

Light microscopy advantages and disadvantages

A

Quick and cheap, identify different stages of eggs

Hard to identify specific species, requires training

229
Q

What agent causes ameobic gill disease and in which species? What type of agent is it?

A

Neoparameoba perurans
Salmons
Sarcomastigophora

230
Q

Neoparamoeba perurans lifecycle, clinical signs, diagnosis and treatment

A

Binary fission in gills of salmon -> trophozoites move through water and spreads via direct contact in intensive systmes -> onto new host gills

Multiple whiteish, swollen foci
Lamellar fusion

Wet mount shows free floating amoeba, histology of gills, molecular techniques

2-6 hours freshwater bath in treatment cage. these are resistant to most parasiticides. Salmons can develop resistance

231
Q

2 ciliates affecting fish

A

Ichthyophthirius multifiliis - freshwater spot disease

Trichodina

232
Q

Ichthyophthirius multifiliis description

A

Ectoparasite protozoa, low host specificity
Disease of freshwater fish
Common temp for outbreaks is 15-25 degrees

233
Q

Ich lifecycle and clinical signs

A

External parasite on surface of fish epithelium -> become well fed -> trophonts go into environment to reproduce -> get membrane around it and become a tomont -> tomites divide inside cyst and burst -> tomites becomes theronts -> penetrate epithelium of host in 5 minutes

Cause osmoregulatory failure and tissue necrosis, ragged fins, skin broken, skin haemorrhaging and secondary bacterial infection

234
Q

Ich diagnosis, treatment and prevention

A

Diagnosis -> microscopic examination of skin and gill tissue. C shaped macronucleus in mature trophont or spherical if immature, body with uniform ciliia

Treatment -> Raise salt concentration in small systems, use formalin in bigger systems or combine treatment with high temperature

Maintain good water quality, quarantine and treat all fish in salt for few hours, quarantine infected ponds, observe fish regularly

235
Q

Trichodina hosts, infection sites, reproduction and pathogenicity

A

Hosts -> freshwater and marine fish

Infection site -> skin, fin, gill

Reproduction -> binary fission

Feed on bacteria and epithelium, hyperplasia of epithelial cells, clubbing of gill filaments, reduces osmoregularity and respiration abilities, secondary bacterial infection

236
Q

Clinical signs of trichodina

A

Rub against surface and damage skin and gills

Scratching, ulcers, not feeding, lethargic, grey film over body

237
Q

Diagnosis, treatment and prevention of trichodina

A

mucous scraping of infected fish, histopathology

Prevention and treatment same as Ich

238
Q

5 species of monogenea affecting fish

A 
Sea lice
Fish lice (argulids)
Dactylogyrus spp - gills freshwater
Gyrodactylus -> viviparous on skin + fins freshwater
Benedenia spp - skin + fins of Kingfish
239
Q

Structure of monogenea

A

Ectoparasitic flukes (flatworm)

Hermaphrodites
Suckers or hooks cause damage
Affect freshwater and marine fish

240
Q

Reproduction and lifecycle of benedinia, dactylogyrus and gyrodactylus (all freshwater fish)

A

Dactylogyrus spp in gills -> oviparous. Eggs -> operculum releases oncomiracidium -> reinfect

Gyrodactylus spp. -> on skin and fins, viviparous. Produce larvae on skin -> reinfect or direct contact transmission

Benedenia (Kingfish skin) -> oviparous. Eggs -> water -> operculum opens -> oncomiracidia hatch -> find new host

All direct, no intermediate hosts

241
Q

Which type of fish do sea lice infect and what do they do?

Which type do fish lice infect and what do they cause?

A

Sea lice -> Marine (only females are parasitic - feed on epidermis, blood and mucous and transmit other diseases

Fish lice -> freshwater. Cause loss of physical condition, bacterial infections and transmit other diseases as they feed. Flashing feeding activities are damaging

242
Q

Fish lice lifecycle and treatment

A

Adults mate on fish -> females leave fish to have eggs on vegetation -> eggs hatch as copepodid -> find host -> moults to adult

Lifecycle takes 40-100d

Raising temp in tank shortens treatment

Organophosphates for treatment. Remove all fish, dry tank and start again

243
Q

When do we treat fish?

A

Water more acidic at night due to plants
Formalin used in day when oxygen supply is better as it displaces oxygen

Treat white spot disease at night time when fish are not moving as much

First time treating -> during the day to observe fish

Parasitology (2 decks)

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