Mid-Semester Exam Flashcards
(243 cards)
1
Q
What is a parasite?
A
An organism that lives off another organism (hosts) for feeding and reproduction
2
Q
What are 3 groups of parasites?
A
Protozoa
Helminths
Arthropods
3
Q
What are 2 zoonotic parasites?
A
Ascaris and hookworm
4
Q
Of the endemic diseases that affect livestock in Aus, which have the largest impact on farm productivity?
A
Parasites
5
Q
What were the 3 spikes in the word parasite in history?
A
Both world wars and the vietnam war
6
Q
What are 2 benefits of parasites?
A
Maggots - heal amputations
Hookworms can help to control allergies
7
Q
Define endoparasite
A
Parasites that live inside internal organs of the host
8
Q
Define ectoparasite
A
Parasites that lives on the external parts of the host
9
Q
Define obligatory parasites
A
Parasite that cannot live without host
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
11
Q
What is a definitive host?
A
Host affected by the adult stage of the larvae
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
13
Q
Define paratenic host
A
Larvae that do not develop in host
Alive but inactive inside host
14
Q
Define direct life cycle
A
eggs picked up from the ground to definitive host for example
- Disease happens quick
15
Q
Define indirect life cycle
A
different hosts included like an intermediate
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
17
Q
Define non-migratory life cycle
A
pick up parasite and it stays there (inhale = goes to lung and stays there
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
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
20
Q
Define infective stage
A
one in which the parasite is capable of entering its host and continue its development within the host
21
Q
Define free living stage
A
parasites survive outside the host in this period until they find a new host
22
Q
What is the latin name for strongyles?
A
Trichostrongylus sp.
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
24
Q
What is the latin name for liver fluke?
A
Fasciola hepatica
25
How do we write latin names?
Genus and species
Genus capital letter
Species lowercase
always in italics
26
What are 6 host factors affecting infection, parasitism and pathogenicity?
```
Age and exposure
Quantum of infection
Genetics -> some animals more resistant
Periods of stress
Pregnancy/lactation
Management factors
```
27
what are 6 parasite factors affecting parasitism?
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
28
What is the latin name for hookworm?
Andylostoma duodenale
29
How does hookworm causes haemorrhage?
Grabs intestinal tissue and sucks blood
30
Which parasite can cause thrombus formation?
Strongylus vulgaris -> larval stages can cause thickening of arterial wall and thrombus formation
31
Name 6 problems caused by parasites
1. Necrosis
2. Haemorrhage
3. Thrombus formation
4. Prevent nutrient absorption
5. Digest tissue
6. Allergy and inflammation
32
What are 3 groups of protozoans?
Apicomplexa
Sarcomastigophora (giardia, trypanosoma)
Ciliophora
33
What are 2 groups of metazoans?
Helminths and arthropods
34
How can protozoa be described?
Motile unicellular, eukaryotic microorganisms
35
Contrast extracellular and intracellular protozoa characteristics
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
36
What are 2 groups of sarcomastigophora?
Sarcodina (amoeba) and zoomastigophora (flagellates)
37
How do amoeba replicate?
Binary fission - nucleus and body divided into 2
38
How do flagellates move?
Whip like motion
| Undulating cell membrane
39
How do flagellates reproduce?
Binary fission
40
What 3 groups of flagellates (zoomastigophora) are there?
Diplomonadida (giardia)
Trichomonadida (tritrichomonas)
Kinetoplastida (trypanosoma and leishmania)
41
What is the latin name for giardia?
Giardia intestinalis
part of diplomonadidia -> zoomastigphora -> protozoa
42
What is the host range of giardia?
Diverse mammal host range
43
Where does giardia live during free living stage?
Soil, food and water
44
Describe the structure of giardia in the host and in free living stage
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
45
Describe the lifecycle of giardia
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
46
Name 3 routes of infection for giardia
1. Family member with it
2. contaminated water, food
3. direct person to person
47
Clinical signs of giardia
fatty diarrhoea, cramps, weight loss, dehydration, blood, bile function affected
48
How do we diagnose giardia?
Faecal sample to look for cysts and live parasites (trophozoit)
49
How do we treat giardia? how do we prevent it?
Medication for pain and symptoms
If no symptoms -> no treatment
Handwashing, hygiene, wash vegetables
50
How do we
51
Explain the structure of tritrichomonas foetus
Pear shaped, 3 anterior flagella, undulating membrane
Trichomonadida -> zoomastigophora -> protozoa
52
How does tritrichomonas replicate?
Binary fission
53
Where is tritrichomonas found?
Bull penis and prepuce, membranes inside sheath, not normally in semen
Vagina, uterus and oviduct
54
Tritrichomonas lifecycle
Veneral pathogen, infected bull -> passes trophozoites to cow -> lives in reproductive tract
No cysts form as no free living stage
55
Symptoms of tritrichomonas in cows and bulls
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
56
How do we diagnose tritrichomonas?
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
57
what are 2 kinetoplastida
leishmania and trypanosoma
Part of zoomastigophora -> protozoa
58
What is an amastigote and promastigote?
Amastigote - Form of parasite with no external flagella
Promastigote - flagella comes from front of body
59
what is an epimastigote and trypomastigote?
Epimastigote - flagella comes from posterior part of body but not past the nucleus
Trypomastigote - completely posterior flagella
60
What variations of flagella does leishmania have?
Where does it live?
What does it cause?
What are the hosts?
Kinetoplastida -> zoomatigophora -> protozoa
Amastigote (in wbc) and promastigote (in fly)
Immune system and targets macrophages
Causes fever, anaemia, lethargy
host sandfly and vertebrates
61
Leishmania lifecycle
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
62
How do we diagnose leishmania?
Blood smear to detect amastigote in white blood cells
| Cutaneous leishmania - sample these areas
63
Leishmania treatment
Liquid nitrogen to skin lesions - freeze lesion killing tissue causing lesion healing
64
Is trypanosoma intracellular or extracellular and what does it cause?
Kinetoplastida (like leishmania) -> zoomastigophora -> protozoa
Extracellular -> swims between rbc and exposed to antibodies and other defence systems
Clinical signs -> vessels blocked, anaemia, emaciation
65
Trypanosoma lifecycle
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
66
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?
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
67
How are apicomplexa described? What are the developmental stages?
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)
68
What are 2 types of apicomplexa?
Eimeria (coccidia) and piroplasms (malaria)
69
Route of infection of Eimeria and clinical signs
Oral to intestine - uses apicomplex structure to go into enterocytes
causes diarrhoea, dehydration and lethargy
70
Lifecycle of Eimeria
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
71
Diagnosis of eimeria, control + prevention
```
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
72
Control/treatment and prevention of Eimeria
Vaccinate chickens in first week -> prevent overstocking and contamination of litter
Use anticoxidials
Treat infection with sulphonamides, monensin
73
What sort of parasite is toxoplasma gondii? What are the hosts? What are the effects?
Apicomplexa, intracellular, zoonotic
Definitive -> cats (gametogony)
Intermediate -> beetles and humans
Abortion in humans
Causes behavioural changes in intermediate hosts
74
Lifecycle of toxoplasma gondii
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
75
Human toxoplasmosis
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
76
Diagnosis of toxoplasma gondii
Find oocysts in cat faeces
| Humans -> serology for specific IgG and IgM antibodies, symptoms
77
Cryptosporidium -> where is it, hosts
Apicomplexa found in blood, one group found in tissue
| C Parvum -> found in cattle intestine, zoonotic, waterborne transmission
78
Cryptosporidium lifecycle
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
79
Clinical signs and diagnosis of cryptosporidium
Clinical signs -> asymptomatic, young immunocomprimised animals, villous atrophy, malabsorption
Diagnosis -> visualise oocysts in faeces, immunofluorescence, RAT, PCR
80
Plasmodium spp. 4 species infecting humans
| Type of parasite
P. Malariae
P. Ovale
P. Vivax
P. Falciparum
Apicomplexa
81
Malaria transmission
Caused by bites of infected anopheles mosquito vectors - only females
82
Plasmodium lifecycle
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
83
Symptoms and diagnosis of plasmodium
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
84
Prevention and control of plasmodium
Anti-malarial drugs, insecticides
- resistance to both of these
- chemical repellents, bed nets
85
Describe babesia spp. -> distribution, definitive host, name of disease
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
86
Lifecycle of babesia
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
87
Clinical signs, control and animal susceptibility of babesia
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
88
Describe Theilieria spp.
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
89
Diagnosis, pathology and clinical signs of Theileria spp.
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
90
Name 4 types of helminths
Platyhelminths
Nematodes
Acanthocephala
Annelida
91
Characteristics of platyhelminths
No body cavity, incomplete to no digestive system, hermaphrodites
Classified as:
- Turbellaria (free living)
- Monogenea
- Trematoda
- cestodes
92
Describe fasciola species - 2 types, distribution, hosts
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
93
Fasciola hepatica lifecycle
```
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
94
Fasciola hepatica location
south east QLD, coastal and tableland NSW, all victoria, eastern tas
95
Fascioliasis - acute vs chronic
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
96
Diagnosis of fasciola hepatica
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
97
Prevention and control of fasciola hepatica
Drench
Cook watercress
Pasture management for draining/fencing off swampy areas
Quarantine new sheep
98
Fasciola hepatica immunity and resistance
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
Describe the size of paramphistomes and what they are known as
Stomach flukes
<1cm
orange/red as adults
trematode -> platyhelminth -> helminth -> metazoa
100
Stomach flukes lifecycle
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
Paramphistomes (stomach fluke) distribution
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
Stomach fluke clinical signs
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
Immunity towards stomach fluke
Resistance occurs after exposure
| Weaner cattle and lambs are the most susceptible
104
Diagnosis and control of stomach fluke
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
Control of stomach fluke
Draining, fencing off wet areas, alternative water sources and drenching (no drenches registered in nsw)
106
Describe blood flukes - size, where they live, where the adults are
>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
Blood fluke lifecycle
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
How do blood flukes hurt the host?
Interfere with normal blood flow
Parasite products form host response and inflammatory granulomas "egg granulomas"
Immunity is hard to generate
109
How do we diagnose blood fluke?
Eggs in faeces
| Antibodies or antigens in blood or urine samples
110
What schistosoma spp (blood flukes) are found in humans?
S. mansoni
S. hematobium
S. japonicum
111
What schistosoma spp (blood flukes) are found in humans?
S. mansoni
S. hematobium
S. japonicum
112
Schistosoma lifecycle in humans
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
Symptoms of schistosoma in humans
dermatitis (swimmers itch), abdominal pain, diarrhoea, bloody stool, mucosal fibrosis due to inflammatory response to eggs, egg granulomas
114
Diagnosis and treatment of schistosoma
Histology, eggs in urine or stool, symptoms
Praziquantel
Eliminate snails, dont swim in snail water
115
Benefits of schistosoma to humans
Inject antigens to reduce incidence of type I diabetes in mice
Immunotherapy
116
Describe the morphology of cestodes
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
3 classes of cestodes
Cyclophyllidea, pseudophyllidea and diphyllobothridea
118
Diphyllobothrium latum lifecycle
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
Where is diphyllobothrium latum found?
Scandinavia, russia, japan, north america
120
Clinical signs of diphyllobothrium latum
Can last decades - most asymptomatic
Diarrhoea, weight loss, abdominal discomfort, vitamin B12 deficiency, pernicious anaemia, intestinal obstruction
121
Diagnosis of diphyllobothrium latum
Operculated eggs, broad proglottids in stool
| Check for anaemia with complete blood count
122
Control + prevention of diphyllobothrium latum
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
Describe characteristics of pseudophylidiae
```
2 bothria
single, central uterine pore
ciliated, free living larvae
water essential for transmission
Oval eggs
2-3 IH
```
124
Describe characteristics of cyclophyllidiae
```
4 suckers +/- hooks
1-2 lateral genital pores
No free-living stages
water not essential for transmission
Eggs round
1 IH
```
125
Name the species of pseudophyllidean cestode and its lifecycle
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
Moneizia expansa lifecycle
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
Dipylidium caninum lifeycle
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
Which taeniid species are zoonotic?
```
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
List taeniid species and their IH and DH
```
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
What is the echinococcus species found in australia?
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
Diagnosis of echinococcus granulosus in dogs
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
E. granulosus in wildlife
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
How do we treat tapeworms?
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
Describe the structure of nematodes
| Males and females
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
3 terms to describe the egg laying of nematodes
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
4 types of nematodes
Ascarids
Strongylids
Spirurida
Enoplida
137
name 2 strongylids of sheep
Haemonchus contortus (barbers pole worm)
Trichostrongylus colubriformis (black scour worms)
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Haemonchus contortus lifecycle
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
Haemonchus contortus clinical signs
Bottle jaw
anaemia
no diarrhoea
death before weight loss due to anaemia
140
Trichostrongylus colubriformis structure and clinical sign
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
Which nematode demonstrates hypobiosis?
Trichostrongylus colubriformis (sheep) - can sit in intestine or abomasum and wait for conditions to be right before becoming adults
Ostertagia ostertagi (type 2)
142
Name 3 nematodes infecting cattle
Ostertagia ostertagi
Haemonchus placei (barbers pole worm of cattle)
Trichostrongylus axei
143
Ostertagia ostertagi lifecycle
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
Ostertagia ostertagi symptoms and 2 types of disease
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
Name 3 large strongyles and 1 small strongyles infecting horses
Large -> Strongylus vulgaris, S. edentates, S. equinus
Small -> Cyathostomins
146
Strongylus vulgaris lifecycle
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
Strongylus vulgaris disease
Burrows in the walls of arteries -> blood clots -> disrupts flow to intestine -> larvae move to large intestine lumen to mature
Can cause thrombi
148
Lifecycle of S. edentates and S. equinus
Same as strongylus vulgaris but migrate to liver not arteries
149
Cyathostomins lifecycle
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
Cyathostomins disease mechanism
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
Diagnosis of cyathostomins
Egg of immature larvae count in faeces
152
Name and describe structure of 1 nematode strongyloid infecting dogs
Ancylostoma caninum - hookworms
zoonotic
Large buccal capsule, 3 pairs of marginal teeth and dorsal gutter
Well developed bursa
common in coastal areas
153
Ancylostoma caninum lifecycle and PPP
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
Ancylostoma caninum in people
Risk factors - bare feet, humidity, dogs
Causes itch
Townsville and north QLD
155
Ancylostoma caninum signs in dogs
Black, tarry faeces
pups have reduced haematocrit
microcytic, hypochromic anaemia
Poor coat, loss of appetite, weakness
156
Ancylostoma caninum control
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
Name one enoplida, ascarid and spirurida of dogs
Enoplida -> Trichuris vulpis
Ascaridida -> toxocara canis
Dirofilaria immitis -> spirurida
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Toxocara Canis Lifecycle
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
Toxocara canis clinical signs and post mortem
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
Toxocara canis diagnosis and treatment
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
Trichuris vulpis lifecycle
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
Trichuris vulpis control and diagnosis
Whipworm - Enoplida - Nematode
Diagnosis - eggs in faeces
Control - canine all wormer with praziquantel, pyrantel and oxantel every 3 months
163
2 ascardid nematode in horses
Parascaris equorum - affects foals and young stock
Oxyuris equi
164
Parascaris equorum lifecycle
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
Parascarid equorum clinical signs
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
Oxyuris equi lifecycle, pathogenicity and control
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
Describe the lifecycle of tongueworms (Linguatula serrata) and their zoonotic transmission
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
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What family do fleas of vet importance belong to, and what 4 genera are we concerned about?
family - pulicidae
Genera -> echidnophaga, ctenocephalides (flea allergy dermatitis), pulex and spilopsyllus
169
What are fleas?
Arthropods -> insects -> flea
170
What genera of fleas have both pronotal and genal combs, and just a genal comb?
Both -> ctenocephalides
| Just genal -> spilopsyllus
171
What genera of fleas have no genal or pronotal combs?
Echidnophaga
| Pulex
172
Flea lifecycle and ideal conditions
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
Facts about fleas jumping
About 250x their own height
| fleas have protein resilin in leg hinges - elasticity high
174
Flea morphology
Head, thorax, 3 pairs of legs and abdeomn
chitinised
3rd pair of legs adapted for jumping
Lateral compression
175
Describe flea allergy dermatitis signs
hypersensitivty to saliva - pruritis and scratching = self trauma
Skin thickening, hair loss form middle of back to tail base, down rear legs
176
Diagnosis, treatment and control of fleas
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
List diseases fleas can carry in rats, rabbits and dogs
Rats -> bubonic plague
Rabbits -> myxomatosis
Dogs -> dipylidium caninum (tapeworm)
178
What are ticks?
Arthropods -> arachnids -> ticks
179
Explain the difference between hard and soft ticks
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
General tick lifecycle (one host)
adults drop off host to lay eggs -> 6 leg larvae -> crawl onto host and blood meal -> 8 leg nymph blood meal -> adult
181
2 host tick lifecycle
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
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3 host tick lifecycle
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
Disease mechanisms of ticks
Blood loss - anaemia
reduces growth rate of host
produces toxins when capitulum attaches
hypersensitivity to saliva
184
3 steps for ectoparasite treatment in companion animals
1. Isolation -> of animal to prevent spread to non-infested individuals
2. Medication -> to kill the parasites
3. Treatment -> of the animals environment
185
Describe and name the dog tick AKA australian paralysis tick
Ixodes holocyclus - hard tick
vectors of infectious agents including babesia
Most medically important
186
Hosts of the australian paralysis tick
Natural hosts - bandicoots, possums, kangaroos (immunity protecting against toxins), birds, humans, dogs and cats
spring peak season when develop into adults
187
Australian paralysis tick effects on humans and lifecycle
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
Distribution of ixodes holocyclus
Australian paralysis tick
East cost
Dogs infected by walking through long grass
189
Morphology of capitulum of australian paralysis tick
Palp -> leg like sensory structures to find things
Chelicera -> pierces the skin
hypostome - anchors tick
190
Pathogenesis of ixodes holocyclus
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Anaemia
toxicosis
Inhibits immune processes
Transmit pathogens - babesia
one tick can cause paralysis
change in bark -> wobbly back legs -> paralysis
```
191
Diagnosis and treatment of ixodes holocyclus
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
Describe the southern paralysis tick morphology and distribution
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
Describe hosts of bush tick, distribution and clinical signs - haemophysalis longicornis
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
Distribution, host lifecycle number and distrinctive characteristic of brown dog tick - Rhipicephalus sanguineus
3 host cycle
domestic dogs DH
large eyes distinctive characteristic
Found in tropics and subtropics, mainland aus
195
Pathogenesis of brown dog tick
```
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
tick removal
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
What is the most important cattle disease in Aus?
What other animals is it found on and where is it found?
Rhipicephalus microplus -> asian blue tick
also found on sheep, horses, dogs, pigs, marsupials
found across northern austrlaia and nsw north coast
198
Rhipicephalus microplus lifecycle
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
Rhipicephalus microplus disease, treatment and control
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
Name, morphology and distribution for buffalo fly in cattle
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
Lifecycle of buffalo fly
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
Clinical signs of buffalo fly
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
Describe sheep lice morphology, scientific name and cost
Bovicola ovis - biting lice
flat body, 1.6mm long, bite
cost to treat eith chemicals and for lower quality wool cuts
204
Lifecycle of bovicola ovis
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,
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Disease from bovicola ovis
Seasonal pattern
Diagnosis
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
Eradication and control of bovicola ovis
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
Management and control of bovicola ovis
Shearing, chemical control (dose rate, sufficient time in dip, maintain dip at full strength
Break cycle
208
Name of the australian blowfly
Lifecycle
clinical signs
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
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5 forms of flystrike
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
Management of flystrike
chemical control - some break lifecycle moulting points but dont kill maggots, others kill maggots
Surgical mulesing with pain relief
Genetic selection
211
Management of flystrike
chemical control - some break lifecycle moulting points but dont kill maggots, others kill maggots
Surgical mulesing with pain relief
Genetic selection
212
Morphology of mites
```
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
Name 4 species of mites
Demodex canis
Sarcoptes scabiei
Otodectes cynotis
Canine nasal mites
214
What is the most common form of mange in dogs?
| Lifecycle, disease, diagnosis
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
Sarcoptes scabiei lifecycle, clinical signs and hosts
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
Morphology, lifecycle and clinical signs of otodectes cynotis
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
Diagnosis and clinical signs of canine nasal mites
Diagnosis - endoscopy, CT
Sneezing, nasal discharge, head shaking, epistaxis
No drugs to treat them
218
2 mites of birds
```
Ornithonyssus
Dermanyssus (poultry)
```
Feed on blood causing anaemia and reduced egg production
219
Lifecycle of a spirurida in dogs (nematode)
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
Dirofilariae immitis clinical signs
Thickened arteries
Thrombi and infarction
Pulmonary artery dilated and increased pressure
221
Dirofilariae immitis diagnosis and preventatives
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
Human dirofilariosis signs
Dying larvae in pulmonary arteries produce granulomas called coin lesions
Cough, chest pain and fever
223
Filaroids osleri type of egg layer, symptoms, treatment
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
What is a PCR? 2 advantages and disadvantages
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
What is ELISA, advantages and disadvantages
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
Faecal egg count advantages and disadvantages
A -> quick, cheap
| D -> large margin for error in diagnosis and hard to find eggs of some species
227
How is a dipstick for heartworm performed, advantages and disadvantages
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
Light microscopy advantages and disadvantages
Quick and cheap, identify different stages of eggs
Hard to identify specific species, requires training
229
What agent causes ameobic gill disease and in which species? What type of agent is it?
Neoparameoba perurans
Salmons
Sarcomastigophora
230
Neoparamoeba perurans lifecycle, clinical signs, diagnosis and treatment
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
2 ciliates affecting fish
Ichthyophthirius multifiliis - freshwater spot disease
Trichodina
232
Ichthyophthirius multifiliis description
Ectoparasite protozoa, low host specificity
Disease of freshwater fish
Common temp for outbreaks is 15-25 degrees
233
Ich lifecycle and clinical signs
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
Ich diagnosis, treatment and prevention
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
Trichodina hosts, infection sites, reproduction and pathogenicity
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
Clinical signs of trichodina
Rub against surface and damage skin and gills
| Scratching, ulcers, not feeding, lethargic, grey film over body
237
Diagnosis, treatment and prevention of trichodina
mucous scraping of infected fish, histopathology
Prevention and treatment same as Ich
238
5 species of monogenea affecting fish
```
Sea lice
Fish lice (argulids)
Dactylogyrus spp - gills freshwater
Gyrodactylus -> viviparous on skin + fins freshwater
Benedenia spp - skin + fins of Kingfish
```
239
Structure of monogenea
Ectoparasitic flukes (flatworm)
Hermaphrodites
Suckers or hooks cause damage
Affect freshwater and marine fish
240
Reproduction and lifecycle of benedinia, dactylogyrus and gyrodactylus (all freshwater fish)
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
Which type of fish do sea lice infect and what do they do?
Which type do fish lice infect and what do they cause?
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
Fish lice lifecycle and treatment
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
When do we treat fish?
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
