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Animal Disease 1 > Protozoa > Flashcards

Protozoa Flashcards

1
Q

Describe the protozoa kingdom.

A
  • Single celled organisms
  • Very small organisms measured in microns
  • Eukaryotes – so have a nucleus and complex sub-cellular organisation
  • Unknown until the invention of the microscope in 1675
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2
Q

What are 6 examples of disease caused by parasitic protozoa?

A

Amoebic dysentery
Malaria
Sleeping sickness and animal trypanosomiasis
Tick-borne diseases of livestock
Toxoplasmosis
Coccidiosis

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3
Q

What are the most important 4 phyla a parasitic protozoa can be?

A

Phylum apicomplexa – apicomplexans move by body flexion, all are parasitic and use the apical complex to invade host cells.

Phylum euglenozoa – flagellates move by 1 or more whip like processes or flagella.

Phylum ciliophora – ciliates move by short hair-like processes or cilia.

Phylum ameobozoa – amoeba move by processes or pseudopodia.

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4
Q

Distinguish direct and intermediate hosts.

A

Definitive host – one in which a parasite reaches maturity and usually reproduces sexually.

Intermediate host – one in which the parasite develops, but does not reach maturity or reproduce sexually.

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5
Q

What host does a vector require?

A

Definitive host and intermediate host vector.

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6
Q

What are enteric pathogens?

A

Direct and indirect life cycles and live in GI tract. Water borne or soil transmitted

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7
Q

What are haemoparasites?

A
  • Indirect life cycles and live in the blood
  • Vector borne – transmission by mosquitos, tsetse fly, tick
  • Cause fever, anaemia and worse
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8
Q

What are systemic pathogens?

A

Have examples form both enteric pathogens and haemoparasites

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9
Q

What are some examples of coccidia?

A

A broad grouping of apicomplexan parasites

  • Eimeria
  • Isospora
  • Cryptosporidium
  • Toxoplasma
  • Sarcocystis
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10
Q

What are trophozoites?

A

Feeding stages that move around in tissues are trophozoites. Have gametes that can be fertilised to form oocysts.

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11
Q

What is the structure of apicomplexa?

A

Rhoptries
Micronemes
Polar rings
Conoid

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12
Q

What does the structure of apicomplexa allow them to do?

A

Anable parasite to penetrate host cell. Activated by the release of sequestered calcium ions into the parasite cytoplasm.

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13
Q

Describe the process of apicomplexa entering the host cell.

A
  1. Receptor detects ligand in a host cell
  2. Re-orientation so apical complex is ready to invade cell
  3. Parasitophorous vacuole forming
  4. Parasite inside vacuole where it lives are evades destruction by the immune system.
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14
Q

How do apicomplexa multiply?

A

By schizogony – multiple nuclear division precedes cytoplasmic division.

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15
Q

What are Eimeria?

A

A major enteric coccidian pathogen of global importance. Numerous individual species affect poultry and other livestock causing the disease coccidiosis.

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16
Q

What is the lifecycle of Eimeria?

A
  1. Spend part of their lifecycle in poultry and another part of their lifecycle in the environment.
  2. Unsporulated egg like structure passed out of the intestine.
  3. Undergoes sporulation and develops internal structures known as sporocysts
  4. Host becomes infected upon ingestion.
  5. Sporozoites are released and enter the gut epithelial cells, where they multiply by schizogony – asexual cycles.
  6. Breaks up into new parasites called merozoites.
  7. There is a last schizogony event and there is development of microgametes for male gametes and macrogametes for female gametes.
  8. Fertilisation to form a zygote which is passed up as an unsporulated oocyst.
  9. Whole cycle is about 3.5-5.5 days.
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17
Q

What do coccidia and disease depend on?

A

Parasite factors:
- Parasite species
- Predilection site in intestine

Environmental conditions:
- Temperature
- Humidity
- Hygiene

Host factors:
- Age – young
- Immunity – naive
- Density – intensification

Typically causes bloody diarrhoea

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18
Q

What is the pathology caused by Eimeria tenella?

A
  • Thickening of mucosa
  • Inflammation
  • Haemorrhage
  • Necrosis.
  • Has predilection for the caeca, which is useful for diagnosis.
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19
Q

What are the infective stages of Eimeria?

A
  1. Unsporulated oocyst
  2. Oocyst require warmth, moisture and oxygen to sporulate
  3. Sporulated oocyst, which can resist disinfection and persist in environment
  4. Oocysts eaten by chicken
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20
Q

Describe cryptosporidium parvum.

A
  • A very tiny coccidian parasite
  • Pathogen of domestic animals and humans
  • Causes cryptosporidiosis
  • Common zoonosis
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21
Q

What are the clinical signs of cryptosporidiosis?

A
  • Clinical signs – intermittent anorexia and diarrhoea
  • No treatment – usually self-limiting
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22
Q

Describe the life cycle of cryptosporidium parvum.

A
  • Direct life cycle but humans get it often from drinking water where other people have been.
  • Lives in brush border of gut epithelium cells
  • Asexual and similar sexual cycle of Eimeria
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23
Q

Describe the locations of cryptosporidium schizonts.

A
  • Located within brush border
  • Parasite develops in a space between the cytoplasm and the cell membrane
  • Located within parasitophorous vacuoles covered by host microvillous membranes
  • Intracellular but extra-cytoplasmic location
  • Infected microvilli are destroyed when the parasite leaves the cells
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24
Q

Describe cryptosporidium oocysts.

A
  • 1 calf can produce up to 10^7 oocysts per gram of faeces
  • Measure 3-5m in diameter
  • Pass easily through normal water filtration systems
  • Highly resistant to chlorination
  • Potential for contamination of municipal water supplies
  • Auto infection is possible – sporozoites released from oocysts within the intestine may re-infect the same individual
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25
Q

Name some flagellate protozoa with direct life cycles.

A

Giardia lamblia (duodenalis)
Trichomonads
Spironucleus (hexamita)
Histomonas

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26
Q

What does giardia lamblia cause?

A
  • Causes diarrhoea in many birds and mammals, including humans
  • Zoonosis
  • Ingestion of a mature cyst results in infection
  • Malabsorptive diarrhoea
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27
Q

Where does giardia lamblia occur?

A
  • Trophozoites attach with suckers to epithelial cells of the small intestine
  • The very distinctive trophozoites can sometimes be found in the faeces
  • Cysts mature in the colon and faeces
  • Excystment occurs in the duodenum to release the trophozoite
  • Trophozoite attaching to surface of the epithelial cells blocks absorption
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28
Q

Name the trichomonas.

A

Trichomonas foetus
Spironucleus (Hexamita)
Histomonas meleagridis

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29
Q

What is trichomonas foetus and how does it present in bulls, cows and cats?

A

Simple direct life cycle. Sexual transmission.

  • Bull – asymptomatic
  • Cow – infertility, abortion, embryonic and early foetal death, foetal pyometra and vaginal discharge
  • Cats – typhlocolitis
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30
Q

Describe spironucleus meleagridis.

A
  • Small, less than 10 m
  • Transmission by faeco-oral route of encysted forms
  • Single flagellum
  • Migrate in portal circulation
  • Direct life cycle possible via faeco-oral route or more usually
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31
Q

What does spironucleus meleagridis cause?

A
  • Catarrhal enteritis in turkey poults and game birds
  • Adult birds are asymptomatic carriers
  • 6-20um in diameter ‘blackhead’ in turkeys and chickens
  • Necrotic lesions in the caecum
  • Cause focal necrosis in liver
  • Cyanosis of head and wattle due to poor blood supply
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32
Q

What is the species of spironucleus that causes a similar disease in pigeons?

A

Spironucleus columbae

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33
Q

Describe the life cycle of histomonas meleagridis.

A

Indirect life cycle via nematode
- Heterakis gallinarum
- Found in caecum
- Histomonas invades nematode
- Histomonas within heterakis eggs

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34
Q

Describe the lifecycle of histomonas meleagridis once eggs have been formed?

A
  1. Heterakis eggs passed in faeces
  2. Birds ingest geterakis eggs or heterakis eggs ingested by and develop within earthworm:
  3. Bird eats earthworm containing heterakis containing histomonas
  4. Becomes infected with both parasites simultaneously
  5. Free range turkeys and chickens
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35
Q

Describe the properties of sarcocystidae.

A
  • Apicomplexa
  • Similar to Eimeria but have indirect lifecycles: asexual stages occur in intermediate hosts. Asexual and sexual stages occur in definitive hosts
  • Examples: toxoplasma, neospora, sarcocystis
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36
Q

What is toxoplasma gondii?

A

An apicomplexan protozoan parasite that infects most species of warm blooded animals, including humans, causing the disease toxoplasmosis.

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37
Q

What does toxoplasma gondii cause?

A
  • Cat family/Felidae are the only known definitive hosts for the sexual stages and so are the main reservoirs of infection.
  • Toxoplasmosis is an important cause of abortion and foetal abnormality in humans, sheep and goats.
  • Also causes significant infections in immunocompromised humans.
  • Important zoonosis
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38
Q

Describe the life cycle of toxoplasma gondii in the definitive host.

A

Domestic cat and other felids.

  • Generally become infected by ingesting infected rodents or birds
  • Shed oocysts which become infectious to most mammals and birds
  • Most commonly infected as kittens
  • Shed large numbers of oocysts but only for 1-2 weeks
  • Develop immunity
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39
Q

Describe the lifecycle of toxoplasma gondii in intermediate hosts.

A

Rodents and birds:

  • Sprulated oocysts – sporulate in 1-5 days
  • Carnivorism/omnivorism or transplacentally (most important in humans, sheep and goats)
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40
Q

What are some accidental hosts of toxoplasma gondii?

A

Sheep, pigs and other mammals

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41
Q

How does toxoplasma gondii pass to organisms?

A

Form tissue cysts that can pass to organisms including humans by ingestion, particularly if food is undercooked or if it gets into foetus.

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42
Q

Once in the intermediate host, how does toxoplasma gondii develop?

A

Tachyzoite - Rapidly multiplying crescent-shaped stage in the development of an acute tissue phase of infection.

Bradyzoite:
- Slow growing, comma shaped forms
- Found in clusters within cysts in the tissues
- Chiefly muscles and the brain, in chronic (latent) toxoplasmosis

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43
Q

Describe tachyzoite movement and multiplication.

A
  • Move by gliding , flexing, undulating and rotating
  • No externally visible means of locomotion such as cilia, flagella or pseudopodia
  • Motion effected by apical complex
  • Rapid multiplication within IH cells
  • Lytic cycle, like viruses
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44
Q

Describe the lytic cycle.

A
  • Enter host cell by actively penetrating cell membrane or by phagocytosis
  • Multiply asexually repeatedly within host cells
  • 2 progeny form within and consume the parent parasite – endodyogeny
  • Host cell ruptures when it can no longer support the growth of tachyzoites
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45
Q

How do bradyzoites develop?

A
  • Multiply asexually within host cells by repeated endodyogeny
  • Tissue cysts first appear 7-10 days post-infection
  • Contain hundreds of bradyzoites
  • Within host cell cytoplasm
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46
Q

What are the properties of the cyst wall?

A
  • Composed of host cell and parasite materials
  • Resistance to digestion by gastric juice
  • Protection from host immune response
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47
Q

Describe the immune response to bradyzoites.

A

Normally the immune response efficiently prevents the dissemination of these tachyzoites.

In immunocompromised hosts, such reactivation may be unchecked or more frequent.

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48
Q

Describe the life cycle of toxoplasma gondii in feline definitive host.

A
  1. Ingest quiescent bradyzoites occupying tissue cysts or rapidly multiplying tachyzoites in recently infected intermediate hosts or sporulated oocysts.
  2. Ingested bradyzoites resumes activity.
  3. Penetrate the epithelial cells of the small intestine.
  4. Initiate the formation of numerous asexual generations.
  5. Sexual cycle, the production of gametes.
  6. 2 walls are laid down around the fertilised zygote.
  7. Kittens and young cats can shed millions of oocysts in the faeces for 3 weeks after infection
  8. Oocyst excreted unsporulated in the faeces.
  9. Sporulated to become infectious 1-5 days after excretion.
  10. Sporulated oocyst contains 2 sporocysts, each containing 4 sporocysts.
  11. Can survive in soil for several months.
49
Q

What are the clinical signs of toxoplasmosis in sheep and goats?

A

Early gestation, abortion – ‘barren ewe’

Mid-gestation – abortion, lesions in cotyledons of placenta and foetus or mummification of dead foetus

Late gestation – still born or weak lambs

50
Q

How does toxoplasmosis in cattle (and perhaps camelids) cause abortions?

A
  • Associated with abortion or birth of weak lambs due to pathological changes in the foetal membranes
  • Grossly the placental cotyledons have characteristic 1-2 mm white or yellow focal lesions
  • Infection of susceptible ewes in the 1st 2 months of pregnancy lead to foetal death with subsequent expulsion or mummification
  • Infection later in pregnancy, apparently normal lambs may be aborted during the last month or brown dead or weak at full term
51
Q

What is neospora caninum?

A

An emerging and now widespread cause of abortion in cattle that has many similarities to toxoplasmosis but with canine definitive host.

52
Q

How does neospora caninum affect dogs?

A
  • Puppies and dogs under a year old
  • Myositis
  • Encephalomyelitis – paralysis
53
Q

How does neospora affect cattle?

A
  • Major cause of abortion – repeated abortions and returns to service
  • Congentially affected calves:
  • Stillborn, weak or apparently normal
  • Vertical transmission – heifers may abort during first pregnancy
54
Q

What is exogenous transplacental transmission of neospora in cattle?

A
  • Infectious resulting from ingestion of sporulated oocysts
  • Involves dog definitive host
  • New infection of naïve herds
55
Q

What is endogenous transplacental transmission of neospora in cattle?

A
  • Infections resulting from reactivation of bradyzoites during pregnancy
  • Principal route of infection of cattle
  • Does not involve dog definitive host
  • Maintenance of infection in endemic herds
56
Q

Summarise the hosts, transmission and clinical importance of toxoplasma.

A
  • Definitive host = cat
  • Intermediate host = rodents, birds
  • Accidental host = sheep, goat, cattle, pigs, horses, humans
  • Exogenous TPT = sheep and goats oocysts, humans oocysts and bradyzoites
  • Endogenous TPT = unusual in sheep and goats
  • Abortion in sheep and goats, human birth defects
57
Q

Summarise the hosts, transmission and clinical importance of neospora.

A
  • Definitive host = cat
  • Intermediate host = cattle
  • Accidental host = horses, sheep, goats
  • Exogenous TPT = cattle oocysts, transmission to niave herds
  • Endogenous TPT = cattle bradyzoites, principle means of transmission for maintenance
  • Abortion in cattle, paralysis in dogs
58
Q

What is sarcocystitis?

A

Indirect life cycles, infecting mammals, birds and reptiles. The carnivore definitive hosts have asymptomatic gut infections while their herbivore prey, the intermediate hosts, have cysts in muscle and other tissues that may lead to clinical signs.

59
Q

Name the host specific combinations of sarcocystis.

A

Cattle:dog = Sarcocystis bovicanis (/cruzi)

Sheep:dog = Sarcocystis ovicanis (/tenella)

Cattle:human = Sarcocystis bovihominis

60
Q

Describe the general life cycle of sarcocystis.

A
  1. Sarcocystic ingested by definitive host.
  2. Sexual reproduction cycles in the lamina propria of the gut of the definitive host.
  3. Sporulated oocysts passed in definitive host faeces sporocysts released.
  4. Sporocysts ingested by intermediate host.
  5. Asexual reproduction in endothelial cells of intermediate host.
  6. Sarcocysts formed in muscles.
61
Q

Describe the specific lifecycle of sarcocystis cruzi.

A
  1. Bovine ingests oocysts contaminating pasture. Could be post mortem lesions or myeloencephalitis.
  2. Initial development in endothelial cells of blood vessels and subsequent encystment of bradyzoites in muscle tissue to form sarcocysts.
  3. Bovine tissue eaten by carnivorous definitive host.
  4. Development of micro and macro gametes in intestine of dog/fox/wolf/coyote definitive host.
  5. Release of sporulated oocysts in faeces, GI disturbance.
62
Q

Describe equine protozoal myeloencephalitis.

A
  • Neurological problem in horses in USA
  • Caudal ataxia and weakness
  • Sarcocystis neurona / falcatula
  • Sarcoysts develop in equine CNS
  • Natural cycle: opossum to and from birds, raccoons, skunks and armadillos
  • Horse is accidental or dead-end host
63
Q

What is besnoitia besnoiti?

A

Clinically affects cattle and goats. Epidemiology poorly understood

64
Q

What are the hosts of besnoitia besnoiti?

A
  • Definitive hosts in Africa are thought to be wild cats and presumed to be domestic cats in Europe.
  • Intermediate hosts: cattle, goats and wild ruminants
65
Q

Describe the transmission of besnoitia besnoiti.

A

Similar to sarcocystis:

  • Intermediate to definitive host by carnivory
  • Definitive host to intermediate host by ingestion of sporulated oocysts (similar to toxoplasma)
  • Possibly also horizontal transmission among intermediate hosts by biting flies
  • Possibly also sexual transmission along intermediate host cattle
66
Q

What is benoitia bennetti?

A
  • Affects intermediate host donkey, horse, mules and zebras
  • Reported in UK donkeys in Devon and Dorset since 2013
  • All originated in UK or Ireland
67
Q

Describe the pathogenesis of besnoitia bennetti.

A

Replicating tachyzoites within vascular endothelial cells – subcutaneous oedema.

Bradyzoites within fibroblasts and endothelial cells:
- Swell to form nodules 0.5-1.0 mm diameter
- Subcutaneous, muscle fascia, blood vessels
- Sclera of eye – diagnostic

68
Q

What are the clinical signs of besnoitia bennetti in cattle?

A
  • Skin and hoof lesions
  • Vulvitis, vaginitis, orchitis, all leading to infertility
69
Q

What are the arthropod borne protozoa of major importance to humans?

A

Plasmodium (malaria)
Trypanosoma (trypanosomiasis)
Leishmania (leishmaniasis)

70
Q

What are the arthropod borne protozoa of major importance to animals?

A

Trypanosoma
Theileria (theileriosis)
Babesia (babesiosis)
Plasmodium (avian malaria)
Leishmania

71
Q

Describe the general life cycle of a tick.

A
  1. Larva
  2. Nymph
  3. Adult
  4. Eggs

Feed on blood and drop of host and moult. Vary on how much time they spend on host as some do moulting on the host.

72
Q

Describe one host ticks.

A
  • Larvae, nymph and adults live on the same host.
  • Adult females give eggs on the host, which give rise to larvae which infect new hosts
73
Q

Describe two host ticks.

A

Larva and nymph live on same host and adult attached to a different host.

74
Q

Describe three host ticks.

A

Each instar has a different host. Feeds, moults, drops off and attaches to another new host.

75
Q

What is transstadial transmission?

A

Disease is transmitted from one stage to the next, between hosts.

Tick can not be reservoir. ‘Pasture spelling’ eliminates disease from ticks if alternative tick hosts are not susceptible.

76
Q

What is transovarial transmission?

A

Female passes on disease to her eggs and the subsequent larva and nymph and so adult developed are infective. Can sustain tick population even in the absence of hosts.

Tick may act as reservoir of disease in absence of disease susceptible vertebrae hosts. Tick survives by feeding on non-susceptible hosts. Pathogen survives by vertical transmission within ticks.

77
Q

What are 3 important European tick species?

A

Ixodes ricinus – sheep tick, castor bean tick. I. hexgonus, I. canisuga

Rhipicephalus sanguineus - brown dog tick, kennel tick

Dermacentor reticulatus – marsh tick, meadow tick, ornate cow tick. Uncommon in UK, important vector in Belgium? (Claerebout E. et al. 2013. Parasites & Vectors 6:183)

78
Q

What is babesia?

A
  • Tick-borne protozoan parasites of red blood cells
  • Cause of babesiosis
  • A variety of species infect various host and vector species, e.g. Babesia canis
79
Q

What is texas fever?

A
  • Splenic or ‘redwater’ fever – Pyrexia, splenomegaly and haemoglobinuria
  • Parasite of red blood cells qNamed “Pyrosoma bigeminum”
  • Disease was spread by cattle ticks – First demonstration of any vector-borne disease
  • Later renamed Babesia bigemina
80
Q

Describe the babesia life cycle.

A

Multiplication mammal red blood cells. Multiplication in tick gut and migrates to salivary gland and cells there produce sporozoites that are released in the tick saliva and go back to infect the dog. Both transstadial and transovarian transmission.

81
Q

What is babesia canis?

A

Transmitted by Dermacentor reticulatis. Main species in Europe

82
Q

What is babesia vogeli?

A
  • Transmitted by Rhipicephalus sanguineus
  • Mediterranean area
  • Less pathogenic than B. (canis) canis
83
Q

What is babesia gibsoni?

A
  • Probably transmitted by Rhipicephalus sanguineus
  • Sporadically reported in Europe
84
Q

What is babesia vulpes?

A
  • AKA Theileria annae, Babesia microti-like species
  • Suspected vector: Ixodes hexagonus
  • Probably reservoir in foxes (Vulpes vulpes)
  • Endemic in northern Spain
85
Q

What is the pathogenesis of babesia?

A
  • Rapid division of parasite in erythrocytes
  • Haemolytic anaemia
  • Splenomegaly
86
Q

What are the acute clinical signs of babesia?

A
  • 1-2 weeks post tick-feeding
  • Fever, haemoglobinuria (red water), jaundice, anaemia
  • Neurological signs
87
Q

What is the treatment for babesia?

A
  • Antiprotozoal drugs
  • Blood transfusion
88
Q

How is babesia diagnosed?

A
  • Blood smear – giemsa stain
  • Do not confuse with nucleated red blood cells – appear in regenerative anaemia
  • PCR
89
Q

What is babesia divergens?

A

Vertebrate host: cattle

Vector: Ixodes ricinus

Disease: redwater fever

90
Q

What are the clinical signs of babesia divergens?

A
  • Pyrexia, anorexia, depression
  • Anaemia, haemoglobinuria, icterus
  • Diarrhoea or constipation
  • Occasionally neurological signs
91
Q

How haemoglobinuria distinguished from haematuria?

A

RBC settle on standing in haematuria

92
Q

What are the factors affecting the epidemiology of bovine babesiosis in the UK?

A
  • Restricted to pastures that support high numbers of ticks
  • Disease outbreaks associated with peaks of tick feeding activity
  • Principally a disease of older animals (Redwater)
  • Inverse age resistance - animals up to 6 months old in endemic areas are protected by colostral immunity and an innate resistance
  • Infected cattle develop non-sterile immunity (premunity). Carriers of a low level of infection, which prevents further infection
  • Enzootic stability develops in endemic areas - high challenge, low disease.
93
Q

Describe enzootic stability?

A

A state of host–tick–pathogen interaction in which there is:

  • A high level of challenge of calves by infected ticks
  • Absence of clinical disease in calves despite infection – due to their inverse age resistance
  • A high level of immunity in adult cattle
  • Consequently a low incidence of clinical disease
94
Q

What are the risk factors of bovine babesiosis?

A
  • Introduction of Babesia naïve adults to tick areas
  • Introduction of tick-infested cattle to naïve herds
  • Fluctuations in tick numbers
95
Q

What causes fluctuations in tick numbers?

A
  • Set aside schemes
  • Changes in pasture harvesting
  • Presence of dipped sheep
  • Use of endectocides for helminths
  • Purturbation of ‘enzootic stability’
96
Q

How is bovine babesiosis controlled?

A
  • Ensure adequate exposure of young animals to tick challenge – before 6 months of age
  • Treatment of affected animals
  • Monitor introduced adult cattle for evidence of infection – timely treatment to prevent disease but also allow immunity to develop
  • Tick reduction measures e.g. dipping (not in UK)
  • Vaccination (in Australia, but not available UK)
97
Q

What are some treatments for bovine babesiosis?

A
  • Imidocarb diproprionate or long acting oxytetracycline
  • Diminazene aceturate in some countries
  • Supportive therapy
98
Q

List some other babesia species in animals.

A

B. bovis, B. bigemina in cattle in tropics/subtropics

Sheep: mild infection – B. ovis, B.motasi

B. capreoli deer Scotland/sheep

Horses: Theileria equi (was B. equi) severe clinical signs abroad

Pigs: mild to severe clinical signs abroad

99
Q

What is leishmania?

A

A flagellate parasitic protozoan of animals and man transmitted by the sandfly. Causes leishmaniasis. Important zoonosis.

100
Q

What are the hosts and vectors of leishmania?

A

Vertebrate hosts: human, dog, wild animals. Infects host macrophages

Vector: bloodsucking phlebotomine sandfly – phlebotomus sp. (Old World) and lutzumyia sp. (New World)

101
Q

What are the 2 main forms of leishmania?

A
  • Visceral (humans & dogs)
  • Cutaneous (humans)
  • Also a mucocutaneous form (humans)
102
Q

What is canine leishmaniasis?

A
  • Vectors not (currently) present in UK
  • Recent case of canine leishmaniosis in the UK in a dog without a foreign travel history
  • Congenital and venereal transmission, or biting?
  • Incubation period months to years – disease may appear after return to UK
103
Q

What are the variable clinical signs of canine leishmaniasis?

A
  • Skin lesions, ocular abnormalities, epistaxis
  • Frequently: weight loss, lethargy
104
Q

What is the pathology of canine leishmaniasis?

A
  • Anaemia
  • With or without thrombocytopenia
  • Hyperglobulinemia
105
Q

How is canine leishmaniasis diagnosed?

A
  • Cytology on Giemsa stained lymph node or bone marrow aspirates §
  • PCR
  • Serology
106
Q

How is canine leishmaniasis diagnosed?

A
  • Cytology on Giemsa stained lymph node or bone marrow aspirates §
  • PCR
  • Serology
107
Q

How is canine leishmaniasis treated?

A
  • Pentavalent antimonials (toxicity)
  • Allopurinol
  • Miltefosine (safer, expensive)

Treated dogs may remain carriers, may relapse and may remain infectious to sand flies.

108
Q

How is canine leishmaniasis prevented?

A
  • Insecticides: topical or impregnated collars
  • Imidacloprid, deltamethrin
109
Q

What is trypanosomiasis?

A
  • Major problem in sub-Saharan Africa
  • Causes anaemia and loss of production in animals
  • Zoonosis: fatal in humans
  • Other species of trypanosomes found elsewhere, including non-pathogenic forms in UK
110
Q

Describe trypanosome antigenic variation.

A
  • Variable surface glycoprotein coat (VSG)
  • Vast repertoire of VSG genes
  • Antigenic variation evades host immune response
111
Q

Describe trypanosome antigenic variation.

A
  • Variable surface glycoprotein coat (VSG)
  • Vast repertoire of VSG genes
  • Antigenic variation evades host immune response
112
Q

Name 2 factors that straw bedding provides, which are conductive to infection with Eimeria tenella.

A

An intact faeco-oral cycle. High moisture and temperature suitable for development to the infective stage.

113
Q

Name the 3 lifecycle stages in Eimeria.

A

Schizogony or merogony
Gametogony
Sporulation

114
Q

What disease does trypanosoma brucei cause in humans?

A

Sleeping sickness, or human African trypanosomiasis

115
Q

What are the consequences for an adult cat infected with toxoplasma gondii?

A

None or minimal, possibly some transient diarrhoea. Kitten can be infected In utero and born weak.

116
Q

What are the consequences of a pregnant sheep infected with toxoplasma gondii?

A

Abortion, stillborn or apparently barren

117
Q

What are the consequences of a pregnant woman infected with toxoplasma gondii?

A

Possible miscarriage. A child infected in utero can develop retinal lesions and vision loss.

118
Q

What are the consequences of toxoplasma gondii on a healthy, non-pregnant, immunocompetant person?

A

Non or minimal flu-like signs. Bradyzoite cysts can establish in the brain but are unlikely to lead to clinical disease, though could affect behaviour.

119
Q

Can giardia be zoonotic?

A

In principle, yes. In practice, most strains seem to circulate separately in dogs and humans, and in fact there is probably more human-to-dog than dog-to-human transmission.

Animal Disease 1 (25 decks)

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