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81 Cards in this Set
- Front
- Back
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Protozoology
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The study of unicellular organisms
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Apicomplexa members
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Coccidia, Piroplasmidia, and Haemosporidia
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General Apicomplexan life cycle
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1. Sporozoites enter host cells and being to develop
2. Sporozoites become trophozoites that multiply asexually (schizogony) in a schizont, developing daughter cells called merozoites 3. Merozoites are released and enter new host cells; can be several rounds of schizogony 4. Merozoites will trasform into gametes (gametogony) producing micro- and macrogametes which fuse together to form a zygote 5. A wall is formed around the zygote to form an oocyst 6. Oocyst is released by rupture of the host cell and passes into environment with the host's feces 7. When environmental conditions are right, the single cell within the oocyst undergoes sporogony to form a oocyst with sporozoites |
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Members of Coccidia with direct life cycles
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Eimeria, Isospora, and Cryptosporidium
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Members of Coccidia with indirect life cycles
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Toxoplasma, Neospora, Sarcocystic, Besnoitia, Hammondia, Hepatozoon
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Eimeria sporulated oocysts
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Thick walled, spherical
Possible micropyle cap Contains 4 sporocysts with 2 sporozoites in each |
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Isospora sporulated oocysts
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Thin walled, spherical
Contains 2 sporocysts with 4 sporozoites in each |
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Transmission of Eimeria and Isospora
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Fecal-oral route
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Do animals develop immunity after Eimeria and Isospora exposure?
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Yes, animals develop immunity after exposure. Immunity can be complete or partial.
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Clinical signs of coccidiosis
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Profuse, chronic, watery diarrhea
Possible hemorrhage of the GIT Impaired absorption from GIT Poor weight gain, weakness, dehydration, ill thrift Abdominal pain, tenesmus |
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How is a diagnosis of coccida made in a live animal?
How is a post-mortem diagnosis of coccidia made? |
Demonstrating oocysts using a sugar or salt fecal flotation technique
Based on gross and microscopic lesions and on the demonstration of sexual or sexual stages of the parasite in direct/squashed smears or histological sections of affected portions of the GIT. |
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How can you treat coccidiosis?
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Sulpha-drugs, amprolium or ionophores
Supportive treatment (fluids, electrolytes, etc) |
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Is there a vaccination for coccidiosis?
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Yes, but ONLY in poultry
Immunocox, Paracox (live vaccines) |
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Types of non-tissue cyst forming coccidiosis that affects dogs
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Isospora canis, I. ohioensis, and I. burrowsi
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Type of non-tissue cyst forming Coccidiosis that affects cats
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Isospora felis and I. rivolta
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Types of non-tissue cyst forming coccidiosis in cattle
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Eimeria bovis: invades the endothelial cells of the central lacteal of villi in the lower small intestine and epithelial cells of the cecum and colon
Eimeria zuernii: invades the connective tissue cells of lamina propria in the lower small intestine and epithelial cells of the cecum and colon Eimeria alabamensis: common in calves after spring turnout |
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Types of non-tissue cyst forming coccidiosis of goats and sheep
Which species is more susceptible? |
Goats: Eimeria ninakohlvakimovae
Sheep: Eimeria ovinoidalis Goats |
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What are important predisposing factors for coccidiosis outbreaks?
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Unhygienic conditions and stress
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Type of non-tissue cyst forming coccidiosis of horses
Type of non-tissue cyst forming coccidiosis of pigs |
Eimeria leuckarti
Isospora suis |
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What is responsible for one of the most considerable losses in the poultry industry?
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Intestinal coccidiosis, especially subclinical infections
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Types of caecal coccidiosis in poultry
Types of intestinal coccidiosis in poultry |
Eimeria tenella
Eimeria necatrix, E. brunetti, E. acervulina, E. maxima |
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Morphology of Cryptosporidium oocysts
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Very small (4-8 um)
Each oocyst contains 4 naked sporozoites |
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Where does Cryptosporidium infect the host?
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Intestinal epithelium cells
Can also infect epithelial cells of the gall bladder, respiratory tract and kidney, especially in immune-compromised hosts |
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Cryptosporidium found in the stomach of
Cryptospidium found in the abomasum of cattle |
C. muris
C. andersoni: it is larger than most of the other spp and occurs in older animals |
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Cryptosporidium parvum
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Infects the small intestines
Has 2 genotypes: 1. C. hominis = infective for humans only 2. C. parvum = infects bovine, humans, and more (zoonotic); usually occurs in calves younger than 3 weeks |
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Transmission of Cryptosporidiosis
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Fecal-oral route
Waterborne outbreaks Possible aerosol transmission |
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Clinical signs of Cryptosporidiosis
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Foul-smelling yellow diarrhea 3-5 days post-infection
Reduced food intake, weight loss Depression Malabsorption, fluid loss, and dehydration when severe |
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How to diagnose Cryptosporidium
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Clinical signs and age
Acid fast stains - modified Ziehl Nielsen, Safranin methylen blue, fluorescent staining PCR |
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How do you treat Cryptosporidiosis?
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Difficult!
No specific drugs available, but Halofuginone (Halocur) is commonly used Symptomatic treatment |
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How do you prevent Cryptosporidiosis?
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Avoid contact of neonates with oocysts
Good hygiene --> cresol based disinfectant Avoid overcrowding of animals Protect water supplies No vaccine available!! |
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Members of Sarcocystidae (coccidia with indirect life cycles) that are of veterinary importance
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Toxoplasma
Neospora Sarcocystis Besnoitia Hammondia |
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What type of oocyst do members of Sarcocystidae have?
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isospora-like
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What members of Sarcocystidae have oocysts that are excreted unsporulated?
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Toxoplasma and Neospora
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General life cycle of member of Sarcocystidae
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1. The final host becomes infected by ingestion of the tissue cysts in the meat of various intermediate hosts
2. Gametogony takes place in the intestinal epithelium of the small intestine 3. Oocysts are excreted (usually unsporulated) in the feces and sporulation occurs in the environment 4. Intermediate hosts ingest oocysts and the sporozoites are set free inside the intestine to pentrate cells. 5. Schizogony occurs leading to pseudocysts being produces which are filled with merozoites/tachyzoites 6. Tachyzoites are released after bursting of pseudocyst, infecting other cells 7. After several cycles, tissue cysts are formed, filled with bradyzoites |
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Final hosts of Toxoplasmosis
Intermediate hosts of Toxoplasmosis |
All felids, but the domestic cat is of most importance
All mammals, including birds and humans. Most important is sheep, goats, pigs, and humans. Cats can also serve as intermediate hosts |
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What is the one species responsible for Toxoplasmosis?
Are final hosts of toxoplasmosis affected? |
Toxoplasmosis gondii
Usually no significant pathology Only the superficial cells at the tips of the villi in the small intestine are affected |
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Sources of infection for toxoplasmosis
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Finals hosts- by ingesting tissue cysts from infected intermediate hosts
Intermediate hosts- accidental ingestion of oocysts from the environment, eat raw/undercooked meat infected with tissue cysts, transplacental transmission in acute phase of disease, organ transplant, or blood transfusion |
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Clinical signs of toxoplasmosis
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Cats- rare
Dogs- young dogs can have nervous signs, coughing, dyspnoea Sheep/goats- perinatal mortality, abortion, resorption of fetus Pigs- rare, some respiratory symptoms Humans- rare in adults unless pregnant --> abortion or birth defects |
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How do you diagnose toxoplasmosis?
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Serologic or histocytologic examination
DT, IFAT, latex agglutination test, ELISA, PCR, demonstration of tachyzoites in tissue sections or smears of body fluid |
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How do you treat toxoplasmosis?
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No satisfactory drug.
Clindamycin used in cats to reduce shedding of oocysts |
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Prevention of toxoplasmosis
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Avoid contaminated cat feces, raw/uncooked meat, dispose of aborted fetuses/placentas
Vaccine available in sheep! --> Toxovac! |
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What is the definitive host for Neosporosis?
What are the intermediate hosts for Neosporosis? |
Dog
Dogs, cattle, horses, sheep, goats, deer |
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What is the most common route of transmission of Neospora in cattle?
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Transplacental transmission (occurs in all the intermediate hosts)
Transplacental transmission frequently recurs in subsequent pregnancies once infected |
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Clinical signs of Neosporosis
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Cattle: abortions, usually at 5-7 months of gestation ; newborn infected calves may be underweight and unable to rise, and they may also show neurological signs (ataxia, limbs flexed or hyperextended) ; exophthalmia
Dogs: ascending paralysis, especially when involving several littermates |
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Diagnosis of Neosporosis
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Clinical signs
Serology - ELSA, IFAT, LAT ; Titres of equal to or more than 1:800 in dogs usually indicative of acute infection ; immunohistological staining of brain lesions Oocysts in feces of dogs |
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Treatment of Neosporosis
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None in cattle
Sulphonamides and/or pyrimethamine and clindamycin have been used with some success in dogs |
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Prevention of Neosporosis
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A killed vaccine (NeoGuard) available in USA
Don't feed raw meat or aborted fetuses to dogs Prevent contaminated of feed/water Maintain biosecurity |
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What are important Sarcocystis species?
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Sarcocystis bovihominis
S. cruzi S. suihominis S. neurona --> Equine Protozoal Myeloencephalitis (EPM) |
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Clinical signs of Sarcocystis in cattle
Clinical signs of Sarcocystic in sheep |
Protracted fever, anemia, lymphadenopathy, anorexia, diarrhea, hypersalivation, weakness, hair loss on eyes, neck and tail switch
Anemia, hepatitis, myocarditis, neurological signs and lesions of encephalomyelitis |
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Treatment for Sarcocystis in cattle, sheep, pigs
Prevention/control measures of Sarcocystis |
No effective treatment, in final or intermediate host
Good hygiene |
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Definitive hosts of Sarcocystis neurona
Intermediate hosts of Sarcocystis neuron |
Opossums (Didelphis spp)
Nine-banded armadillo in the natural intermediate host ; other mammals have been found to be experimentally ; horses are "dead-end" hosts as no sarcocysts develop |
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Where does Sarcocystis neurona parasitize?
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Neurons, mononuclear cells and glial cells in all regions of CNS of the horse
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Clinical signs of Sarcocystis neurona in the horse
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Determined by the area of the CNS parasitized
Spinal cord is most frequently affected, leading to gait abnormalities Can also have multifocal areas of hemorrhage, nonsupportive inflammation, and necrosis |
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Diagnosis of Sarcocystis neurona
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Clinical signs
Immunoblot analysis of serum and CSF |
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Treatment of Sarcocystis neurona
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Sulphonamides, pyrimethamine, the coccidiostats diclazuril and toltrazuril can kill the early stages of the parasite and may be used as prophylactic drugs
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Prevention of Sarcocystis neurona
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Provisionally licensed vaccine available in USA
Protect food/water supplies |
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Describe the life cycle of Besnoitia besnoiti
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Still unknown
It infects both domestic and wild bovids as intermediate hosts but the definitive host has not been identified |
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Distribution of Besnoitiosis
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Africa, Middle East, and Europe
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Clinical phases of Besnoitiosis
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1. Febrile stage (lasts 2-10 days): associated with intense miltiplication of tachyzoites within macrophages, fibroblasts and endothelial cells of blood vessels. Photophobia, epiphora, ocular and nasal discharges, ruminal stasis, anorexia, increased heart and resp rate, and possible abortion
2. Normal/slightly increased temp, enlargement of lymph nodes and oedematous swellings of head, limbs, and lower parts of the body, skin is warm, thick and painful, congestion of udders/teats, acute orchitis with painful testes and transient or permanent infertility in bulls 3. Chronic phase: formation of numerous tissue cysts containing bradyzoites, commonly found in the dermis, upper resp tract, connective tissues, sclera conjunctiva, muscles. Skin becomes thickened with hyperkeratosis and alopecia |
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Diagnosis of Besnoitiosis
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Clinical signs (chronic cases especially) - cysts likely visible
ELISA, IFA PCR to detect parasite in skin biopsies or cell cultures |
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Treatment of Besnoitiosis
Prevention of Besnoitiosis |
None. Sulfamides used to diminish severity of clinical signs
Attenuated live tachyzoite vaccine in Israel and South Africa, but not Europe |
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Describe the morphology of the Babesia bigemina, B. bovis, and B. divergens trophozoites
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B. bigemina - pairs are at acute angles
B. bovis - pairs are at obtuse angles B. divergens - pairs are at obtuse angles and located in the periphery of the cell |
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Distribution of Babesia
Susceptible hosts of babesiosis |
Worldwide
Most mammalian hosts - livestock, domestic animals, rodents, game, and humans |
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Transmission of Babesia
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Transmitted biologically through ticks of the family Ixodidae
Transmission is transstadial, but transovarial transmission occurs in some species (B. divergens) |
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Inverse age resistance
Endemically stable |
Natural non-specific immunity to the disease in young ruminants between 6-9 mo of age
When >80% of the herd is immune; develops under conditions of high tick challenge as most animals become infected at a young age when they are still protected |
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Endemically unstable
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When only 20-79% of animals become infected during their first year of life; frequent outbreaks of disease occur if tick numbers increase
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How long can the infection of Babesia divergens be maintained in a tick population in the absence of bovine hosts?
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Up to 4 yrs
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What does the pathogenesis of Babesia chiefly revolve around?
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The destruction of RBCs when the parasites exit the cell following replication
In some Babesia spp, there is also an increased fragility of the RBCs. The destruction of RBCs can lead to anemia, haemoglobinuria, and haemoglobinemia. B. gibsoni can also cause anoxia |
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Clinical signs of Babesia
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Dependent on the strain as well as host factors
Fever, anemia, and haemoglobinuria usually appear 8-16 days after tick engorgement Haemoglobinemia and anoxia Depression, anorexia, weakness, cessation of rumination, dehydration, death --> B. divergens |
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Diagnosis of Babesia
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Clinical signs
Microscopical examination of thin blood smears prepared from the ear or tail tip and stained with Giemsa stain PCR IFAT, ELISA |
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Treatment of Babesia
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Reduce parasitemia ASAP
Imidocarb used in Ireland, but be aware of withdrawal periods! Non-specific supportive therapy - iron, dextrose, vitamin, and blood transfusion Attenuated live vaccines available for use in Ireland |
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Prevention of Babesia
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Control of ticks with acaricides
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Morphology of Theileria
Distribution of Theileria |
Schizonts/Koch's bodies in lymphocytes
Piroplasms in RBCs - small (1-2 um), oval/comma shaped with nucleus at one end Usually more than one parasite in an RBC Maltese cross in Theileria equi Africa, Asia, Middle East |
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Hosts of Theileria
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Cattle, small ruminants, and some wildlife spp.
Cats and dogs Horses and donkeys |
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Transmission of Theileria
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Transmitted biologically by ticks of the family Ixodidae
Only transstadial transmission occurs Iatrogenic spread reported Intrauterine infection in horses |
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Lymphoproliferative group of Theileria
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T. parva, T. annulata and T. lestoquardi
Phase of hyperplasia and expansion of lymphoblast population leading to lymph node enlargement and spreading infected lymphocytes throughout the body |
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Haemoproliferative group of Theileria
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T. mutans, T. equi, and T. orientalis
Infected RBCs are destroyed as the parasites exit the RBC; also evidence of oxidative damage of RBCs --> anemia and organ damage |
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Clinical signs of Theileria
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Severity of disease is dose-dependent
First symptoms (8-14 days after tick attachment) - regional lymph nodes enlarge followed by fever 1-2 days later Animals anorectic with nasal discharge Resp distress and mucohaemorrhagic diarrhea develops at terminal stages Some develop nervous disorders Anemia in T. annulata and haemoproliferative group Fever, malaise, anorexia, depression, icterus, haemoglobinemia/hemoglobinuria, pale mucous membranes, tachycardia, tachypnea, and sudden death signs of T. equi |
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Diagnosis of Theileria
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Clinical signs
Demo of parasite in smears of lymph node aspirate and RBCs, stained with Giemsa |
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Treatment of Theileria
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Quinazolines (Halofuginone), coccidiostats that target the schizont stage or naphthaquinones targeting both the schizont and prioplams stage are the drugs of choice
Most anti-babesial drugs, especially Imidocarb, are also effective in the case of T. equi |
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Prevention of Theileria
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Acaricides used to eliminate tick vectors
T. parva and T. annula have vaccines No vaccine for T. equi |
