Parasitology PROTIST Flashcards
Protozoa define, 2 forms of pathogensis, reproduction, lifecycle, size, locomotion and nutrition
Eukaryotic unicellular organisms
• Pathogenesis Intraintestinal OR Extraintestinal
• Reproduction Intracellular OR Extracellular
• Life cycle -> Direct (faecaloral route generally) OR Indirect (e.g. vector-borne)
• Size -> 5-40 μm
• Locomotion -> Gliding, via flagella, cilia or pseudopodia, other
• Nutrition -> Usually absorption via the pellicle (cell membrane)
What are the 4 structures used for locomotion and describe them
1) Flagella ->elongate ‘whip-like’ extensions of the cell membrane
2) Pseudopodia -> temporary extensions of the cell body or ‘false feet‘
3) Cilia -> small ‘hair-like’ extensions of the cell membrane
4) Undulating -> tiny undulatory waves in cell membrane imparting forward gliding motion
What are 8 important diseases caused by protozoa
1) avian trichomoniosis
2) leishmaniosis
3) cattle - neosporosis
4) canine babesiosis
5) malaria
6) feline tritrichomoniosis
7) porcine coccidiosis
8) cogenital toxoplasmosis
Phylum - apicomplexa what is an important feature and its function and the reproductive aspect
Apical complex - Allows for penetration - Cytoskeletal and secretory function - Central to cell penetration and invasion - Parasitophorus vacuole Reproductive - sexual and asexual - highly prolific
What are the 3 phases of reproduction in apicomplexa and what produce
1) Schizogony (=Merogony) -> Asexual (Schizont)
- Replication of merozoites (multiple generations) - HIGHLY PROLIFIC
- Pathogenetic stage
2) Gametogony -> Sexual (Gamont) Gametes
> Macro-gametocytes (M) & micro-gametocytes (m)
> Gametes (M + m) > Zygote > unsporulated oocyst
3) Sporogony -> Asexual (Sporont)
- Sporulation of the oocyst (sporocyst > sporozoites) external environment or within the host
- “infective unit”
What are the general 6 steps in apicomplexa lifecycle
1) parasite within cell within a cyst
2) ingested
3) sporozoite comes out and invades the cells
4) within cell within vesicle -> replication - schizogony
5) gametongy
6) sporogony
What is the general sporulated Oocyst morphology and how differentiated
Oocyst contains sporocyst which contain sporozoite/(s) -> infective stage
1st number - number of oocyst
2nd number - number of sporocyst
3rd number - number of sporozoite within one sporocyst
What are the main differences between non- cysts and cyst forming coccidia in terms of lifecycle and location
Non-cyst forming
- Direct LC/rapid
- Mainly in intestines and associated organs cause coccidiosis
Cyst-forming
- Indirect LC/slow
- DH - intestines, PH/IH in tissues - pathogenic
What is the main different between eimeria and cystiosospora and cryptosporidium
Eimeria and Cystisospora
- Go deep into cell, destroy cell via rupture and self-infective -> lots of tissue destruction (haemorrhagic)
○ Different from cryptosporidium
Coccidia what are the 2 main different effects in the definitive host and what are the husbandry risk factors
DEFINITIVE HOST:
- Strong species-specific immunity develops with exposure (‘trickle immunity’)
- Subclinical / asymptomatic self-limiting
OR
- scours/ diarrhoea ± haemorrhagic
○ naïve’ most affected especially weaners
○ Immunity, dose, virulence
Husbandry risk factors:
- Overcrowding, stress (climate), poor hygiene, poor nutrition
Eimeria what are the hosts and the main pathogenic effects and the main spcies involved
Hosts: - Birds, Ruminants, Lagomorphs Significance: - Economic losses – Poultry*** - Hepatitis - Enteritis (watery/bloody diarrhoea) - Many species – differing virulence - Mostly SI – E. Tenella LI
Eimeria lifecycle what type, pre-patent period, sporulation and virulence
- Direct – rapid
- Pre-patent period varies from 3-21 days - RAPID
- Sporulation 1-3 days (21-30ºC, humid optimal)
- Many species, vary in virulence, low - severe
What are the 11 steps in the Eimeria lifecycle
- oocyst shed in faeces
- Sporulate in the environment via Sporogony and form sporozoites
- Ingested by host
- Passes through stomach
- In intestines the oocyst ruptures, sporocyst ruptures and sporozoites come out
- They get onto epithelial cells in gut - location species dependent
- Bind on and penetrate via apical complex
- Sit within cell in parasitophorous vacuole membrane where suck nutrients from the cell
- Undergo Schizogony -> thousands of schizonts produced which ruptures the cell
- Now called merozoites which ruptures the cell
- CAN EITHER
a. repeat steps 7-9 (cycle) through pathogenic stage causing haemorrhagic diarrhoea
b. Undergo developmental change and go through gametogony where they form gametes (ovum and sperm) which then invade a cell, form either Macro-gametocytes (M) or micro-gametocytes (m), gametes then fuse and become the zygote which becomes oocyst completing the lifecycle
Eimeria pathogenesis what parasite factors and host factors involved and what occurs
High mortality is rapid - 2nd schizogony phase - lamina propria destruction/sloughing off - haemorrhagic diarrhoea Parasite factors: - species, dose, location Host factors: - age, nutrition, immunity
Eimeria diagnosis what are the 3 main ways this occurs
- Post-mortem (fresh!) - generally have high mortality when called out
- Gross observation - predilection site, pathology
- Samples:
○ Multiple fresh mucosal smears / scrapings + fixed gut sections for histology
§ schizonts with merozoites - diagnosis
§ gametes - Ante-mortem:
- Faecal flotation -> saturated sucrose or saline
○ McMaster method for oocyst counts and identification
- Unsporulated oocysts -> sporulation in 2% potassium dichromate soln - Feed sample: if coccidiostats incorporated to check dosage
What are the 3 types of treatment for Eimeria and what is the most common
- Curative treatment?
- Supportive treatment - most common
a. fluids/electrolytes -> wait for immune system to remove the parasites - Preventative treatment
○ Arrests development
○ None registered for layers!
What are the 3 groups of common anti-coccidial agents, the most common, examples within and species used on
- Ionophore Antibiotics
- Affect cell membranes (e.g. Na2+ influx)
- Coccidiostatic – extracellular stages only
- Monensinchicken, cattle, sheep, goats, turkeys Lasalocid sheep, cattle
- Salinomycin , Narasin, Maduramycin – chickens - Toltrazuril
- Drugs affect plastid-like organelles
- Coccidiocidal (ALL STAGES)
- Long acting – single dose prophylaxis, multiple for treatment
- Long withdrawal period for meat
- Poultry, dogs, cattle, sheep, pigs - Sulfonamides: - MOST COMMON
- Coccidiocidal
- interfere with folate production and nucleotide (DNA) production.
- Birds, dogs, cats, pigs
What are the 2 main control strategies within controlling coccidiosis in poulty
- Vaccine
- live and live attenuated vaccines
- sporulated oocysts
- species-specific immunity -> low exposure dose so acquire a level of immunity
○ Can do combination of species within one vaccine
- inoculate chick or hatchery - Hygiene
- Resistant oocysts
○ Ammonia-based disinfectants - very effective
§ Irritation to the animals so need to remove before treatment
○ Desiccation - steam and heat - if dry out die quickly
- Treat and introduce – quarantine
- On-farm biosecurity
- Chicken housing -> break the faecal oral route cycle -> bring chicken on slatted flooring to make faeces fall through the floor
What is an issue of controlling coccidiosis via hygiene alone
- ‘too clean’ – immunity?
○ Low level exposure is the best as can gain immunity
○ Get the major issue when outbreak in naïve group of animals - HIGHER MORTALITY
Intestinal and hepatic coccidiosis in rabbits what are the effects and necropsy findings with hepatic
Intestinal coccidiosis in rabbits - Scours, haemorrhagic diarrhoea Hepatic coccidiosis in rabbits Eimeria stiedae - Merogony in bile duct / gall bladder epithelium - Jaundice, diarrhoea, sudden death ○ Up to 50% fatality in weanlings Necropsy findings: - Focal white-yellow nodules or cords in liver along path of bile ducts - Cholangitis
Coccidiosis in cattle what are the two species, what age most common, what lead to, risk factors and treatment
E. zuernii , E. bovis
- 1-2 months <1 year old
- Calf diarrhoea / bloody scours
○ Secondary colibacillosis
- Subclinical – production losses
- Overcrowded barns, weaning to pasture/ feedlots
- Coccidiostats in milk replacer, feed (monensin, lasalocid) or single drench (toltazuril) before weaning
Coccidiosis of lambs what are the two main species, what age most common, risk factors and prevention strategies
- Lambs 1-5 months old (E. crandallis and E. ovinoidalis)
- Lambing pens, weaning, introduction to feedlots
- Prevention: coccidiostats in feed
○ late gestation in ewe, 21 days prior to lambing
○ prior to weaning in lambs!
Cystoisospora what age group mainly occur in and why and main pathogenic effects
strong acquired immunity
○ Therefore mainly in young animals -> puppies, kittens, piglets
- ± diarrhoea (not usually bloody), ill thrift
Cystoisospora lifecycle what type, stages in which host or environment and steps
- Direct life-cycle
○ rapid and host-specific
○ Can use a paratenic host - Schizogony – multiple phases - intestines
- Gametogony – gametes (sex) - intestines
- Sporogony – in environment
Same as Eimeria HOWEVER - less asexual merogon penetration of tissues and repeating cycle that way
- Can have paratenic host - rodents ingest oocyst, hatch, penetrate through the tissues and remain dormant in tissues until ingested by definitive host (Cystoisospora felis)
What are the 2 mechanisms of diagnosis of cystoisospora and what detecting
1) faecal flotation
○ Unsporulated oocysts
2) Schizonts/merozoites via histology
What are the 3 treatment options for cystoisospora
1) Supportive care
2) Sulphonamides for 1 – 2 weeks -> can still be shedding through this time
3) Toltrazuril for 1-3 days
What are 3 prevention and control strategies for cystoisospora
1) Mass treatment of all animals including mothers
§ As for other coccidia PLUS
□ Dogs - before whelping and during lactation
2) Faecal oral Hygiene, biosecurity
§ Cleaning out bedding, hang in the sun (to kill)
3) Prevent predation / feeding of raw meat
List some control options for cystoisospora in piglets and treatment options
- Hygiene, biosecurity, all-in-all-out system
○ Hose the area DO NOT BROOM then allow to dry - Medicate the sow feed with coccidiostats
- Piglets:
○ Single oral dose of toltazuril (Baycox) at 3-5 days
OR
○ Long acting sulphonamide injection at 6 days of age
Cryptosporidiosis what are the 3 main forms of disease in which animals occur in and what important consideration with treatment
- Intestinal: diarrhoea / steatorrhea - mammals
○ Generally before weaning calves
○ Not haemorrhagic diarrhoea as epicellular (sit on top of cells don’t invade and lyse cells) - Gastric: Postpandrial regurgitation
○ In animals such as snakes -> hyperplasia and distention of cloaca (almost always fatal) - Respiratory – mainly in birds
Resistant to heat / chlorination!!!!!
Whihc of the cryptosporidium is less host-specific
C. parvum - zoonoses (particularly a problem in children)
Cryptosporidium lifecycle type, where sporogony occurs, special location where in the host
- Direct - faecal-oral route
- Sporogony occurs within the host – infective immediately
- ‘Epicellular’ position – intracellular but extracytoplasmic
- Gastric or intestinal
- Respiratory epithelium poultry – C. baileyi
What are the 7 steps in the lifecycle of Cryptosporidum and two ways transmitted
- Oocyst (1:0:4) ingested move through stomach
- cues in intestines/gastric/respiratory system that trigger release such as bile acids
- hatch and emerge as sporozoites
- attach to the surface of the gut (via apical complex) and causes the plasma membrane of the epithelial cells to engulf them and sit on top of the cell within the membrane
a. Parasitophorus vacuole membrane in epicellular position - parasite proteins that suck nutrients from host cell
- Undergo Schizogony producing schizonts into gut lumen merozoites
- CAN EITHER
a. repeat steps 4-6(cycle) through pathogenic stage causing diarrhoea OR
b. Undergo developmental change and go through gametogony where they form gametes (ovum and sperm) which then invade a cell, form either Macro-gametocytes (M) or micro-gametocytes (m), gametes then fuse and become the zygote which becomes oocyst completing the lifecycle
i. Two types of oocyst formed
1) Thick walled - passed in faeces
2) Thin walled - autoinfection
Cryptosporidum pathogensis what are the 3 main effects on host
1) Villous atrophy ○ Parasite destruction ○ T-cell induced apoptosis 2) Epithelial mucosa release cytokines ○ ↑H20 and ↑Chloride 3) Watery diarrhoea (frequent and can last weeks) and malabsorption Destroy mucus membrane
Cryptosporidum what are the 2 main significance
1) Neonatal / post-weaning diarrhoea
○ Livestock, foals, pigs, pups, kittens
○ Poor colostrum intake
○ Immunocompromised
2) MAJOR water-borne pathogen – oocysts resistant to chlorine
○ Self-limiting diarrhoea (2-4 weeks in healthy)
○ Chronic life threatening diarrhoea in HIV-AIDs patients
○ Zoonoses! - C. parvum*
Cryptosporidum in calves what age, infectious dose and excretion
- Only calves up to pre-weaning < 4 weeks infected with C. parvum, not adult cattle!
- High intensity of oocysts excretion
- Low infectious dose (5-10 oocysts) - very hard to control, way all cattle will probably be infected within first few weeks of life
Cryptosporidum diagnosis what are 4 mechanisms
- Difficult if not trained eye
1) Zinc or sucrose floats (S.G. 1.12-1.18)
○ Oocysts small (5-6 μm)
○ immunofluorescence - oocyst wall protein
2) Smear - Ziehl-Neelsen, Modified Acid Fast stain - most common
3) ELISA or immunochromatography (dip-stick)
4) PCR – species ID
Cryptosporidum treatment options
- No curative treatment
- Supportive care
○ Fluids, electrolytes - Hyper-immune bovine colostrum
- Following shown some success
○ Halofuginone (quinazoline derivative) – prevention clinical signs - reduces oocyst output calves, not ‘cure’!
○ Nitazoxanide (anti-protozoal) and paromomycin/ azithromycin humans (HIV aids)
What are the 3 main control strategies for cryptosoporidum
- Hygiene (heat >70ºC – steam, flame gun, dry, ammonia based disinfectants)
○ All in all out -> flame thrower - Biosecurity/ quarantine
- Adequate colostrum
What are the 13 main steps in cys forming coccidia
- Sporulated oocyst in faeces of infected cat (2-4 days)
- Oocyst ingested can involve parenetic host but ultimately ingested by intermediate host (any mammal)
- Typical lifecycle cat to rodent - Sporozoite comes from the oocyst moves into tissues where form 2 different specialist cells
- Form tachyzoite -> move around the blood through blood stream, gets into cells replicates under schizogony and ruptures the cells -> repeat this cycle
○ Where replicate leads to clinical disease - When the Immune response or treatment occurs results in death of some tachyzoite and move into the cells
- In cell without replication forms bradyzoite -> dormant stage (cyst stage) waiting to be ingested
- Then Ingested by the definitive host where they get onto epithelial cells in gut - location species dependent
- Bind on and penetrate via apical complex
- Sit within cell in parasitophorous vacuole membrane where suck nutrients from the cell
- Undergo Schizogony -> thousands of schizonts produced which ruptures the cell
- Now called merozoites which ruptures the cell
- CAN EITHER
- Become tachyzoite in its own right and cause issues in the definitive host
- OR Undergo developmental change and go through gametogony where they form gametes (ovum and sperm) which then invade a cell, form either Macro-gametocytes (M) or micro-gametocytes (m), gametes then fuse and become the zygote which becomes oocyst - In environment unsporulated -> sporulate then infective (takes 24-48 hours)
○ Oocyst (1:2:4 morphology)
