Parasitology Flashcards
Types of damage caused by parasites (6)
- Mechanical damage (eg occlusions in intestine)
- Traumatic damage
- Inoculation of pathogens
- Malabsorption (eg increase in intestinal permeability, loss of epithelial barrier function)
- Malnutrition
- Pressure and atrophy
Classification of parasites
- Protozoa
- Helminths
- Arthropoda
- Single eukaryotic cells, genetic material carried on chromosomes
- These are worms. include: i) Plathelminthes (flatworms) → ie Trematoda (bi-lateraly symmetrical and leaf-like, no body cavity) and Cestoda (extremely elongate and segmented as adults, no body cavity). ii) Nematoda (roundworms) elongate, usually circular in cross-section, tapered at both ends and with a body cavity
- Insects, ticks, mites. Usually metamerically segmented
Cattle PGE
a) Define parasitic gastroenteritis (PGE)
b) Clinical signs of PGE (5)
c) Biggest impact of PGE
a) Syndrome of symptoms characterised by a number of parasitic infections of nematodes in the GI tract
b) 1) Weight loss. 2) Loss of production. 3) Hypoalbuminemia. 4) Diarrhoea. 5) Seasonal
c) Economic losses associated with parasitic disease. Clinical disease often only evident in cattle with heavy parasitic burden
Cattle PGE
Four main parasites causing PGE and where they infect
- Ostertagia ostertagi (Abomasum nematode)
- Haemonchus spp. (Abomasum nematode)
- Nematodirus spp. (Small intestine)
- Oesophagostomum spp (Large intestine)
Cattle PGE
Describe direct lifecycle of Ostertagia ostargi
Eggs passed in faeces. Under optimum conditions develop within pat to the infective L3 within 2 weeks. When moist conditions continue, L3s migrate from herbage, ingested by graxing cattle. On ingestion, L3s exsheath in rumen, furhter development in abomasal glands. After ~18 days after infection, L5s emerge from glands, become sexually mature on mucosal surface.
Pre-patent period is 3 weeks - 6 months
Cattle PGE
Pathogenesis of Ostertagia infection (5) and causes of these symptoms
Parietal cells are replaced by rapidly dividing, undifferentiated, non-acid secreting cells, initially just in parasitised glands, but then changes spread. Results in a thickened gastric mucosa. Lesion is a raised nodule with a visible central orifice.
Cattle PGE
Ostertagia ostertagi epidemiology summary and environmental risks
- Immunologically naive calves experience clinical disease and spread eggs on pasture
- Adults do not significantly contribute to spread of eggs and do not experience disease
- Dairy calves are highest risk group, autumn beet calves are lower risk, and spring beef calves are lowest risk
- Environmental risks: Short winter, or early summer increases risk. Highests risk of type 1 disease in autumn, lowest risk in spring
Cattle PGE
Epidemiology of Ostertagia ostertagi in dairy calves
Many L3s can survive winter on pasture, sometimes enough to cause type 1 disease in calves after spring turnout, but this is unusual and usually results in subclinical infection. Overwintered L3s have high mortality, so pastures are safe for grazing after mid summer
Eggs newly deposited in spring can develop rapidly in mid-summer, so reach infective stage by mid July. Sufficient number of ingested L3s cause Type 1 disease until October.
Cattle PGE
Epidemiology of Ostertagia ostertagi in spring beef calves
Unlikely to show disease as L3 mortality has occurred before they are turned out
Catle PGE
Epidemiology of Ostertagia ostertagi in autumn beef calves
Can result in disease after summer turn out, but being alongside immune adult cattle reduces this chance
Cattle PGE
Diagnosis ofOstertagia ostertagi (6)
- Clinical signs
- Season (July-September Type I, March-May Type II)
- Grazing history (Type I where calves are grazed on same field for several months, Type II where calves have grazed on a field from spring to mid-summer, then moved, then brought back in autumn
- Faecal egg count (Type I: >1000 eggs)
- Plasma pepsinogen levels (>3.0 IU tyrosine, vs normal 1.0)
- Postmortem examination
Cattle PGE
Treatment for Ostertagia ostertagi
Type I responds well to modern benzimidazoles, pro-benzimidazoles (febantel, netobimin, thiophanate), levamisole, or avermectins/milbemycins. These drugs are active against developing larvae and adult stages.
Type II requires drugs that are effective against arrested larvae as well as developing larvae and adult stages: modern benzimidazoles (albendazole, fenbendazole, oxfendazole) or avermectins/milbemycins
Infected field may be grazed by sheep/rested until following june
Cattle PGE
Controls for Ostertagia ostertagi Type I disease (5)
- Use clean pasture - not grazed by cattle in the previous year
- Delay turn out - after spring mortality of overwintered L3
- Dose ‘n’ move - anthelmintic treatment in early July, then moved immediately to a new pasture (although does not prevent against clinical ostertagiosis in Spring)
- Strategic treatment - Treatments after mid-July, Doramectin treatment before mid-July at 0 and 8 weeks of turnout
- Intraruminal Anthelmintic devices - minimise autoinfection, but are expensive
Sheep PGE
Summary of main causative agents of ovine PGE (3) - site of infection and important features
- Nematodirus battus: Small intestine. Has high mortality, causing watery diarrhoea. L3 hatch from eggs, and eggs survive up to 2 years on pasture. Infection in Spring
- Haemonchus contortus : Abomasum. Causes anaemia. Not viable in cold weather. Can arrest L4s. Single annual cycle. Infection in Summer
- Teladorsagia circumcinta: Abomasum. Causes low albumin, watery diarrhoea and an increased rumen pH. Can cause type 1 or 2 disease. Infection in Autumn
Sheep PGE
Lifecycle of Nematodirus
- Direct lifecycle
- Preparasitic phase unusual as L3 development occurs within the eggshell. Hatching requires a long period of chill, followed by mean temperature of >10°C (late spring)
Sheep PGE
Epidemiology of Nematodirus
- Eggs can survive up to 2 years on pasture
- Hatching requirements mean large numbers of L3s on pasture May-June, annual cycling of parasite (although clinical nematodirosis is not annual)
- Negligible role of ewes, so considered lamb-to-lamb disease
Sheep PGE
a) Pathophysiology of Nematodirus infection
b) Clinical signs
c) Diagnosis
a) Lambs infected during weaning. Disease caused by massive flush of L3s in Spring where there is a disruption of small intestine mucosa by L3s → severe villus atrohpy, acute inflammation, protein and water loss
b) Yellowy-green diarrhoea can occur during prepatent period. Animals are thirsty. High mortality in untreated animals
c) Faecal flotation egg identification. Larval culture. Faecal PCR. Post-mortem
Sheep PGE
Lifecycle of Haemonchus
- Eggs hatch to L1s on pasture, develop to L3s quickly in optimal conditions (warm)
- Once ingested, exsheathment in rumen, then larvae moult twice close to gastric glands
- Just before final moult they develop lancet that allows them to obtain blood from mucosal vessels
Sheep PGE
Epidemiology of Haemonchus
- Tropical and Subtropical climates: favourable environment → multiple cycles annually (outbreaks depend on local rainfall)
- Temperate climates: less favourable → single annual cycle (eggs deposited in spring, ingested by lambs in summer, arrested L4s in abomasum in winter, adults develop following spring)
Sheep PGE
Pathogenesis of Haemonchus infection
- Pathogenesis due to blood-sucking habit of the worms, high worm burden = high blood loss
- Different symptoms depending on type of case (hyperacute vs acute vs chronic)
- Hyperacute occurs with very high worm burden (up to 30,000 worms)
- Chronic occurs when there is neglibible reinfection, so small number of worms
Sheep PGE
Teladorsagia lifecycle
- Eggs in faeces develop to L3s within 2 weeks (optimal conditions)
- After ingestion, L3s exsheath, further development occurs in abomasal glands, then two further moults to be L5s (~18 days after infection) to be sexually mature on mucosal surface
Sheep PGE
Epidemiology of Teladorsagia
- Depends on clean vs contaminated pasture
- PPR in ewes is most important source of contamination
- In clean pasture, no overwintered L3s so only source of infection is resumed development of hypobiotic larvae → Type 1 disease in lambs from July
- In contaminated pasture also have overwintered L3s → Type 1 disease can be in May/June as well as from July
Sheep PGE
Pathogenesis of Teladorsagia
Sheep PGE
Groups of anthelmintics used against sheep PGE (3) and novel anthelmintics (2)
Group 1 - Benzimidazoles → Broad spectrum. Effective against arrested larvae in abomasum. Variable efficacy against Nematodirus immature stages. Resistance of Teladorsagia and Haemonchus
Group 2 - Imidothiazoles/tetrahydropyrimidines → Broad spectrum. Highly effective against adult and larvae Nematodirus. Effective against arrested larvae. Resistance of Teladorsagia
Group 3 - Macrocyclic lactones/milbemycins → Broad spectrum. Variable efficacy against Nematodirus. Resistance of Teladorsagia
Monepantel → effective against resistant populations, MUST USE SPARINGLY
Closantel → higly effective against Haemonchus
Lice
General life cycle of lice
Lice
How to differentiate between chewing and sucking lice
Lice
Cattle lice (5). Chewing or sucking? Life cycle span. Region affected
Lice
Sheep lice (3) and goat lice (2). Chewing or sucking? Life cycle span. Region affected
Lice
Horse lice (2). Chewing or sucking? Life cycle span. Region affected
Lice
Chicken lice (4). Chewing or sucking? Life cycle span. Region affected
Lice
Dog lice (3) and cat lice (1). Chewing or sucking? Life cycle span. Region affected
Lungworm
Dictyocaulus viviparus cattle lungworm lifecycle
- First stage larva are found in faeces
- Direct lifecycle
- L1 used for diagnosis
- After ingestion, L1-L3 migrate to mesenteric lymph node, before migrating to lungs
- PPP = 3-4 weeks
Lungworm
Dictyocaulus viviparus
a) Source of infection
b) Important information
a) Carrier animals that have hypobiotic larvae. New infected animals brought into herd. Fungal spores of Pilobolus (grows on cow pats) -> meaning when fungus releases spores, spreads Dictyocaulus
b) Very high biotic potential (produces many larvae). Larvae are susceptible to heat and drying. Infected animals can develop some immunity
Lungworm
Dictyocaulus viviparus
Epidemiology (dry weather vs warm and wet weather)
Dry weather: L3s remain in faeces and there is little spread via formites. Few eaten by calves, so low level infections, which can induce immunity. End of summer may show calf immunity.** Slow infection rate**
Warm and wet: Pilobus fungus helps spread L3s via spores. Sudden L3 exposure to naive calves. Immunity unlikely to prevent disease. Clinical disease
Epidemiology is very unpredictable, depends hugely on the environment
Lungworm
Pathogenesis of Dictyocaulus viviparus clinical signs (7)
- Salivation and anorexia
- Air hunger
- Coughing (especially with exercise)
- Increased respiratory rates
- Dyspnoea (irregular breathing), tachypnoea (fast breathing)
- Marked milk drop
- Smallest calves most severely affected
Lungworm
Pathogenesis of Dictyocaulus viviparus
a) Pre-patent phase
b) Patent phase
c) Post-patent phase
Lungworm
Dictyocaulus viviparus
a) Diagnosis
b) Pharmaceutical treatment
c) Vaccination
a) 1. Baermann apparatus 2. Endoscopy 3. ELISA (seroconversion takes 4-6 weeks, also some cross-reactivity with other nematodes) 4. Post-mortem
b) All drugs are effective (benzimidazoles, ivermectin, levamisole), but in severely affected animals, can worsen disease (as cause a sudden mass in the lungs of dead worms), may require antibiotics/fluid.
For calves that need to return to grazing after treatment - Ivermectin, doramectin or moxidectin. Parenteral (residual effect)
c) Live attenuated vaccine (Huskvac). Calves must be 8 weeks old, two doses 4 weeks apart. Immunity lasts 6 months (boosters required)
Lungworm
Dictyocaulus filaria lifecycle, pathogenesis, treatment
- Sheep lungworm
- Same pathogenesis, same lifecycle, same treatment as Dictyocaulus viviparus
- No vaccine available for sheep
- Only sporadic outbreaks
Lungworm
Angiostrongylus vasorum Canine French Heartworm lifecycle
- Not actually a lungworm, but grouped with them
- Indirect lifecycle
- Particularly prevalent in Europe
- Intermediate host are slugs and snails
Lungworm
Angiostrongylus vasorum Dog French Heartworm
a) Epidemiology
b) Pathogenesis (clinical signs) (7)
c) Pathology of infected hosts (4)
a) Widely distributed with endemic foci. Spread by consumption of infected snails/slugs
b) Very variable (depending on worm burden). 1. Swelling and haematomas 2. Mild exercise intolerence 3. Anaemia, ascites 4. Coughing, dyspnoea, respiratory distress 5. Bruising and bleeds (especially chest) due to reduced clotting due to parasite secreting anticoagulants 6. Reduced appetite 7. Death
c) 1. Chronic condition 2. Adult worms found in large vessels of lungs 3. Eggs and larvae found in arterioles and capillaries 4. Heavy worm burden can lead to congestive cardiac failure
Lungworm
Angiostrongylus vasorum Dog French Heartworm
a) Diagnosis (5)
b) Treatment
a) 1. Baermann apparatus (but only large numbers of worms are detected, must repeat 3 times) 2. Rapid antigen test 3. Post-mortem 4. Broncho-alveolar lavage 5. Radiography
b) Moxidectin (dose 4-weekly). Restrict access to snails
Lungworm
Oslerus osleri Dog lungworm
Lifecycle
- Direct lifecycle
Lungworms
Oslerus osleri Dog lungworm
a) Pathogenesis (4)
b) Clinical signs (4)
c) Diagnosis (4)
d) Treatment
a) 1. Fibrous nodules at the tracheal bifurcation 2. Pinkish-grey granulomas 3. Most nodules are small 4. Adults rarely found in lungs
b) 1. Often inapparent 2. Persistent cough, respiratory distress 3. Exercise intolerance 4. Loss of appetite in heavy burden infections
c) 1. Pharyngeal swab 2. Bronchoscopy 3. Radiography 4. Baermann apparatus (but low specificity)
d) Fenbendazole, Albendazole
Lungworm
Aelurostrongylus abstrusus Cat lungworm
Lifecycle
- Very rare in UK, but very prevalent in continental Europe
- Indirect lifecycle, using a paratenic host
- PPP is 7 weeks
Lungworm
Aelurostrongylus abstrusus Cat lungworm
a) Pathogenesis
b) Clinical signs
c) Diagnosis
d) Treatment
a) 1. Low pathogenicity 2. Infections discovered incidentally at post mortem 3. Small, grey foci or consolidated granulomas
b) 1. Very mild 2. Coughing following exercise 3. Nasal discharge, dyspnoea 4. Diarrhoea, weight loss (only with a very heavy worm burden)
c) 1. Broncho-alveolar lavage 2. Baermann apparatus (again, low sensitivity) 3. Radiography 4. Post mortem
d) Fenbendazole
Cestodes
Label anatomy of Cestodes
- Proglottids: immature are a simple shell (closest to neck). Mature have both male and female organs - self and cross fertilise. Gravid are full of eggs, no sexual organs, shed in faeces
- Different species of cestodes have different types of larvae
Cestodes
Echinococcus granulosus Dog tapeworm
a) Lifecycle
b) Type of larvae
a) Zoonotic
8 genotypes of E. granulosus, but only zoonotic in sheep genotype
Humans are terminal hosts
Indirect lifecycle
b) Hydatid cysts for larvae. Have 3 membranes: Outer pericycst (made by hosts). Middle laminated membrane. Inner germinal layer, containing many (>100,000) larvae. Germinal layer can give rise to new cysts within the same cyst
Cysts are huge, found in liver, lungs, heart etc
Cestodes
Taenia hydatigena Dog tapeworm
Lifecycle
- cysticerus oncospheres
Cestodes
Dipylidium caninum Dog Tapeworm
Lifecycle and treatment
- Intermediate hosts are fleas or lice (Trichodectes canis )
- Treatment - Praziquentel for adults, flea treatment important
Cestodes
Taenia solium (Pig Tapeworm)
Lifecycle
- Humans can act both as definitive and intermediate hosts, if acting as intermediate, can form cysts in human tissues
Cestodes
Taenia saginata (Cattle Tapeworm)
Lifecycle
- Humans are definitive host
Cestodes
Anoplocephala perfoliate (Equine tapeworm)
Lifecycle
- Oncospheres are irregularly shaped (used for diagnosis)
- Very common in UK
- High worm burden can be fatal as worm is often found in ileocaecal junction, causing ulceration and intussusception (telescoping of intestine) -> causing spasmodic colic
Cestodes
Moniezia spp (Sheep and goat tapeworm)
Lifecycle
- Indirect lifecycle
- Definitive hosts are sheep/goats, sometimes cattle
- Intermediate hosts are forage mites
Trematodes
Describe the life cycle of Fasciola hepatica in sheep
Trematodes
Describe the relationship between acute fasciolosis and Black disease
Black disease - infectious necrotic hepatitis caused by Clostridium novyi type B
Ticks
Describe the overall structure of the tick body
- Idiosoma is the main, single segmented body
- Gnathosoma: mouthparts (made of idiosoma, palps, hypostome and chelicerae)
Ticks
Describe a three host life cycle
- Eggs hatch into 6-legged larva
- Larva latches on to small mammal host
- Larva will engorge, drop off first host, then moult into an 8-legged nymph
- The nymph will quest, latch on to birds or slightly larger mammal, drop off and moult into 8-legged adult
- Adult then latches to large mammal reproductive host, females engorge, drop off, lay eggs
3-year life cycle, and only 2-3% of lifecycle is spent on a host, so control is very difficult
Ticks
Complete table of tick-borne pathogens of dogs and cats
Ticks
Complete table of livestock tick-borne pathogens
Myiasis
a) What is the primary agent of blowfly myiasis in sheep
b) Lifecycle stages of this fly
c) Important features of infection
d) Treatment of blowfly strike
a) Lucilia sericata
b) See image. Eggs require high humidity to hatch (rain or faecal soiled fleece)
c)
- larvae secrete proteolytic enzymes and can abrade the skin with mouth hooks at later stages
- Small numbers of larvae will do just superficial damage, lesions usually heal cleanly (single infestation)
- Multiple infestations can cause severe toxaemia, lethargy
- Most lowland flocks (warm) will have at least one case
- Highly seasonal, temperature and rainfall dependent
- Shearing will reduce susceptibility (double shearing very useful) and tail docking can reduce susceptibility
d)
- Most effective treatments are insect growth restrictors (IGRs)
- Pyrethroids are less effective, act more as a repellent
- Can use organophosphate dip, but used less as OP is reserved for sheep scab treatment
Protozoans
Describe the lifecycle of Eimeria species (6 stages)
- Direct lifecycle
- Main three phases - sporogony, merogony (schizogony) and gametogony
- Each ingested sporozoite penetrates epithelial cell, becoming a trophozoite
- Trophozoite divides to form schizont (each containing many merozoites). When schizont is mature, epithelial cell ruptures and merozoites invade neighbouring cells
- Merozoites give rise to male and female gametocytes (macrogametocytes = female -> single nucleus, microgametocytes = male -> divide to form many micorgametes). Gametocytes fuse forming an unsporulated oocyst
- Unsporulated ocysts passed in faeces
- Under suitable conditions, unsporulated oocyst nucleus divides and protoplasm forms four sporocysts, each containing two sporozoites (now a sporulated oocyst)
Protozoans
Difference between Eimeria-like sporulated oocysts and Isospora-like sporulated oocysts
- Eimeria-like: 4 sporocysts, 2 sporozoites
- Isopora-like: 2 sporocysts, 4 sporozoites
Protozoans
Lifecycle of Toxoplasma gondii - intestinal phase
- Occurs in definitive host (a felid - commonly house cat)
- Host infected by ingestion of 1. sporulated oocyst (direct transmission betwee cats) 2. infected animals (usually rodents) with bradyzoites or tachyzoites. Mature bradyzoite ingestion is most important
- Cyst wall digested in cat’s stomach, releasing bradyzoites in intestinal epithelium
- Bradyzoites initiate merogonous and gametogonous development, resulting in oocysts after 3-10 days (shed for 1-2 weeks
Protozoans
Diagnosis of T. gondii
a) Direct
b) Indirect
a) Detection of oocysts in faeces. Detection of tachyzoites in blood/secretions
b) Detection of antibody types
Arthropod-borne parasites
Describe Babesia life cycle
Vertebrate host:
- Stage of merogony (asexual reproduction)
- Tick bite releases sporozoites from salivary glands into mammalian host
- Sporozoites enter RBCs and multiply by binary fission to form merozoites
- These leave RBCs and invade other cells
- Asexual cycle continues indefinitely
Tick host:
- Stage of gametogony (sexual reproduction) and sporogony (asexual reproduction)
- When tick ingests gametocytes from infected RBCs these reproduce in the tick’s gut, forming kinetes which infect tick ovarian cells (eggs)
- The infected eggs become infected larvae -> infected nymph -> infected adult
- Parasite enters tick salivary glands and undergo sporogony, creating infective sporozoites
Arthropod-borne parasites
Leishmania - describe the life cycle
- indirect lifecycle
- female sandfly transfers promastigotes to human/dog during feeding
- promastigotes phagocytosed by macrophages, where they transform into amastigotes and multiply by simple division
- amastigotes leave macrophages to invade new cells
- female sandfly takes a blood meal and ingests amastigote-infected macrophages
- in midgut, amastigotes transform to promastigotes, which migrate to proboscis
Arthropod-borne parasites
Diofilaria immitis life cycle
Canine heartworm
Mosquito species that infect: Culex pipiens, Ades albopictus
