Mamalian coccidiosis

Coccidial Protozoa whilst most important in the chicken, can actually affect an entire host range.

• Isospora/eimeria strains. 
• Cattle, sheep, pigs and rabbits.
• Isospora== 2 sporocysts with 4 sporozoites. PPP= longer than eimeria (7 days eimeria). Differentiate by ID cysts. 
• Pathogenic and non pathogenic species.
• Few treatments available.

Sheep:

• Disease in lambs (2-3 months). 
• 10 species.
• Caecum/colon.
• Diarrhoea, dehydration, abdominal pain & anorexia. 
• Diagnose= clinical signs + oocysts. 

Cattle:

• Below 1 year old.
• 20 species.
• Housed, older animals.
• Caecum/colon.
• Dystentery, diarrhoea, and dehydration.
• Sulphonamide treatment. 
• Diagnose by clinical signs/oocysts. 

Pigs:

• Young piglets.
• Isospora suis-> S.I. 
• High morbidity, low mortality. 
• Diagnosis difficult-PM.
• Sow prophylaxis.

Rabbits:

• E.Stiedae.
• Wasting, diarrhoea & jaundice. 
• Bile duct epithelia. Enlarged liver & white nodules
• Diagnose-> PM, oocysts in faeces. 
• Treatment/prophylaxis.

Horses:

• E.Leukarti. 
• Intermittent diarrhoea. 
• Difficult diagnosis. 

Dog 

• Isospora.
• Differential diagnosis.

Rain Scald

A short post today about this condition in horses. This condition is also called dermatophilosis. I also wondered what this meant in my pathology lectures and now I know it is the curious condition called rain scald in horses, which presents in this characteristic pattern. I'll also remember it because my boyfriend said his horse also suffered with it. 

Caused by dermatophilus congolensis. It is a very common and contagious disease. Affects areas commonly/ persistently soaked. More severe in Winter (more rain), resulting in matted hair, adherent crusts with a purulent base (sounds a nasty disease to me. 

The pain is usually only mild. To heal the horse needs to be in a dry environment, the matted hair and crusts need to be removed (apparently the horse really likes this bit), and treated with diluted chlorhexidine antimicrobial washes. Systemic antimicrobials administered in extreme cases. 

(I'm also running for the position of LUVS secretary.. here's to hoping I get it ). :) 

Bird Ectoparasites

Lice- pretty disgusting creatures. Eurgh. 

I struggle to remember bird parasites, rather like the worms. Hence I'm collating them all here. This may also be due to the fact they're not my main species of interest.. although I will have some chickens when I graduate (ex battery :D). 

Mites

Knemidocoptes

• K.Mutans-> feet and legs. Poultry. Causes extensive crusting. 
• K.Pilae-> budgies, parrots. Light feathered areas with a scaly face.
• K.Laevisgallinae-> poultry & pheasants. Known as 'depluming itch.' Can be treated topically.

 Dermanyssus Gallinae 

• Nocturnal-> hide in accommodation structure in daylight. 
• Bright red poultry mite. 
• Can survive for months in empty accommodation. 
• Rapid population build ups. 
• Pruritis, papules & crusts. 
• Acaricides-> treat the accommodation. Eradication difficult. Not normally seen on the bird. 

Ornithonyssus Sylvarium

• Permanent blood sucking mite found on the bird themselves. 

Ticks

Argas Reflexus

• Pigeon tick.
• Heavy infestations may be fatal. 
• Soft tick. 
• Can cause severe allergies in humans. 

Lice

• Lipeurus Caponis (wings, tail).
• Menacnthus Stramineus (body).
• Menopongallinae (shaft). 
• Feeds on feathers. 
• Irritant, decreased body weight and egg production.
• Autumn/winter.
• Control-> OP/carbamate dusts. 

Hookworms

Ancylostoma- imported worm.

Uncinaria Stenocephala 

• Direct life cycle.
• Eggs in faeces.
• L1-L3 with warmth and moisture.
• Small intestine.

Life Cycle

• L3 infective.
• Ingestion with/without migration. 
• Subcutaneous infection.
• Migration-> penetrate buccal mucosa and travel via the lungs and blood to the small intestine.
• PPP= 15 days. 

Pathogenesis

• Anaemia, weight loss and diarrhoea. 
• Kenneled dog. 
• Pedal dermatitis due to repeated L3 exposure. 

Treatment 

• BZ treatment. 
• Dry conditions and treat runs. 

Ancylostoma

• Dogs & foxes. Imported dogs.
• L3 ingested with/without migration.
• Skin penetration. 
• L3 in milk reservoir of infection in the bitch (dormant L3).
• Severe puppy anaemia. 
• Hypobiosis in the bitch tissues. 

Bunostomum

• B.Phlebotomum cattle (also sheep).
• Percutaneous/oral inf.
• Oral not followed by pulmonary migration.
• PPP= 1-2 months.
• Light infection and anaemia >300 worms.

Strongyloides

Ruminants, pigs, horses and dogs.

Transmammary in the young animal.

Free living/parasitic stags.

• Build up in warm, dark and moist environments.
• Percutaneous infection.
• Female only= parasitic.
• L1/larvated eggs in faeces. L3 infective.
• 15 day PPP. 

Switch= adverse environment. Alternate switch= host immunity or overcrowding. 

Cause diahorrea and weight loss. 

Treat-> BZ. 

Ascarids

Found in the small intestine. Females lay large numbers of resistant eggs. L2 develop inside the egg, larvae in egg infective stage. Direct life cycles. 

• Hepatotracheal migration which causes a profound inflammatory response. The adults browse on intestinal contents resulting in mechanical blockage due to size. 
• No Mucosal Damage. 
• Susceptible to all anthelmintics. 

Ascaris Suum- see pigs. 

Poultry Ascarids- see poultry. 

Horse Ascarids- see horses (parascaris equorum). 

Toxocara Canis

Life Cycle

• Development outside the host takes 2 weeks. 
• PPP= 4-5 weeks or 3 weeks if prenatal inf. 

Infection Routes 

• Puppy ingests eggs directly. Hepato-tracheal migration. 
• If the puppy is above 5/6 weeks old the L2 larvae migrate to the muscles where they remain arrested and viable. By 6 months of age, all larvae ingested do this. 
• If an adult female is infected, at 42 days gestation the L2 react and leave the muscles crossing the placenta to affect the fetus. L2-L3 in foetal lung and then matures in the gut. PPP= three weeks. 
• Transmammary transmission. 
• Paratenic host-> L2 ingestion by dog.

Disease

• Diagnose by age, clinical signs, eggs, or adult worms may be passed or vomited.
• Heavy puppy worm burden-> pot belly, poor weight gain & intestinal obstruction. 
• No diarrhoea. 
• Human toxicariosis can cause unilateral blindness.

Treatment 

• Decrease zoonotic risk by decreasing environment contamination with eggs.
• Dose older dogs annually and bitch post whelping.
• Programme to prevent transplacental transmission (fenbend) costly.
• Worm puppy 2, 4, 6 weeks of age, and then 3, 6 months and then annually. 

Toxocara Cati

• Ingestion of L2 & migration. 
• Ingestion of paratenic host/transmammary= NO migration.
• No transplacental transmission. 

Toxoascaris Leonina

• Cats and dogs.
• Mixed infection and no migration.
• Eggs in faeces.
• L2= 3-4 week development.
• Infection via L2 in the egg or L3 in mice.
• No prenatal inf. 
• 10 week PPP (8 week if paratenic host).

T.Vitulorum 

• Cattle and buffalo.
• Tropics.
• Increasing UK reports.
• Transmammary inf.
• Poor thrift & weight loss.

Horse Parasites

There are a whole variety of horse parasites. The main ones will be talked about here.

Parascaris Equorum

• Horses & donkeys.
• Lifecycle= A.Suum. 
• 12 week PPP.
• Small Intestine. 

Disease

• Foal to foal as adults immune.
• Transient cough, poor weight gain, unthriftiness. 

Control

• Resistance to Ivermectin. 
• Pasture rotation but eggs resistant & short lived. 
• Diagnosis-> 1000/epg significant faecal egg count. 

Oxyuris Equi (NOT an ascarid- oxyuroidea family)

• ' Pinworm.' 
• Affects horses and ponies.
• Colon, caecum & rectum. 

Life Cycle 

• Direct.
• Female lays eggs on peri-anal skin and dies.
• Eggs drop to the ground.
• Develop to L3 in egg.
• Ingested.
• Larvae develop in colonal mucosal crypts. 
• 5 month PPP. 

Clinical Signs

• Anal Rust. Pruritis. 
• L4 feed on & erode colonal mucosa-> principal harm. 

Diagnosis

• Selotape test.
• Female-> rubbing, broken hair & sore patches.
• Horse may be unmanageable.
• Eggs in faeces rare. 

Control

• Anthelmintics.
• Little immunity to re-infection.
• Wash peri-anal area daily. 
• Anthelmintics not very effective. 

Trichinellosis & Other Worms

Actually a picture of the Pinworm of the horse- oxyuris equi.

Trichuris

• Whipworm found in the colon.
• Characteristic eggs are highly resistant. 
• Common. 
• Resistant to many anthelmintics.
• Egg containing L1= infective stage.
• Doesn't cause a problem.

Capillaria- see bird parasites.

Trichinella

• Wide range of hosts- carnivores.
• Zoonotic.
• Humans, pigs and horses.
• Wildlife reservoirs.
• No eggs or larvae in faeces and no free living stages. 

Life Cycle 

• Adults in the small intestine.
• Small & short lived.
• Females larviparous.
• L1 pass through the wall of the small intestine & encyst in muscles.
• Transmission occurs when muscle cysts are eaten. 
• L1 released, adults mature, reproduce and die. 

No disease in domestic animals, but serious disease in humans. Fever, oedema, muscle pains, peri-orbital oedema & myocarditis. 

11 million cases worldwide affected by eating undercooked contaminated meat. 

Control

• Meat inspection- automated muscle digestion systems.
• Cooking & freezing.
• Important reservoirs in wildlife. 

Dictyocaulus Viviparus

Causes parasitic bronchitis 'husk' in cattle. Common in the wetter west UK. 

• Trichostrongyle superfamily (not metastrongyle like the other lungworms).
• D.viviparus-> cattle. D.filaria-> sheep. D.arnifieldi-> horse respiratory disease. Patent donkey infection (carriers).
• Trachea & bronchi. 

Life Cycle

• Direct life cycle. Female ovoviviparus-> gives birth to larvated eggs which hatch immediately.
• L1 in lungs, coughed up, swallowed and pass out in the faces.
• Lympho-tracheal migration. 

L3 infective stage. L1-L3 stages all ensheathed to protect them from adverse weather conditions. Takes 5-7 days to develop. 

ppp= 25 days (slightly longer than nematodirus, PGE and ostertagia). 

1. Penetration Phase

• 0-7 days.
• Lymph-tracheal migration (mesenteric lymph nodes). Moults to L4 in the lymph node. L4 in the lung.

2. Pre-patent phase. 

• 8-25 days. 
• L4-L5 in lungs. L5 migrate UP the bronchial tree so the adults reside in the bronchi and trachea. 

Clinical Signs 

• Intense inflammatory response-> bronchitis & bronchiolitis. 
• Interstitial emphysema. 
• Pulmonary oedema-> coughing. 
• Respiratory distess & tachypnoea.
• Weight loss. 

3. Patent Phase

• 26-55 days.
• Adult worms in upper respiratory tract. Eggs and L1 in alveoli. 

Clinical Signs

• Intense inflammatory response.
• Frothy white mucus.
• Emphysema & hypoxia.
• Gasping & coughing.
• Possible death. 

4. Post-patent phase

• 55+ days.
• Immune expulsion of adults and protective immunity.

Clinical Signs

• Some animals epitheliation of the lung tissue & never completely recover. 

Epidemiology

• Unpredictable.

Factors affecting the pre-parasitic stages:

1. Temperature.
2. Moisture.
3. L3 dispersal by Pilobolus Fungi.

L3 overwinter. L1 are also shed by carrier animals.

Disease= AUGUST-> SEPTEMBER. Same as ostertagia etc. 

• Dairy replacement calves.
• First cycle= few L3 so no disease.
• L1 shed->L3.

Only 1000 worms are needed to cause clinical disease. Disease is from turn out to november. Immunity is short lived and needs continual boosting. 

Diagnosis

• Antibody detection ELISA.
• Treat-> anthelmintics, NSAIDS for inflammatory reaction & antibiotics to protect against secondary infection.
• House most severely affected calves.

Control

• No intermediate host.
• No immunity- adult cattle naive and at risk. 
• More break outs in adult cattle than calves.

Vaccines

• Huskvac.
• 1000 live attenuated irridated L3 given orally. 
• Give before turnout.
• Needs natural immunity boosting.

Lungworms

Lungworms are common in species, especially dogs and cattle. Angiostrongylus Vasorum is one of the growing concerns in the canine world. 

M.Apri- see pig section.
D.Viviparus- see own section. 

Meullerius Capillaris

• Common.
• Non pathogenic in sheep, but pathogenic in goats.
• Hair like adults in the lung parenchyma.
• Eosinophilic grey green nodules.

Intermediate host-> slug/snail.

Need to distinguish from D.Filaria by the fact that it has no anterior cuticular knob or food granules and has a kink and spike on the end of the tail. 

Oslerus Osleri

The only lungworm to have a direct life cycle.

• Found in tracheal nodules.
• Bitch-> pup passed via L1 in the bitch sputum the infective stage.

Clinical Signs

• Tracheo-bronchitis. 
• Cough.
• Young dogs below 18 months old.
• 10-18 month PPP (unlike 4 week ppp of m.apri). 

Identify

• Low sensitivity to faecal larvae.
• Can use bronchoscopy to identify the nodules. 

L1 moults to the L2 in the small intestine, migrates via the lymphatics and the vascular system to the lungs. 

Crenosoma Vulpis 

• Another dog parasite.
• Fox reservoir host.
• L1- L3 in snails. 
• Show seasonality.

Found in the mucus of the trachea, bronchi and bronchioles. 

Aleurostrongylus Abstrusus

• Cat parasite.
• Adults in the lung parenchuma.
• L1 in the faeces.
• Snail intermediate host and bird/rodent paratenic host (no development). 

Generally asymptomatic but may cause a cough/respiratory disease.

Treatment= Fenbendazole similar to m.apri. 

Angiostrongylus Vasorum 

• Highly pathogenic.
• Found in the pulmonary artery & right atrium.
• Intermediate host= slug/snail. 
• L1 is released from the adult female-> pulmonary capillaries-> alveoli & trachea-> coughed up, swallowed and pass out as L1 in the faeces.
• Can be diagnosed via the baermann apparatus. 
• Take repeat samples.
• L1-L3 in the snail. Slug ingested by the dog. Migrates lymphotracheal to the heart and pulmonary arteries.
• PPP= 5-8 weeks.

Clinical Signs-> 

• Respiratory signs.
• Coagulopathies (blockage of blood vessels). 
• Neurological signs.
• Dysnpnoea. 
• Weight loss.
• Flunctuating haematoma.
• Bleeding disorders. 

Diagnosis-> 

• Often asymptomatic.
• Sudden death.
• Clinical signs and radiography.
• Enlarged heart and pulmonary artery.
• Patchy alveolar and interstitial pattern.
• L1- resp tract. Repeat samples.

Infection foci- south west extending. Fox reservoir hosts and dog movement.

• Milbemycin Oxime
• Moxidectin.
• Febendazole. 
• Corticosteroids/cage rest. 

Pig Parasites

I promised you I'd make one like I did with the bird one :D. Right Pigs..

Metastrongylus Apri

• Lungworm, so lymphotracheal migration. 
• L1 in the faeces. 

These are little small white worms which exist in the small bronchi and bronchioles. 

They are not very pathogenic. They cause:

• Decreased weight.
• May exacerbate other respiratory pathogens. 

1. L1 ingested by the earthworm. Earthworm is the INTERMEDIATE HOST.
2. L1-L3 inside the earthworm.
3. The L3 is the infective stage.
4. 4 week PPP. 

Control

• Outdoor pig problem- since worms live outside in the soil most of the time. Found in pigs between 4-6 months old.
• Control via fenbendazole in feed. 

Can diagnose via Mg2SO4 flotation solution but this worm is normally present in pigs with no clinical signs. Control is hard due to the earthworm intermediate host- housed, douse pigs and infected pasture cultivated or grazed with other stock. 

• Trichinella- see trichinellosis lecture. 

Ascaris Suum 

• Prolific egg layers. Egg takes 3-4 weeks to develop to the egg L2. 
• Eggs are resistant to disinfectants so remain viable in the environment for years. 

Life Cycle

• L2 hatches in the intestine.
• Migrates to the liver where it moults to the L3 stage.
• Migrates to the lungs-> alveoli-> S.I.
• Develops to the adult in the small intestine.
• PPP= 7 weeks.

Paratenic horse= worms & beetles. 

Disease

• Hypersensitivity response to the migrating larvae resulting in fibrous liver milk spots and transient pneumonia.
• Adults cause poor weight gain and mechanical blockage. 
• Economical losses-> poor weight gain and liver condemnations. 
• Affects young pigs.
• Clinical disease uncommon.

Diagnosis

• Typical faecal eggs.
• MgSO4 flotation solution.
• Abattoir reports & clinical signs. 

Control

• Immunity is rapid. 
• Highly resistant eggs-> steam clean indoor pens as sows contaminated the environment. 
• Problem in outdoor pigs. BZ in feed.
• Routine dose before farrowing of weaned pigs and sows.