Coccidiosis Flashcards
which coccidia species are we concerned about in cattle? how does the prevalence of coccidia species differ geographically?
- Eimeria zuernii & Eimeria bovis - cause severe clinical disease
- To a lesser extent, Eimeria alabamensis also can cause clinical disease
- Prevalence of the different species of coccidia can vary considerably between farms, regions, seasons and age groups
what age group is most susceptible to coccidiosis? how does infection occur?
- Coccidiosis is a common parasitic protozoan disease of cattle - particularly weaned calves
- Calves: 3 weeks to 6 months of age
- Infection occurs from contaminated pastures or lots by older cattle or other infected calves
- Mature cattle may become infected when place in crowded feedlots or barns
Life Cycle of Coccidia
- Bovine coccidia have stages within and outside host
- Microscopic eggs (oocysts) are passed out in the manure
- Oocyst develops within three to seven days and is now capable of infecting cattle
> Affected by temperature, moisture and oxygen - Oocyst contains eight bodies (sporozoites), each capable of invading an intestinal cell
<><> - Sporozoite enters a cell > changes into a meront and divides many times (up to 100,000 offspring called merozoites)
> The numbers produced depend on the species of coccidia involved - Each offspring, in turn, may enter another intestinal cell
> This cycle is repeated several times - Large numbers of intestinal cells are destroyed during the multiplication of parasite stages
<><> - Eventually, the cycle stops and sex cells (macro & microgametocytes) are produced
- Then they produce the next generation of oocysts, which rupture from the intestinal cell and are passed in the manure
- Thousands of oocysts, each containing eight sporozoites when mature, can be passed in the manure of an infected animal
coccidia pethogenesis
- Destruction of intestinal epithelial cells
- Second-generation schizonts/gamonts maturation
- Loss of large bowel epithelium
<><> - Exposes capillaries of lamina propria
- Rupture of capillaries
- Loss of red blood cells
- Loss of plasma
- Non-absorption of water, Na+, K+
coccidiosis patient profile for dairy
- Mainly young cattle (<1 year)
- Dairy calves:
– Young calves (3 weeks - 6 months)
– Older than 17-18 days
– Massive, rapid exposure
– Crowding
– Small, heavily contaminated yards
coccidiosis patient profile for beef
- Beef calves:
– 5-10 months old
– Yearling cattle
– Feedlots
– Stress: overcrowding, early weaning, diet changes, cold wet weather, poor sanitation
coccidiosis disease severity factors
- Number of oocysts eaten
- Species of coccidia present
- Age of the animal
- Animal immunity due to previous infection
Cattle Susceptibility
* Are they all equal?
- Coccidia occur in all breeds of cattle
- Calves may acquire infection as soon as they begin grazing or eating food other than milk
- Common in calves 3 weeks to 6 months of age
- May occur in yearlings & adults
coccidiosis seasonal incidence and where they are relevant
“Summer coccidiosis”
- High humidity, warm weather
- Ontario, Maritimes
- Young, highly susceptible calves
- Sporadic cases
- Unsanitary barns and pastures
- High mortality
<><>
“Winter coccidiosis”
* Calves 5-10 months old
* Feedlots, beef ranches
* Alberta, B.C., Manitoba, Sask, Quebec
* High incidence: January-March
- Stress, confinement
- Lower mortality
- Effects on weight gain
- Up to 25-50% of group affected
clinical signs of coccidiosis?
- Not specific to coccidiosis
- Common signs:
- Profuse diarrhea that may contain blood
- Dehydration, weight loss and death in severe cases
- Loss of appetite regardless of the Eimeria spp. involved
- Feed intake can be reduced as much as 60% during peak infection and can remain low subsequently
forms of coccidiosis?
- Enteric form
> Intestinal coccidiosis - Enteric + nervous form
> Nervous coccidiosis
enteric form of coccidiosis signs
Diarrhea/dysentery
* Watery feces to profuse diarrhea
* Frank blood 2-3 days after diarrhea (hematochezia)
* Mucus 2-3 days after diarrhea
<><>
* Tenesmus
> Rectal prolapse in some cattle
* Depression
* Weakness
* Rough hair coat
* Dehydration
<><>
* Anorexia
* Poor weight gain
* Anemia, pale mucous membranes
* Death in acute, severe cases
* Up to 3% mortality
nervous form of coccidiosis prevalence and timing? signs? mortality?
- Small % of cases affected
- Up to 20-30% in western Canada
- January to March
<><> - Muscle tremors
- Loss of balance
- Recumbency
- Convulsions
- Hyperexcitable
- Paddling
- Frothing at mouth
- Opisthotonus
- Nystagmus
- Strabismus
- Blindness
<><> - Up to 50% mortality
- Die on first day or live 3-5 days
clinical pathology of coccidiosis?
- Hemoconcentration - due to dehydration
- Anemia - due to large intestinal damage
- Hyponatremia/hypochloremia - due to lesions in cecum, proximal colon
- Hyperglycemia - due to convulsive episodes in nervous coccidiosis
diagnosis of bovine coccidiosis?
Combination of:
- Herd history
- Season
- Clinical signs
- Physical examination
- Microscopic examination of manure taken from the rectum
- Fecal flotation for oocysts: > 5,000 egg E. zuernii, E. bovis
<><>
* Diarrhea usually precedes heavy oocyst discharge by one or two days
> May continue after oocyst discharge has returned to low levels
necropsy findings for coccidiosis
Necropsy findings:
* Intestinal mucosal scrapings
* Oocysts/schizonts/merozoites
* No neurological lesions on histopathology
Treatment of Affected Animals for coccidiosis
- Several anticoccidial drugs available
- Outbreaks of coccidiosis in calves and feeder
cattle:
> mass medication added to feed or water
therapeutic plan for coccidiosis - what do we do based on disease progression and what should we keep in mind?
- May be self-limiting disease
- Spontaneous recovery
- Adults usually immune
- No clinical signs until life cycle of Eimeria almost complete
- Gut severely damaged by that stage
<><> - Drugs effective against merozoites and schizonts
- Prevent disease in animals at risk !!
- Fluids (parenteral/oral)
- Tranquilizers (nervous form)
drugs for coccidia
- Amprolium
- Sulfamethazine
- Benzene acetonitrile compounds
> Toltrazuril
> Diclazuril
how does amprolium work for coccidiosis?
- Thiamine antagonist
- Retards generation of 1st-generation schizonts in intestinal epithelium
- Dose: 10 mg/kg for 5 days
how does Sulfamethazine work for coccidiosis?
- Primarily act on the asexual stage
- Aids in permitting normal epitheliogenesis
- Dose: 140 mg/kg for 3 days
Benzene acetonitrile compounds
which are used for coccidiosis and how do they work?
- Metaphylaxis
<><>
Toltrazuril:
* Single dose 15 mg/kg
* Prevents clinical disease and oocyst excretion
Diclazuril:
* 1 mg/kg BW
* Similar results to toltrazuril
Prophylaxis for coccidia
- Amprolium
- Decoquinate
- Monensin
- Lasalocid
coccidiosis prevention
- Good management practices are important when establishing parasite control programs
- Prevent infection of susceptible animals in the herd
- Prevent drinking water and feed from becoming contaminated with manure
- Keep pens dry and supplied with ample dry bedding
- Use pastures that are well drained
- Raise watering troughs above the ground
- Keep grazing to a minimum on grasses
along the edges of ponds and streams - Prevent overgrazing
- Animals forced to graze down to the roots of plants may eat large numbers of parasites
- Heavily parasitized animals should be isolated from the rest of the herd and treated
client for coccidiosis?
- types of housing
-climate factors
- treatment
- Avoid overstocking
- Portable pens, hutches
- Rotate calf paddocks
<><>
Climatic factors - Oocysts very sensitive to sunlight, dryness
- Oocysts survive for months in moist conditions
- Unsporulated oocysts NOT harmed by freezing
<><> - Isolate & treat clinically affected cases
- Put herd on coccidiostatic medication in drinking water or feed
bluetongue virus family, genome, serotypes
- Family: Reoviridae
- Genus: Orbivirus
- Other virus in this genus: Palyam virus, epizootic hemorrhagic disease of deer, African horse sickness
<><> - Double-stranded RNA genome
- 10 segments contained within three concentric shells of structural proteins
- Subcore, outer core and outer capsid.
- Variation in the proteins that make up the outer capsid—VP2 and,
to a lesser extent, VP5—determine serotype
<><> - 30 serotypes worldwide
- 6 serotypes isolated in the U.S.
bluetongue history
- First described in South Africa
- Mediterranean outbreak, 1997-2002
bluetongue transmission and hosts? where are most severe clinical signs seen?
- Insect-borne viral disease
> Culicoides - Ruminants: cattle, sheep, deer, goats and camelids
- Primary host is sheep
> Severe clinical signs are most commonly seen in improved breeds of sheep
Animal Transmission of bluetongue
- Biting midges
> Genus Culicoides
> Principal vector (U.S.)
○ C. variipennis var. sonorensis - Ticks, sheep keds
- In utero
- Mechanical
- Venereal?
<><> - vecotor bites host > intrinsic intubation > vector bites host > extrinsic intubation …
> oral transmision
> transplacental
> persistent infection?
Map of the Estimated Global Range of Bluetongue Virus Prior to 1998.
tropics
Blue Tongue in Ontario / Canada?
- Found in a southwestern Ontario cattle herd
- first time the viral illness has been found outside British Columbia’s Okanagan Valley
- CFIA: In Canada, bluetongue is a reportable disease under the Health of Animals Act, and all cases must be reported to the Canadian Food Inspection Agency (CFIA).
- This excludes bluetongue types 2,10,11,13 and 17, which are listed as immediately notifiable in Canada.
what is a reportable disease vs immediately notifiable?
- Reportable disease: Reportable diseases are usually of significant importance to human or animal health or to the Canadian economy.
- Immediately notifiable: diseases are diseases exotic to Canada for which there are no control or eradication programs.
economic impact of bluetongue
- Trade restrictions
<><> - Cost to U.S.
- Greater impact on cattle industry
> Reservoir for virus - $125 million per year
> Lost trade and animal testing
bluetongue clinical manifestations
- The majority of infected animals: no clinical signs
○ The blue tongue after which the disease was named is seen only rarely and in more serious clinical cases.
<><> - Clinically manifest in 2 ways:
> Reproductive syndromes
> Systemic hemorrhagic viral fever that affects multiple organs but especially the upper gastrointestinal tract, skin, and lungs (blue tongue)
<><> - Cattle and goats rarely manifest clinical disease
Clinical Signs of bluetongue
- The majority of infected animals: no clinical signs
<><> - Clinically manifest in 2 ways:
> Reproductive syndromes
> Systemic hemorrhagic viral fever
<><> - Fever
- Depression
- Lameness
- Edema of the lips, tongue & head
- Conjunctivitis
- Coronitis
- Excessive salivation
- Nasal discharge, hyperaemia & pain at mucocutaneous junctions: i.e. gums & vulva
- Death
<><>
In pregnant animals: - Abortogenic and teratogenic
Following recovery: - Long-lasting secondary effects
- Reductions in milk yield
- Weight gain
- Severe wool break
- Temporary infertility
Morbidity/Mortality: bluetongue inSheep
Severity of disease varies:
○ Breed
○ Strain of virus
○ Environmental stress
- Morbidity
○ As high as 100%
- Mortality
○ Usually 0 to 30%
Morbidity/Mortality: bluetongue in cattle, goats
- Morbidity: up to 5%
- Death is rare
Morbidity/Mortality: bluetongue in deer, antelope
- Severe infection
- Morbidity
○ Up to 100% - Mortality
○ 80 to 90% - Lasting effects
Clinical Signs: Sheep bluetongue
- incubation, etc.
- Incubation period: 5 to 10 days
- Most asymptomatic
- Oral erosions & and ulcerations
-
Tongue
> Swollen, protruding
> Cyanotic
= “blue-tongue” - Reproductive failure
<><> - Coronitis
- Lameness
- Inflammation of
- Painful hooves coronary band
bluetongue clinical signs in cattle and goats
- Usually subclinical
- Erosions, crusts around nose & teats
- Coronitis
- Reproductive failure
bluetongue clinical signs in antelope and deer
- Hemorrhage, death
bluetongue post mortem lesions in sheep
- Face & ears edematous
- Dry, crusty exudate on nostrils
- Coronary bands hyperemic
- Internal hemorrhaging
- Hydranencephaly, cerebellar dysplasia
bluetongue post mortem lesions in cattle
- Skin: edematous, ulcerated, dry, thick folds
- Mouth: vesicles, ulcers, necrosis
DDx for bluetongue
- Foot-and-mouth disease
- Vesicular stomatitis
- Peste de petits ruminants
- Malignant catarrhal fever
- Bovine virus diarrhea
- Contagious pustular dermatitis
- Infectious bovine rhinotracheitis
- Parainfluenza-3 infection
- Sheep pox
- Foot rot
- Actinobacillosis
- Oestrus ovis infestation
- Plant photosensitization
diagnosis of bluetongue
- Clinical signs
- History
> Insect activity
> Wasting or foot rot - Laboratory
> Virus isolation
> ELISA, IFA, VN, CF
> PCR
bluetongue treatment
- No specific treatment
- Supportive therapy
> Protection from the elements
> Fluids and electrolytes
> Antibiotics may be needed - Control of vectors by insecticide
> Reduce transmission
> Protect susceptible animals
bluetongue in humans?
Can acquire the virus but…
* Not a significant threat to humans
* Precautions should be taken
* Disease in humans is not fatal
* Treatment is supportive care
control / prevention of bluetongue?
- Quarantine & movement controls * Prevent spread of virus
- Confine animals indoors (i.e., barn) * When vectors are active
Disinfection for bluetongue
- Cleaning the premises
> Sodium hypochlorite (bleach)
> 3% Sodium hydroxide (lye)
> But that does not stop virus transmission - Insect control
> Pyrethroids
> Organophosphates
vaccination for bluetongue? limitations?
Available
* Serotype specific
<><>
Adverse effects
* Fetal malformations
* Recombination
> New strains of virus
