Diarrhea
What is disease causal theory
Each factor that contributes to the development of disease is a component cause
A sufficient cause is a complete causal mechanism that produces disease
Component causes added together -> sufficient cause
Removal of a component cause -> disease does not develop
What are the treatments for crypto
Halfluginone - effectiveness questionable, must be given before onset of symptoms
Novo-azithromycin - macrolide, used in human medicine, reduces oocyst shedding
Tylosin - macrolide, reduces oocyst shedding
What is immunology
Animals develop immunity to the specific eimeria species
subsequent infections tend not to cause clinical disease
however, oocysts can still develop and be shed
level of immunity dependent on # of oocysts ingested in initial infection
Low levels may not generate substantial immune response
What is the diagnostic challenges with cociddiosis
Primarily based on clinical signs in group + necropsy findings in mortalities
Fecal float for oocysts - false positives (13 species but only 2 are highly pathogenic), false negatives (severe disease can be in early life stages without oocysts production)
Semi-quantitative counts in a group may be useful in assessing threat of infection
What is acute BVD - transient infection
Most infections are subclinical
Infections in immuno-competent animals are often unremarkable
May be transient diarrhea for a few days but often animal recovers and becomes immune
Neutralizing antibodies detected 10-14 days post infection
Virus can cause significant immunosuppression
Severity and manifestation of disease can vary depending on - immune status and virus type
Sometimes TI can be sever and look like mucosal disease - diagnostic testing important
What is the basic diarrhea pathogenesis
Diarrhea -> dehydration and lactic acidosis -> hypovolemic shock -> decreased profusion -> ischemic damage of multiple organs -> translocation of enteric bacteria -> septicemic shock -> death
What is coccidiosis
Widespread, ubiquitous parasite
Most ruminants are exposed
Almost all vertebrate species have species specific coccidia
many infections self limiting, mild or asymptomatic
significant economic losses to cattle
Site of initial invasion for most species -> small intestine
Rupture of enterocytes during replication - late shizogony and even more gamogony, can potentially have clinical signs prior to shedding large numbers of oocysts
Eimeria species that are more pathogenic - cause more severe damage to deeper submucosal layers -> e. bovis, invasion of lymphatic vessels and lymph nodes
How do you environmentally control cociddiosis
Avoid overcrowding
Maintain feed and water hygiene
Well drained calving/lambing areas
Exposure to sunlight and drying
Bedding
Clean quarters for dairy calves
Environmental management is key
What is the link with TI and immunosuppression with BVD
Even though most TI BVD infections are subclinical, many cause a transient immunosuppression
Persistently infected animals may have permanently impaired immune response
Lymphocyte populations are diminished reaching minimal numbers 5-10 days after infection
Also affects function of other WBCs
They are more susceptible to other diseases such as respiratory disease, mycoplasma
How do you minimize pathogen exposure
Preventing effective contacts -> decreasing the number of contacts that results in transmission
- physical separation: dilution, segregation, quarantine
- minimize dose load: prophylactic medicines, sanitation
- minimize contact time
What is the life cycle of coccidiosis
Oocysts in environment
Require 2-4 days to sporulate
Dependent on moisture, oxygen and temperature conditions
Sporulated oocysts can survive in environment for months under moderate conditions in moisture
Extreme dryness and sun exposure will limit survival
Length of cycle dependent on species and environmental conditions
What are the clinical signs of coccidiosis
Loss of blood, fluid, electrolytes, blood protein
most infected animals are subclinical
weight loss, decreased weight gains, high morbidity, low mortality, weakness, anorexia, anemia, dehydration
Diarrhea, dysentery is variable in appearance, anemia, transient fevers
What do you use for control vs treatment of coccidiosis
Prevention - ionophores, decoquinate
Prevention and reduction of shedding - toltrazuril
Treatment of coccidiosis label claims - sulfa drugs
Prevention and treatment - amprolium
How does BVD induce respiratory disease
BVDV - induces lymphopenia, Impairs pro-inflammatory cytokine production, facilitates spread of other respiratory pathogens, damages mucociliary apparatus, negatively impacts macrophage activity in the lung
Damage to the mucociliary apparatus
Results in increased susceptibility to secondary infections
What are crypto lesions
Villous atrophy in small intestine
Parasites embedded in the microvilli of absorptive enterocytes
Villi shortened, with crypt hyperplasia and mixed inflammatory cell infiltrate
What is the asexual phase of life cycle of coccidiosis (shizogony)
Time length of cycle dependent on species of eimeria and environmental conditions
Oocysts sporulate and are ingested by host
Digestive enzymes cause release of 8 infective sporozoites
Each sporozoite invades an enterocyte and starts asexual repro phase
Each shizogony cycle creates hundreds to thousands of merozoites which are formed in each host cell
After one cycle, merozoites leave the host cell and each of them move on to infect a new enterocyte
Most eimeria species undergo 2-3 asexual replication life cycles
severity of disease is directly related to the dose of infective oocysts that are ingested
Dose = severity
Replication of coccidia within host's intestinal cells and subsequent rupture
Light infections -> damage is repaired quickly
What is bovine viral diarrhea
A pestivirus with a wide variety of strains - positive strand RNA virus, BVD is found in most countries of the world
BVD virus are grouped into two genotypes - type 1 (16 subtypes), type 2 (3 subtypes)
Genetic variability is large
BVD viruses are further divided into two distinct biotypes based on their effects on tissue cell culture - non cytopathic virus (can induce persistent infections), cytopathic virus
How does BVD induce thrombocytopenia? Sypmtoms?
Not very common now
Clinical syndrome associated with type 2 viral infections
type 2 BVD virus infects blood cells and bone marrow
Some animals will survive with supportive therapy
Clinical symptoms - depression, fever, bruising, epistaxis, bleeding from injection sites/wounds, hemmorrhage in internal organs, hyphema, bloody diarrhea
What are rotavirus lesions
Virus blunts intestinal villi, villous epithelial cells are replaced with squamous/cuboidal epithelial cells
Malabsorptive diarrhea
Virus also makes an enterotoxin -> secretory diarrhea
Usually resolves in around 2 days in uncomplicated cases
What is the sexual phase of life cycle of coccidiosis (gamogony)
Within the enterocyte, the merozoites form either a microgamont or a macrogamont
Microgamonts are motile and are released to fertilize the female stages
Resulting zygote develops into oocysts
mature oocysts rupture host cell and released into lumen
What is nervous coccidiosis
Neurological symptoms have been associated with enteric coccidial infections
Usually seen in feedlot cattle > 6 months of age
minor muscular incoordination, twitching, loss of balance
intermittent seizures
Recover, rise, and resume normal behaviour
Eventually seizures become more frequent and death occurs
case fatality rate >75%
How is BVD transmitted
Two modes - Vertical (cow to calf in utero - infected calf becomes infected for life), Horizontal (between animals - direct contact, bodily secretions, contaminated fomites, virus able to persist in environment for two weeks, transient infection)
Both transiently infected and persistently infected can shed virus
PI animals are most important source of the virus
How does BVD induce repro/fetal infection
Pregnant, non-immune cow is infected with virus
Fetus also becomes infected
Almost all infections of fetus occur with non-cytopathic virus
Timing of infection will produce a variety of clinical syndrome - embryonic death and fetal resorption, abortion, congenital defects, birth of weak calves, persistently infected calves, normal calves
Cow clears virus, she becomes immune