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101 Cards in this Set
- Front
- Back
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What are some predisposing factors for otitis externa?
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conformation
excess moisture treatments (irritating topical meds, ear swabs) systemic disease |
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What are some primary causes of otitis externa?
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Otodectes
Demodex foreign bodies hypersensitivity neoplasia seborrhea endocrine disorders |
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What are some perpetuating factors (can prevent resolution) of otitis externa?
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bacteria such as S. peudointermedius, Pseudomonas, Proteus, E. coli, Klebsiella
Malassezia yeast Stenosis, fibrosis, calcification otitis media |
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What diagnostic tests should be done for otitis externa?
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microscopy will pick up parasites
cytology for yeast/bacteria culture and sensitivity (if recurrent or won't resolve) radiography if middle ear involvement is suspected or surgery is considered MRI/CT if the middle or inner ear need to be examined |
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How does ear cleaning aid treatment of otitis externa?
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allows examination
removes debris allows medication to reach affected areas antimicrobial properties |
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When are systemic antimicrobials helpful in treatment of otitis externa?
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if otitis media is present or topical therapy isn't possible
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Why does treatment of bacteria in otitis externa not always cause resolution?
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infection usually secondary to something else, must resolve the primary issue to fix
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What does growth of staph or strep tell you from an ear swab?
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nothing really, since they are normal skin flora
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Is pseudomonas normal ear flora?
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no
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What normal household substance has good efficacy against pseudomonas?
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vinegar
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What type of otitis is generally seen in large animals?
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otitis media-interna
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What organisms are often associated with otitis in large animals?
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M. haemolytica, P. multocida, H. somni migrate up the auditory tubes to infect the middle ear
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What ages are affected by Rhodococcus equi?
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foals 3 weeks to weaning, mostly 3 weeks to 3 months of age
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Why are most foals with R. equi not treated until they are very sick?
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early signs are subtle, easily missed (low fever, decreased appetite)
foals learn to compensate for decreased function |
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What signs are seen later in R. equi disease?
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increased respiratory effort
nasal discharge cough |
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What pathological findings are present with R. equi?
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pneumonia with large pyogranulomatous lesions
may have extrapulmonary disorders |
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What are the most common extrapulmonary disorders associated with R. equi?
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diarrhea
synovitis ulcerative enterotyphlocolitis abdominal abscesses abdominal lymphadenitis also can see uveitis, bone lesions, hepatitis, meningitis, nephritis |
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How is R. equi diagnosed?
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gold standard is culture from tracheobronchial aspirate
also thoracic imaging and cytology from TBA |
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What three patterns of infection with R. equi are seen at breeding farms?
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unaffected farms (no problems)
sporadically infected farms endemic farms (recurrent problems) |
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What are the features of R. equi?
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gram positive pleomorphic
facultative intracellular within macrophages found in soil and feces |
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What bioforms of R. equi exist?
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avirulent (has no plasmids)
intermediately virulent (has a large plasmid, no disease in foals) virulent (large plasmid, causes disease in foals) |
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What is the significant virulence factor for R. equi?
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vapA gene makes the vapA protein
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Is presence of R. equi sufficient to cause infection?
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No, must have other factors
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What concentration of R. equi (airborne or soil) is associated with higher incidence of disease?
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airborne concentrations, although the relationship may not be causal
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Are poorly managed farms at higher risk for R. equi than others?
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no, actually the other way around
well managed farms see more disease than others! |
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What effect does pasture vs stall have on R. equi infection?
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disease rates seem higher with animals kept in stalls instead of pasture
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Does R. equi infect other species (including humans)?
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only if immunocompromised
AIDS patients, cats, and goats can get it |
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What immune cells are required to clear R. equi?
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CD4 T lymphocytes must secrete IFN gamma
*expression is low early in life and when immunocompromised which may be why infection is higher then |
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How are individual genetic factors related to R. equi infection?
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weak relationships, unknown if certain genes predispose to infection
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What disease is caused by Streptococcus equi ssp equi?
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Strangles in horses
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What are the features of S. equi?
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gram positive coccus
encapsulated if virulent strep M protein most important virulence factor |
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What is the significance of the strep M protein?
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blocks phagocytosis
used in diagnostic testing |
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How is S. equi transmitted?
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HIGHLY contagious!
via nasal discharge, either directly nose to nose or fomites such as buckets, tack, caretakers etc |
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How do subclinical carriers contribute to disease with S. equi?
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after recovery they can shed periodically via nasal discharge
organisms can live a long time in the gutteral pouch can sicken suceptible animals without showing signs themselves |
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what are chondroids?
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inspissated pus in the gutteral pouch that can harbor S. equi
can persist for years may require surgical removal |
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What is the pathogenesis of S. equi?
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attachment to tonsils
move into cells of epithelium and subepithelial follicles translocation to submandibular and suprapharyngeal LNs accumulation and resistance to phagocytosis, abscess formation |
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What is the disease course of S. equi?
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fever (103+)
increased blood fibrinogen, WBCs, neutrophils abscess development lymph accumulation in afferent lymphatics nasal shedding |
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When does shedding of S. equi begin, and what does this mean for transmission?
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4-14 days after infection until 3-7 weeks after resolution unless persistent carrier
Can usually isolate them before they begin shedding if monitoring for fever! |
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Do recovered horses gain immunity to S. equi?
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yes in 75% of cases
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What are the symptoms of S. equi infection?
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fever
mucopurulent discharge lymphadenopathy anorexia neck extension respiratory stridor (inspiratory noise) depression |
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How would you diagnose S. equi?
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culture of nasal swabs, washes, or pus
(washes more sensitive than swabs) *culture may be unsuccessful early on |
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What diagnostic test is available for the Strep M protein?
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PCR can detect SeM, the gene sequence encoding the protein
*does not determine live vs dead bacteria also an SeM ELISA, also does not tell if current infection |
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Are antibiotics indicated for S. equi infection?
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debatable, most cases only require supportive care
antibiotics may be useful if used very early on |
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When should you NOT use antibiotics with S. equi infection and why?
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when lymphadenopathy is detected, because it prevents maturation of the abscesses and prolongs the course of disease
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What are the complications of S. equi?
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sequelae due to metastatic disease, can go EVERYWHERE
myositis |
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How does the presence of metastatic disease affect recovery from S. equi?
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must have long term therapy, and the prognosis is poorer
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What immune mediated complications can occur with S. equi?
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purpura hemorrhagica thought to be caused by immune complex deposition in vessel walls
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What organism is the major cause of bovine footrot?
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Fusobacterium necrophorum
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What are the characteristics of F. necrophorum?
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gram negative pleomorphic rod
obligate anaerobe non-spore forming |
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What are the most important virulence factors for F. necrophorum?
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LPS endotoxin
leukotoxin |
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What is the natural environment of F. necrophorum?
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mucous membranes, GIT
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What is the pathogenesis of infection with F. necrophorum?
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disruption of normal skin
colonization of wound development of anaerobic conditions |
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What organism is the main cause of interdigital dermatitis in cattle?
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Dichelobacter nodosus
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What organisms contribute to digital dermatitis in cattle?
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F. necrophorum
Prevotella melaninogenica Spirochetes *exact causes unknown, but very contagious! |
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What is the primary treatment/prevention for foot infections in ruminants?
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footbaths!
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Is culture a good test for infections of the foot in ruminants?
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no, will get everything under the sun!
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What other diseases does F. necrophorum cause?
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calf diptheria
thrush of the foot in horses liver abscesses necrotic rhinitis, stomatitis of swine |
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What complications can occur with infections of the digit?
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ascending infection to the tendon sheath
hoof sloughing |
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How are EEE, WEE, VEE and WNV transmitted?
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mosquito
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what is the reservoir host for the encephalitides?
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birds
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What type of host is the horse for the encephalitides?
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dead end
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Are the encephalitides transmissible from horse to horse (or human)?
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no, dead end host so the virus can't complete the life cycle
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Which of the encephalitides can a mosquito get from biting an infected horse?
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VEE
*only one where the horse has a high enough viremia to reinfect the vector |
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Which encephalitis is considered zoonotic?
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VEE (because it can go back into mosquitoes from "dead end" hosts)
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Which protozoan causes myeloencephalitis in horses?
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Sarcocystis neurona
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What are the DH and IH for EPM?
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DH: possum
IH: skunk, racoon, armadillo, cat |
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How is EPM transmitted?
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horses ingest feed contaminated by possum droppings (fecal oral)
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List the encephalitides in order of highest to lowest mortality
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EEE (80-90%)
VEE (50-75%) WEE, WNV (20-50%) |
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What is the treatment for the encephalitides?
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supportive care
if EPM, can try coccidiostats |
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What is the likelihood of recovery from EPM?
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1/3 go back to normal, others get permanent deficit or die
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What other animals are at risk for encephalitides?
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crows, bluejays
farm-raised birds: emu, turkey, pheasant |
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How are the encephalitides prevented?
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vaccination
decrease vector prevalence avoidance (stay inside at dusk etc) |
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Is there a seasonality associated with transmission of the encephalitides?
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yes, highest August to November except in warm climates where mosquitoes are seen year round
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Is there a seasonality associated with EPM?
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some, seen most in the summer and fall but more correlated with the possum population
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What diagnostics can be used to identify infection by an encephalitis?
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CSF tap
virus isolation histopathology immunofluorescence *viremia very low except in brain, so the test may be negative despite having the disease! |
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What are the primary signs seen with infection by an encephalitis?
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CNS signs (ataxia, tremors, inability to stand, grinding teeth, weakness)
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What other differentials should be made with CNS signs?
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EPM, rabies, toxins, leukoencephalomalacia, EHV-1, WNV, EEE, WEE, VEE
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What bacterial organisms contribute to BRDC?
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M. haemolytica
P. multocida Bibersteinia trehalosi Histophilus somni A. pyogenes Mycoplasma |
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What is the normal habitat of M. haemolytica and P. multocida?
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commensal in the URT
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What viruses play a role in BRDC?
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BVD, BHV-1, BRSV, BCV
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What is the pathogenesis of BRDC?
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inhalation of commensals
lack of clearance by lung macrophages LPS and leukotoxin damage the lung tissue |
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What WBCs are associated with the most severe form of BRDC?
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neutrophils (don't get severe disease without them!)
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What alters bacterial clearance in the lungs with BRDC?
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temperature, acidosis, immunocompromise (FPT)
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What are the major factors in BRDC?
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bacteria
viruses stress depressed immune system |
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What are the clinical signs of BRDC?
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depression, anorexia, fever, increased respiratory rate, nasal and ocular discharge, cough, sudden death
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What diagnostics are used to ID BRDC?
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nasal swab or tracheal aspirate culture
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What are the other differentials when considering BRDC?
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Dictyocaulus
Acute bovine pulmonary edema and emphysema |
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How do you prevent BRDC?
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preconditioning (vaccines, weaning, castrating, dehorning)
good nutrition metaphylaxis (mass medication upon arrival at the feedlot) minimize stress |
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What are some sources of stress that contribute to BRDC?
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weaning
transportation (>100 miles) sale barns |
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What organism causes interdigital dermatitis in sheep, and how is that different from cattle?
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caused by F. necrophorum instead of Dichelobacter nodosus
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What organism causes ovine footrot and how is that different from cattle?
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caused by Dichelobacter nodosus, instead of Fusobacterium necrophorum as in cattle
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What causes strawberry footrot in sheep?
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Dermatophilus congolensis
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What are the important virulence factors associated with Ovine Footrot?
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LPS
fimbriae exotoxin (extracellular proteases) |
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How are virulent and benign forms of D. nodosus differentiated?
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virulent forms have more potent exotoxin that causes hoof sloughing
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What are the characteristics of Dermatophilus congolensis?
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gram positive pleomorphic rod/filamentous
aerobic makes motile zoospores that can cause spreading lesions commensal organism of foot |
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How is contagious ovine footrot transmitted?
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obligate foot pathogen, must be brought in via fomites or infected sheep
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How long does it take to see clinical signs of ovine footrot after infection?
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10-20 days
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How are ovine foot infections diagnosed?
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clinical signs
culture generally not helpful may use scabs/crusts for gram stain or culture to check for D. congolensis ("railroad track" appearance) |
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How are ovine foot infections prevented and treated?
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footbaths
disinfect new animals quarantine new animals pasture management clean vehicles, trailers |
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How does F. necrophorum act in ovine contagious footrot?
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sets up the environment for D. nodosus to proliferate
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What are some predisposing factors for bovine and ovine infectious foot diseases?
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moisture, trauma
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