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170 Cards in this Set
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Most common cause of severe pneumonia in foals > 2-3 weeks to 3 months of age
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Rhodococcus equi
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Incidence of clinical signs at affected farms with Rhodococcus equi
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5-15%
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Case fatality rates of foals with Rhodococcus equi
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typically 10-30%
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CS of Rhodococcus equi
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* Pneumonia
* Extrapulmonary disorders * Diarrhea * “Immune-mediated” synovitis * Ulcerative enterotyphlocolitis * Intra-abdominal abscessation * Intra-abdominal lymphadenitis * Septic synovitis * Vertebral body osteomyelitis (and paravertebral abscessation) * Uveitis - poor prognosis |
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CS of foals with pneumonia caused by Rhodococcus equi
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* Low grade fever
* Mild increase in RR * Insidious progression * Decreased appetite * Labored breathing * Mild coughing * Bilateral nasal discharge |
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Where are avirulent isolates of Rhodococcus equi found? Do they cause problems in foals?
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found in feces and soil, do NOT cause disease in foals
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What do the virulent isolates of Rhodococcus equi posses that makes them virulent?
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• Posses 85-90 kb plasmid encoding for vapA (virulence associated protein A)
• vapA is necessary to cause disease in foals, is in essentially all isolates from foals with pneumonia |
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What would be the best thing to culture in a foal with pneumonia suspected from Rhodococcus equi?
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Culture from a tracheobronchial aspirate from a foal w/CS of pneumonia
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What diagnostic testing should be done in foals with suspected Rhodococcus equi?
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1. Culture
2. Cytology 3. Thoracic radiographs 4. PCR of Tracheobronchial aspirate 5. Fecal Testing |
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What would you expect to see on a cytology from a foal with Rhodococcus equi?
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gram + pleomorphic rods and septic inflammation
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What are the disadvantages of getting a culture from a tracheobronchial aspirate from a foal with clinical signs of pneumonia?
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* Requires time for growth
* Invasive * Can be life threatening if foal has severe respiratory compromise |
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What can a culture from a tracheobronchial aspirate from a foal w/CS of pneumonia tell you about Rhodococcus equi?
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Identifies genus and species but not virulence status
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What has a high sensitivity for detecting virulent Rhodococcus equi in TBA fluid?
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PCR of Tracheobronchial aspirate
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What is the disadvantages of doing a PCR of Tracheobronchial aspirate for R. equi?
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Doesn’t allow antimicrobial susceptibility testing, isolation of concurrent pathogens, or genotyping
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Why are nasal or nasopharyngeal swabs not good for diagnosing R. equi in foals?
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NO VALUE because unaffected foals can excrete virulent R. equi in breath
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Why is Serology (ELISA, AGID) not a good diagnostic tool for foals with suspected R. equi?
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* Evidence shows they are not useful
* Likely to be a marker of exposure – maternal antibodies, etc |
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What are the predisposing factors for foals with R.equi?
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* Need more than just virulent R. equi to have disease
* Think aqbout the Infectious disease triad: Agent, Environment, Host |
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What is being done to detect R. equi in foals?
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Screening with ultrasound – can detect milder, earlier disease in lungs
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Most feline corona viruses (FCOVs) are pathogenic or non-pathogenic?
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non-pathogenic
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FCOVs have an affinity for what?
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intestinal epithelial cells
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2 thoughts on how pathogenic FCOVs result?
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1. Pathogenic FCOVs result from a mutation offeline enteric coronaviruses (FECVs) in the intestinal tract, allowing them to infect macrophages and cause systemic disease. Mutations to pathogenic FCOVs result from chronic stress in the infected cat, which increases the rate of replication of virus and with it the chance of mutations.
2. Another theory is that FIP is just the result of a high load of FCOVs rather than any mutations in the virus. |
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Effusive FIP is the result of what?
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the result of an inappropriate strong humoral immune response leading to antibody mediated inflammation and inadequate cell mediated response.
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2 types of FIP
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Effusive FIP (more severe form) and Non-Effusive FIP
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What causes effusion of fluid in cats with FIP?
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* Vasculitis leads to leakage of protein rich “urine like” fluid, which can be present in many body cavities, most often noted in the abdomen.
* The non-effusive form has a less severe vasculitis which causes pyogranulomas in many organs: kidneys, meninges, and brain, others. |
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Predisposing factors of FIP
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* Stress or total load of virus
* FIP (Systemic disease) is more likely to occur if the cat develops a strong humoral response. Cell mediated response can prevent systemic disease. * Young cats (6 months to 3 years) are more likely to get disease, especially if exposed to chronic carrier’s feces. |
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3 CS of cats with either form of FIP
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* Fever
* Weight loss * Lymphadenopathy |
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CS of cats with effusive form of FIP
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* Tissue damage
* Antibiotic resistant fever, dyspnea * Icterus * Abdominal masses * Ascites * Muffled heart sounds * Scrotal enlargement |
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What is the life expectancy of cats with the effusive form of FIP?
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Most patients die within a few weeks.
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CS of cats with the non-effusive form of FIP?
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* Less obvious CS
* Chronic disease with perivascular pyogranulomas * Ocular lesions (iritis, keratic precipitates, hypopyon; retinal perivascular cuffing, hemorrhages, detachments) * Neuro signs occur in 25-33% - depression, ataxia, tremors, seizures, paresis, hydrocephalus |
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What is the life expectancy of a cat with the non-effusive form of FIP?
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Fatal in weeks to months.
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Do any cats survive an FIP infection?
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FIP is uniformly fatal. No animals have ever been reported to survive
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What causes the tissue damage in the effusive form of FIP?
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Due to perivascular inflammatory response caused by antigen-antibody complexes
“Immune-mediated” coronaviral vasculitis |
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What is the best diagnostic tool for FIP?
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* Tissue biopsy or necropsy
• Histopath plus immunohistochemical ID of FCOV antigen in pyogranulomas |
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Why should serology testing not be used for diagnosing FIP?
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Can’t distinguish between pathogenic and non-pathogenic, current infection and past exposure
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What would you expect to see on a CBC of a cat with FIP?
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* Lymphopenia
* Neutrophilia + left shift * +/- non regenerative anemia |
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What would you expect to see on a chem panel of a cat with FIP?
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* Hyperglobulinemia
* Polyclonal gammopathy * Other findings based on affected organs: hyperbilirubinemia (liver) or azotemia (kidney) |
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What would you expect to find on a fluid analysis from a cat with FIP?
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• A cloudy, straw colored fluid
* High protein content * Non-septic exudate/modified transudate * Sterile * Increased globulin from exaggerated immune response |
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Albumin: Globulin ratio in an effusion fluid analysis: what excludes FIP? What is diagnostic for FIP?
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* >0.8 excludes FIP
* <0.45 with protein >3.5 g/dL + non-degenerative neutrophils, macrophages, some plasma cells and lymphocytes plus protein precipitates is diagnostic for FIP |
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Rivalta test for FIP
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o A drop of effusion fluid + water and 98% acetic acid. If fluid congeals at top of test tube then suspicion for FIP is higher.
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How is immunofluorescence used to analyze effusion fluid from a suspected FIP cat?
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Detection of coronavirus in macrophages in fluid by immunofluorescence
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Diagnosing FIP is done by excluding other diseases
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Use signalment, background, history, ocular/neuro findings, presence of antibiotic resistant fever
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Treatment for FIP
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Supportive only
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Prevention of FIP
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**GOOD HUSBANDRY is key**
* Minimize early FCOV infections in kittens * Reduce fecal exposure * Early weaning, isolation of kittens, reducing stress and overcrowding, enhance health care and nutrition |
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Why is there not outbreaks of FIP?
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Because animals with systemic disease still only shed enteric form - FECVs in their feces.
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Transmission of FeLV
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* Adolescent/young adult cats exposed to chronically or persistently viremic cats shedding virus in saliva.
* Neonatal transmission through milk and blood transfusions or vertical transmission from viremic queens. |
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Life expectancy of a cat with FeLV
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Infection is fatal, almost all asymptomatic cats are dead within 3 years of detection
* Symptomatic cats die sooner. |
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Transmission of FIV
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Transmitted through inoculation of infected saliva into bite wounds or through blood transfusions. Vertical transmission is unlikely.
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Life expectancy for a cat with FIV
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Persistently infected cats live for many years with good preventive healthcare, as immune function declines they are predisposed to terminal illness.
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What occurs during stage 1 of FeLV? How long does it last?
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(1-4days)
* Virus replicates in LNs near site of exposure |
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What occurs during stage 2 of FeLV? How long does it last?
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(2-14 days)
* Small numbers of infected circulating B-cells and plasma cells. * Weak + ELISA, - IFA |
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What occurs during stage 3 of FeLV? How long does it last?
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(3-21 days)
* Virus replication is amplified in spleen, LNs, GALT, crypt epithelial cells, and bone marrow precursor cells. * More + ELISA, +/- IFA. |
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What occurs during stage 4 of FeLV? How long does it last?
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(14-28 days)
* Infected neutrophils and platelets in circulation. * + ELISA, + IFA |
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What occurs during stage 5 of FeLV? How long does it last?
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(28-56 days)
* Widespread epithelial cell infection. Virus shed in large quantities in saliva and other secretions. * + ELISA, + IFA |
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Possible Outcomes of FeLV Infection
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* Clearance in adult cats
* Persistent viremia and early death in kittens and young cats * Sequestered infection in bone marrow/epithelial cells, inactive latent infections (most common outcome) |
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3 Phases of FIV
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1. Acute Phase
2. Chronic Phase 3. Terminal Phase |
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What occurs during the acute phase of FIV?
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* Rapidly increasing viremia for 6-8 wks, then virus load declines.
* CD4+ cell numbers decline when viremia peaks. * Initial lymphopenia, robust anti-FIV antibody production, may be asymptomatic or show subtle signs of illness (fever, depression, peripheral lymphadenopathy) |
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What occurs during the chronic phase of FIV?
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* Lasts several years, usually asymptomatic.
* Progressive decrease in CD4+ cell counts and cell-mediated immunity. * Abnormalities in cytokine production. |
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What occurs during the terminal phase of FIV?
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* Overt signs of illness due to opportunistic infections or neoplasia resulting from profound immunosuppression.
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What is the disease of friendly cats?
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*FeLV*
Young cats in multiple cat environment |
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Prevalence of FeLV in household cats.
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Prevalence is 1% or less in household cats.
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Predisposing factors of FeLV
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Overcrowding of young cats
* Age related immunity – cats older than 1 year won’t get a new infection. |
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What is the disease of feral cats?
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* FIV*
often intact males |
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Presdisposing factors of FIV
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cats living outdoors, especially intact adult males who fight.
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Clinical signs of FeLV
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* May be asymptomatic
* +/- fever * Diarrhea * Leukopenia * Marked lymphadenopathy at stage 3 * Weight loss * Chronic infections * Hematopoietic dyscrasias * Neoplastic Disease * Bone marrow dyscrasias * Secondary infections |
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Clinical signs of FIV
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* Weight loss
* Anemia * Lymphadenopathy * Persistent/opportunitstic infections * Neurological changes * Neoplastic diseases * Chronic ulceronecrotic gingivostomatitis * Chronic infections |
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best screening test for FeLV?
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ELISA
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What is detected in ELISA and IFA tests for FeLV?
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p27 antigen
* ELISA = detects p27 in blood * Immunofluorescent antibody test (IFA) = detects p27 in neutrophils and platelets |
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What does a positive Immunofluorescent antibody test (IFA) indicate with regards to FeLV?
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Indicates stage 4 infection with persistent viremia
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How can PCR be used to detect FeLV?
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* Detects proviral DNA
* May be used to detect latent/sequestered infections when other tests are negative or inconclusive. |
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What is the target antigen for FeLV vaccines?
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gp70 (envelope)
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Antibody detection and FIV?
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* Accurate detection of antibodies in cat older than 6 months is compatible with infection.
* Kittens may acquire colostral anibody from infected queen. Antibody should have cleared by 6 months of age. (Antigen levels are below detection levels throughout most of infection.) |
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screening test of choice for FIV?
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ELISA
• Vaccine – produces antibody – not distinguishable from infection with ELISA, Western blot, or PCR. |
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When should you test a cat for FIV who you believe was exposed?
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Wait 60-90 days after exposure before testing due to slow seroconversion.
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What is expected to be seen on a CBC/Chem of a FIV + cat?
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* Neutropenia
* Non-regen anemia * Lymphopenia * Hypergammaglobulinemia |
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How to prevent FeLV?
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Prevalence is reduced by testing, removal, vaccination. Vaccinate cats that are at risk, use non-adjuvanted vaccine.
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How to prevent FIV?
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neuter cats, keep cats indoors. Vaccination CANNOT be recommended at this time.
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How do cats become infected with feline calcivirus?
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Infection by oronasal or conjunctival routes
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Where does feline calcivirus replicate?
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replication in oral and respiratory tissues
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What is the incubation period of feline calcivirus?
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2-5 days
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CS of feline calcivirus?
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* Depression
* Fever * Lingual ulceration * Salivation * Mild sneezing * Oculonasal discharge * Open mouth breathing |
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CS of the virulent systemic feline calcivirus strain?
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* Generalized facial and limb edema
* High fever * Multiple organ involvement – liver, pancreas, lungs * Sudden death |
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Mortality rate of cats with the virulent systemic feline calcivirus strain?
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67% mortality in adult cats
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CS of chronic carrier state of feline calcivirus?
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** Up to 50% cats still shed FCV at 75 days in saliva from tonsils
* Oral lesions associated with long term shedding: * Glossopharyngitis * Lymphoplasmacytic ginvivostomatitis – can lose teeth. |
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Where does feline herpesvirus-1 commonly infect?
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Infects conjunctiva, turbinate mucosa, soft palate, tonsils, occasionally trachea
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Incubation period of feline herpesvirus-1?
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2-6 days
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CS of feline herpesvirus-1?
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* Depression
* Pyrexia * Salivation * Anorexia initially * Multifocal areas of epithelial necrosis * Turbinate osteolysis * Rhintotracheitis – serous to mucopurulent discharge * +/- coughing * Dyspnea * Ocular lesions |
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Chronic carrier state of feline herpesvirus-1?
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* Most likely lifelong latent infections after acute disease.
* May be asymptomatic carrier even if vaccinated |
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Where does feline herpesvirus-1 persist in the chronic carrier state?
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Persists in trigeminal ganglion
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When does reactivation of shedding of feline herpesvirus-1 occur?
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* Occurs 7-10 days after stress, illness, or medication
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How long does reactivation of shedding of feline herpesvirus-1 last?
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* Lasts 10-14 days
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3 microbes that were discussed that less commonly cause respiratory disease in cats
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1. Chlamydophila felis
2. Bordatella bronchiseptica 3. Mycoplasma spp. |
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CS of Chlamydophila felis
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* Conjunctivitis without sneezing or nasal conjunctivitis
* Conjunctival hyperemia; * Serous to mucopurulent conjunctival discharge |
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How long does it take Chlamydophila felis to resolve?
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Usually resolves in 3-4 weeks, may relapse.
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CS of Bordatella bronchiseptica in cats
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**normal flora**
* Disease in young cats living with dogs * Coughing * +/- sneezing and ocular discharges * +/- submandibular lymphadenopathy * +/- bronchopneumonia |
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What is an important secondary infection in cats with asthma?
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Mycoplasma- likes to live in existing mucus but can’t cause mucus production itself so is 20 pathogen
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3 Canine Ehrlichiosis Cell Tropisms
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1. Monocytotropic species
2. Granulocytotropic species 3. Thrombocytotropic species |
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3 Monocytotropic species of Canine Ehrlichiosis
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* Ehrlichia canis
* Neorickettsia risticii * Ehrlichia chaffeensis |
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2 Granulocytotropic species of Canine Ehrlichiosis
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* Ehrlichia ewingii
* Anaplasma phagocytophilum |
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Thrombocytotropic species of Canine Ehrlichiosis
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Anaplasma platys
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Geographic distribution of Ehrlichia canis
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worldwide distribution
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Vertebrate hosts of Ehrlichia canis
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domestic dog, coyote, fox, jackal
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Tick host of Ehrlichia canis
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Rhipicephalus sanguineus, the "brown dog tick."
** (3 host tick – all on dog), transstadial transmission |
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Pathogenesis of Ehrlichia canis
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* Replicates in circulating monocytes and phagocytic cells throughout the body.
* Forms a morula: multiple organisms in cell vacuole. Spreads hematogenously, causes multisystemic disease. * The chronic stage of disease reflects bone marrow suppression. |
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What cells are most effective against Ehrlichia canis?
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TH1 – cytotoxic T-cells most effective against intracellular pathogens
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Predisposing factors of Ehrlichia canis
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**Exposure to ticks in an endemic area**
* German Shephards more susceptible, get more severe disease, appear to have poor cell mediated immune response. |
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ACUTE Clinical signs of Ehrlichia canis
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* Fever
* Anorexia * Lethargy * Lymphadenopathy * +/- bleeding disorders * +/- uveitis * +/- CNS signs |
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CHRONIC Clinical signs of Ehrlichia canis
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* Petechia & ecchymosis
* Weight loss * Bleeding disorders * Polyarthritis * +/- seizures * Multisystemic signs |
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Treatment of Ehrlichia canis
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Doxycycline for 28 days. Imidocarb single injection, repeat in 2-3 weeks
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Polymicrobial infections involving 2+ tick borne pathogens are being recognized more
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**much more severe disease, poor prognosis**
* If animal is + for one, consider testing for others. |
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Large babesia
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Babesia canis
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Small babesia
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Babesia gibsoni
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Predisposing factors of babesia
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Tick exposure in endemic area
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B. gibsoni clinical presentation
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* Sometimes fatal
* Chronic carriers common * Pups more severe than adults * May resemble autoimmune hemolytic anemia |
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CS of Hemolytic anemia
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* Pale mucous membranes
* +/- hematuria * Fever * Anorexia * Lethargy * Depression * Splenomegaly |
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abnormalities expected on a cbc/chem in a babesia patient
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* Low PCV, Hb
* Thrombocytopenia * +/- hypergammaglobulemia * +/- hypoalbuminemia * +/- elevated ALK phos, ALT, GGT |
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Why do you need fresh blood to do detect babesia on a stained blood film?
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won’t find pathogen in old, cold blood because they need high O2 content.
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level of parasitemia in carrier phase of babesia
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Low parasitemias in carrier phase!
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Reticulocytes and babesia?
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reticulocytes present = Look for Babesia
*** No retics = probably not Babesia. |
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standard Babesia treatment
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*** Imidocarb a single injection, repeat in 2-3 weeks.****
* Also azithromycin, doxycycline, atovaquone combos. NO immunosuppressives. |
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Babesia from Vietnam mostly seen in what breed?
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pit bulls, suspected to be husbandry related (fighting)
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Lyme, Borrelia, Ehrlichia, and Babesia Preventatives
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**** Tick avoidance, prevention, and removal**
* Borrelia – vaccine available * Ehrlichia - can be 2 days after tick attaches before transmission – removal is essential! |
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Bovine babesia species?
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B. bigemina, B. bovis
** reportable to USDA and TAHC |
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Equine Babesia species?
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B. caballi and B. equi
reportable to USDA and TAHC |
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Predisposing factors of pyoderma
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* Almost always secondary to another disease:
* Anatomic abnormalities * Inflammatory pruritic skin disease * Cornification defects/seborrhea, endocrinopathies * Follicular dysplasias * Allergic skin disease * Demodex * Trauma |
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CS of pyoderma
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* Surface lesions (hot spots, alopecia, erythema, comedones)
* Superficial lesions (papules, pustules, crusts, annular spread, epidermal collarette) * Deep infections (draining tracts, gelatinous skin, nodules, hemorrhagic bullae, lick granuloma, cellulitis interdigital cysts) |
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Intertrigo
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infection of skin folds
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most common pathogen of pyoderma in the dog
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Staphlococcus pseudintermedius
* This is a natural organism of skin microflora and can be cultured from healthy dogs |
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Diagnostic testing for pyoderma
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* Cytology
* Dermatophyte test medium * Biopsy * Culture and Sensitivity |
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Treatment of surface pyoderma
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may only need topical therapy (EX: chlorhexidine) to remove bacteria and excessive sebum
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Treatment of superficial pyoderma
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Beta-lactamase stable antibiotic – minimum 3 weeks Tx (Treat 1 week beyond clinical resolution)
* May use topical for focal lesions or adjunctive topical tx with systemic antibiotics. |
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Treatment of deep infections caused by a superficial lesion that has gone deep
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* Require a minimum of 6-8 weeks of appropriate systemic tx. (Treat at least 2 weeks beyond clinical resolution)
* Use Culture and Sensitivity to choose antibiotic, adjunctive topical therapy helpful. |
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Morphology of Bordatella bronchiseptica
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Gram – coccobacillus
facultative anaerobe |
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Bordatella bronchiseptica commonly lives where
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lives in upper respiratory tract of mammals and birds
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How is Bordatella bronchiseptica transmitted?
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transmitted via aerosol, direct contact, fomites
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Virulence factors of Bordatella bronchiseptica
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* Fimbriae
* Tracheal colonization factor * Capsule * Exotoxins * Lipopolysaccharide, endotoxin |
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What results from the fimbriae and tracheal colonization factor of Bordatella bronchiseptica?
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increased mucus and fluid in URT
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What are the 2 exotoxins released by Bordatella bronchiseptica? What results from their release?
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1. Tracheal cytotoxin
2. Dermonecrotic toxin * Destruction of ciliated resp. epithelium; depressed respiratory clearance mechanisms |
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Why is serology not a good test for Bordatella bronchiseptica?
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only indicates exposure and Bordatella bronchiseptica is normal flora
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Predisposing factors of Bordatella bronchiseptica?
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* High density populations, carrier animals
* Inadequate ventilation |
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Prevention of Bordatella bronchiseptica?
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* Isolate animals with clinical signs
* Reduce predisposing/associated factors |
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2 types of vaccines available for Bordatella bronchiseptica?
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• Intranasal vaccine – modified live virus with avirulent B. bronchiseptica
•IM vaccine – modified live virus bacterin/toxoid |
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primary pathogen of kennel cough
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B. bronchiseptica usually primary pathogen, but usually is part of a complex
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most common cause of severe viral pneumonia in dogs
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Canine distemper virus
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Common canine viruses involved in kennel cough/pneumonia
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* Canine parainfluenza virus
* Canine adenovirus-2 – tracheobronchitis * Canine herpesvirus * Canine distemper virus |
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Common bacterial causes of kennel cough
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* Streptococcus equi ssp. zooepidemicus
* Mycoplasma |
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Common causes of fungal pneumonia
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Histoplasma, Blastomyces, Coccidiodomycosis
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Common cause of protozoal pneumonia
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Toxoplasma gondii is common in cats, rare in dogs.
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Atrophic Rhinitis is caused by what?
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Bordatella bronchiseptica + Pasteurella multocida
•Initial infection is with B. bronchiseptica • If P. multocida not present, just get mild, reversible turbinate hypoplasia |
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What virulence factor of B. bronchiseptica damages epithelial cells and allows P. multocida to adhere
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Dermonecrotic toxin
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Virulence factors of P. multocida
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* Lipopolysaccharide, Endotoxin – toxic to respiratory epithelial cells, decreases phagocytosis, elicits inflammatory reaction
* Exotoxin – P. multocida toxin - induces destruction and atrophy of nasal turbinate bones – osteolytic, induces bone resorption |
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Bovine Respiratory Disease Complex (BRDC) AKA
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Bronchopneumonia, fibrinous pleuropneumonia
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When does an outbreak of Bovine Respiratory Disease Complex (BRDC) occur?
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10-14 days after stress
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First sign of Bovine Respiratory Disease Complex (BRDC)
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drop in feed consumption, sudden death
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Morbidity? Fatality of Bovine Respiratory Disease Complex (BRDC)?
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Variable morbidity, case fatality is 5-20%
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Clinical signs of Bovine Respiratory Disease Complex (BRDC)?
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* Non-specific
* Depression * Anorexia * Fever * Increased respiratory rate •Calves – 15-40 bpm •Adult – 10-30 bpm |
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What is the most common and virulent bacteria associated with BRDC?
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Mannheimia haemolytica
(Commensal of mucosa of oropharynx and GIT) |
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How is Mannheimia haemolytica transmitted?
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shed from nasal cavity – inhalation, direct contact, and ingestion of contaminated feed.
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Virulence factors of Mannheimia haemolytica?
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* Leukotoxin and LPS – drive a tissue destroying inflammatory response
* Capsule, Fimbriae, Adhesin 1, Fibrinogen-binding proteins, other exotoxins |
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Diagnositics for Bovine Respiratory Disease Complex (BRDC)?
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Clinical signs, history, necropsy, lab tests
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Prevention and control for Bovine Respiratory Disease Complex (BRDC)?
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• Eliminate reservoirs
• Reduce predisposing factors • Reduce stress • Increase resistance • Vaccine makes disease worse - results in over stimulated immune response |
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What makes up the BRD complex?
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****M. haemolytica***
• P. multocida • Mycoplasma, Histophilus somni, A. pyogenes, Bibersteinia trehalosi |
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3 most significant organisms in conjunctivitis in cats
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1. Chlamydophila felis
2. Mycoplasma spp. 3. Haemophilus felis |
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When a dog is infected with Ehrlichia canis, in which cell does the organism replicate?
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Macrophages
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Point of care Enzyme-linked immunosorbent assay (ELISA) tests, which are sensitive and
specific, are available to help in the diagnosis of infections with Ehrlichia and Anaplasma. What is the best interpretation for a positive test for Ehrlichia on this ELISA test? |
Evidence for exposure to Ehrlichia sp.
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When a dog gets infected with Anaplasma platys, in which cell does the
organism replicate? |
Platelets
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Clinical signs of a dog infected with Ehrlichia canis include petechial and ecchymotic
hemorrhages. What is the pathogenesis of these findings? |
Thrombocytopenia due to platelet-bound and circulating anti-platelet antibodies
causing the destruction of platelets |
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Describe the use of blood cultures to help diagnose Ehrlichia canis?
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Highly specific for identifying the causative agent, but takes up to 8 weeks to yield
results |
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What antibiotics was Mannheimia haemolytica found
resistant? |
Tetracyclines
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Bronchoalveolar lavage is a useful diagnostic procedure to aid in diagnosing disease caused by what pathogens?
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bacteria, protozoa, and viruses
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What protozoal pathogen has pulmonary involvement in approximately
25% of infected cats? |
Toxoplasma gondii
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