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232 Cards in this Set
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when does infection occur, as opposed to colonization?
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infection occurs when the innate immune system is overwhelmed. Infection is proliferation somewhere where they are not supposed to be, as opposed to colonization in a normal location
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URT immune system and vaccines
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IgA production required. Functions via immune exclusion- does not activate complement well. Immunity is not long lived, and requires frequent reboostering. It is difficult to obtain good secondary responses
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LRT immune system mediator
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IgG
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Is it preferable for a vaccine to stimulate the URT or LRT?
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upper, to prevent a pathogen from ever entering the system
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Sample considerations: URT vs LRT
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URT will have normal flora, LRT should essentally be sterile.
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methods of getting LRT sample
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TTW, endotracheal, BAL, FNA, percutaneous lung biopsy
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is TTW quantitative?
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no, need to look at combo of culture and cytology
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conchiformibius spp. Description and significance
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normal inhabitant of oropharyngeal mucosa. Gram neg gliding bacteria. Multicellular filaments made up of flattended cells stacked one against the other. (formerly called simonsiella). If seen on LRT sample, means that there is contamination from the URT
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major problem with endotracheal sampling
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contamination form the URT
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FNA / biopsy pros/cons
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Invasive. Gives a very small sample. Most useful for focal abnormal areas in the lung (With U/S guidance). Potential to lacerate lung or vessel
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most URT infections are _____
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opportunistic
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opportunistic predisposing infections
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other infectious agents (viruses), trauma, temp extremes, transportation/stress, dust/smoke, etc
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Bullnose
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aka necrotic rhinitis in swine. Caused by: fusobacterium necrophorum, an anaerobic gram negative rod. Infections characterized by necrosis and foul-smelling exudate (necrobaccillosis). Results in nasal discharge and nasal deformities. Not contagious
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can dogs and cats be infected with fusobacterium necrophorum?
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yes, but rare and usually secondary to viral infection, chronic smoke exposure, etc
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calf diphtheria
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fusobacterium necrophorum (+/- others). Necrotic laryngitis or laryngeal necrobaccillosis. Affects calves 3-8 months old, esp veal/feedlot animals. Causes loud inspiratory snore (caused by trauma to the lining of the larynx and subsequent swelling). trauma is usually initiated by dust, allergens, or BRD (anything that causes constant and persistent opening and closing of hte larynx). calves will have high fever and foul breath, throat will be swollen/painful, dyspnea/open mouth breathing, difficulting chewing/swallowing. may develop secondary pneumonia
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sinusitis
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inflammation of paranasal sinuses. Bacterial or fungal infections from: dental dz (eq), URT viral (fel), trauma, tumors, dehorning, etc. No specific agent.
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two diseases of the equine gutteral pouches
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gutteral pouch mycoses and gutteral pouch empyema
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gutteral pouch mycosis
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aspergillus most common. Manifests as serosanguinous to hemorrhagic nasal dischearge with or without cranial nerve signs. May see suddent death. (erode vessels -> fatal hemorrhage from the internal carotid artery)
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guttural pouch empyema
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infection manifested by purulent nasal discharge (uni or bi), parotid swelling, difficulty eating, labored breathing, and/or cranial nerve deficits. Streptococcus most common isolate (equi or zooepidemicus). Chondroids (pus stones) may form; abscessed LNs may rupture. OFten seen with strangles. Some animals = chronic carriers. There can be airway compression if pouch is full
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nasal aspergillosis
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dogs = rhinosinusitis. A. fumigatus most common- ubiquitous fingus. Associated with dolichocephalic breeds. Causes sanguinous discharge, epistaxis, sneezing, pawing/rubbing nose, pain and ulceration of the external nares. Destruction of turbinate bones and local blood vessels. Infection usually localized.
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diagnosing nasal aspergillus
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clinical signs, rhinoscopy for fungal plaques, biopsy for histopath/cytology/culter, serology (AGID), radiology (destruction of turbinate bones resulting in radiolucent areas)
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is serology effective for diagnosing nasal aspergillus?
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has a 6% false positive right. Determines if the animal has fought off infection before, not current infection
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aspergillus microscopy / culture
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wet mounts (KOH preps). Hyaline septate hyphae that branch dichotomously (forks). Easy to culture and ID via characterist conidial arrangement (phialoconidia, medusa head).
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aspergillus TX
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topical AZ delivered as a 1 hour infusion (under anesthesia). Prognisis is good with proper tx. Not zoonotic, but caution to immunosuppressed due to aerosol risk
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cryptococcus neoforms
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encapsulated dimorphic. We only see yeast form in vet med. Capsule allows disuigse from the immune system and prevents phagocytosis. Causes granulomatous nasal dz and occasionally CNS dz. Common in cats > dogs. Reservoir: soil, esp pigeon poop (high levels of urea).
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cryptococcus pathogenesis
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inhalation of unencapsulated yeast cells from environemtn. Capsulation of yeast in vivo at the nasal mucosa. Lesions range from expansive granulomas to little host tissue response (ulcerative lesions, nasal dischrage, chronic-> nasal deformity). Cats- nasal granoulomas and ulcerative lesions predominate. may cause pneumonia, may extend to ocular and CNS tissues)
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which form of cryptococcus is more common in dogs?
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disseminated. Poorer prognosis
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diagnosing cryptococcus
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clinical signs, impression smear, biopsy, KOH preps, diffquik/NMB stain, india ink (csf/clear exudates), culture (biopsy, exudate, CSF- on blood agar). Xr/ct- see thickening of nasal turbinates. Serology, Ab titers
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what does the latex agglutionation test detect?
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present of capsular Ag
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cryptococcus tx / prognosis / control / prevention / zoonotic potentional
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excision/ debulking/debridement. Antifungals (polyenes +/- flucytosine or azoles) long term. Prognosis: usually favorable response to tx. Cats depends on felv/fiv status (if felv positive, will need lifelong tx). Neuro signs = guarded prognisis. Avoid sources of fungus /bird guano. Zoonotic potential very low except immunocompromised.
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streptococcus spp
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gram positive cocci in pairs or chains. Non motile. Divide in one plane. Catalase negative
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streptococcus spp habitat
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most are commensals that colonize the upper resp and lower genital tract of animals. Enterococcus spp colonize the GI tract. A few more virulent species are found in carrier animals- usually in the URT, tonsils or nasopharyngeal area. Reservoir is the animal- they dont survive long in environment
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types of hemolysis
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beta, alpha, gamma
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b hemolytic strep spp.
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usually more virulent, cause the most severe dz
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a-hemolytic strep spp
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aka "viridans". Enterococcus spp and some mastitis strains, generally less virulent but still cause some dz
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gamma hemolytic strep spp.
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least virulent, rarely involved in infections
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define lancefield groupings
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based on differences in CHO extract from cell wall (group Ag or C-substance)
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Lancefield Group A: Strep
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strep pyogenes
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Lancefield Group B: Strep
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strep agalactiae
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Lancefield Group C: Strep
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strep equi equi, strep equi zooepidemicus, strep dysgalactiae equisimilis, strep dysgalactaiae dysgalactiae
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Lancefield Group D: Strep
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enterococcus spp, strep suis
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Lancefield Group E: Strep
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strep porcinus
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Lancefield Group G: Strep
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strep canis
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Lancefield ungroupables: Strep
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s. uberis, s. pneumoniae
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s. pyogenes
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group A, beta hemolytic. Virulent. Involved in URT infections; necrotizing fasciitis; streptococcal toxic shock syndrome (due to superAg). May cause mastitis. It is a human pathogen that may be transmitted to animals
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s. pneumoniae
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ungroupable, a-hemolytic. Pneumonia in hroses, pocket pets and primates. Sometimes septicemia in other animals especially small rums
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three bacteria that can cause toxic shock syndrome
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staph aureus, strep pyogenes, strep canis
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describe the pathogenesis of TSS
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crosslinking of MHC2 and T-cell Rc results in activiation of T cells in the absence of a specific peptide. Massive release of the cytokines IL1 and TNFa resulting in a systemic reaction of fever, decreased BP, shock, diarrhea, and DIC. "cytokine storm."
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s. agalactiae
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group b, a-hemolytic. Contagious mastitis, usually no systemic illness
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s. equi equi
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group c, b hemolysis. Equine strangles
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s. equi zooepidemicus
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group c, b hemolysis. Secondary pneumonia and pyogenic infections in horses. Commensal that causes oppotunistic infections. "shelter dog pneumonia."
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s. dysgalactiae equisimilis
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group c, b hemolysis. misc suppurative infections in horses (metritis), swine (septicemia and skin infection), and dogs (UTI)
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s. dysgalactiae dysgalactiae
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group c, ruminant mastitis
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enterococcus spp
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group d, alpha hemolysis. Opportunistic, low virulence. MDR concerns in human hospitals
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s. suis
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group D, alpha hemolysis. *Zoonotic*, septicemia and meningitis in piglets and humans. Misc suppurateive conditions in other species (abscesses)
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s. porcinus
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group E- b hemolytic. Cervical lymphadenitis (jowl abscesses) in swine.
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s. canis
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group G- b hemolytic. Feline cervical lymphadenitis, misc pyogenic conditions in dogs/cats, including repro tract infections and neonatal septicemias. Can cause TSS
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s. equi equi virulence factors
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hyaluronic acid capsule (antiphagocytic) and M-protein (long fibrillar protein that sticks out through capsule. Antiphagocycic. Fibrillar surface proteins bind serum proteins such as fibrinogen- hides from immune system. Ab to the outer portion of M protein effectively opsonize the bacteria.). Streptolysin O (membrane damaging enzyme that hemolyzes RBCs- b hemolysis-, also toxic to other cells including PMNs. will lyse WBC by membrane by binding to cholesterol). streptokinase (hydrolyzes fibrin, may play a role in spread of bacteria in tissue
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pathogenesis of s equi equi
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enters mouth/nose and attaches to cells in the crypts of the tonsil. Spreads to LNs of pharyngeal area as well as local pharyngeal and nasal mucosa. It will not survive withoin phagocytes, but the capsule and M protein prevent phagocytosis. Attracts large numbers of neutrophils (characteristic pyogenic response). most horses can halt spread of bacteria at local lymph nodes
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strangles clinical signs
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2-14 days post exposure: depression, anorexia, fever, submandibular LN enlargement. Nasal discharge begins as serous, becomes mucopurulent. LNs enlarge and abscess.
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strangles transmission
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direct contect with infected horses and nasal discharge or abscess exudate. Contaminated clothing, buckets, etc. survival in environment is short lived. Most recovered are not long term carriers
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strangles TX
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isolate. Penicillins. **If horse has LN swelling or abscessation: do not treat unless horse is dyspeneic or signs of dissemination occur- may prolong abscess maturation*
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strangles sequelae
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chronic carrier state. Gutteral pouch empyema (chondroids?) . Purpura hemorrhagica - type III hypersensitivity response; aseptic vasculitis. Bastard strangles (internal abscess formation). Streptococcal immune mediated myositis (muscle wasting)
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strangles vaccines
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killed whole cell bacterin; m-protein extract; intranasal avirulent
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acute pneumonia /pleuropneumonia of adult horses
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equine shipping fever. Usually polymicrobial (s equi zooepidemicus in conjunction with anaerobes and faculative anaerobes)
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zoonotic potential of animal streptococcal infections
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s. suis - meningitis in humans.. S. iniae- b hemolytic strep assoc with fish
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mycobacteria
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rod with gram positive type wall- but WILL NOT Stain with gram stain "ghost bacteria." Unique because of high lipid content in ell wall: superficial lipids, mycolic acid, lipoarabinomannan, waxes.
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unique characteristics of the mycobacterial cell wall
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more ristant to acids, alkalis and disinfectants *requires medium level disinfectant*. Resistant to drying. Resistant to most of the commonly used antimicrobials- requires combination therapy
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acid fast stains
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ziehl neelson or kinyoun. Basic fuchsin (alcohol and phenol added). Decolorized with acid-alcohol, counterstained with methylene blue
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acid fast bacilli
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slender, often beeded red staining rods against a blue background
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mycobacteria group 1
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tubercla mycobacteria: m tuberculosis; m bovis
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mycobacteria group 2
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lepromatous mycobacteria: m leprae, m lepraemurium
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mycobacteria group 3
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saprophytic mycobacteria- m. avium-intracellulare compex. M avium ssp paratuberculosis
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know the reservoirs for group 1 mycobacteria
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m. tuberculosis -human. M bovis- bovine
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pathogenesis of tubercle mycobacteria
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enter via resp tract. Phagocytosis by alveolar macrophages. Survive within macrophages (facultative intracellular). Infection of draining LN and granuloma formation. Possible dissemination as well as local spread of infection. Immunity is T- cell mediated. (CD4/Th1 -> y interferon -> activated macrophages / cd8-> cytotoxic cells that lyse macrophages and and release mycobacteria which can be engulfed by activated macrophages). Lesions represent host cell mediated response -> granuloma. Dz may range from focal lesion to widespread dissemination
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what is the classic granuloma?
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tubercle
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define granuloma
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focal area or nodule of granulomatous inflammation
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mycobacterium tuberculosis. Reservoir? Main host? Spread?
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reservoir and main host: human. Spread by aerosol droplot. Anthropozoonosis.
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mycobacterium bovis Reservoir? Main host? Spread?
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reservoir/host: cattle. Spread by aerosol droplet and milk ingestion. Zoonotic. State programs exist to control /eradicate
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diagnosing mycobacterium
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demonstration of acid fast bacilli (does not indicate species; negative does not rule out). Intradermal skin testing. Culture (Slow, definitive, IDs species). PCR (some labS),
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tuberculosis tx
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report! LA- slaughter. SA- depends on type. If bovis or tubercolusis- can transmit to toher animals/humans. Therapy expensive and long term. Not generally recommended
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mycobacteria group 2: lepromatous mycobacteria
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m. leprae (humans, hansen's dz- armadillo reservoir), m. lepraemurium (Cats/rats). Obligate intracellular organisms
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feline leprosy
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m. lepraemurium. Granulomatous nodular/ulcerative dz of the skin and or subcut tissue of the head/limbs/trunk. Transmitted by cat or rat bites
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saprophytic mycobacteria
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opportunistic pathogens usually acquired from the soil. Slow growers (m avium paratuberculosis and m avium intracellulare complex) or fast growers (m. fortuitum, m smegmatis, m chelonae). Usually involved in opportunistic subcutaneous infections in a wide variety of animal species
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m .avium intracellulare complex
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a group of genetically related bacteria. M avium: bird rservoirs, intestinal infections of wild/domestic fowl. (subspecies: avium, paratuberculosis or silvaticum). M intracellulare: saprophyte and opportunist; involved in infections in a wide variety of animals ranging from subcut to GI tract to pulm infections to disseminated dz
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m. avium intracellulare complex: Reservoirs, mode of transmission, species report in, transmissoin.
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reservoirs: wild birds/poultry, soil and water. Inhalation of ingestion. Mainly reported in poulytr, swine, dogs and cats. Not transmissible from one animal to another. Not reportable
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avian tuberculosis
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m. avium
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swine tuberculosis
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usually m avium, bt can be m. bovis
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rhodococcus equi
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a dz of foals (2wk-7mo) with most cases in foals from 4wk-10wks. Bronchopneumonia or embolic pneumonia of foals with formation of pulmonary abscesses
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r. equi reservoir and source
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saprophyte found in soil- multiples dramatically with the presence of horse manure. Transmitted by nhalation of organism on dust partles.
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r. equi culture and gram stain
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mucoid colonies that become salmon pink after several days. Gram stain: small gram positive coccobacilli or short to medium rods (pleomorphic)
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r. equi pathogenesis
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infection likely occurs in first week after birth. Organism inhaled and deposited in LRT. (FPT can be predisposing factor). Macrophages are unble to kill organism, so intracellular infection occurs. Formation of pyogranulomatous bronchopneumonia and granulomas in lung. Hematogenous spread can occur, and extrapulm signs are common (uveitis, diarrhea, synovitis).
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r. equi virulence factors
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encapsulated bacterium, Vap plasmid
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encoding proteins for r. equi
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VapA, VapC-VapH. VapA is needed to cause dz
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what does r equi do once phagocytosed?
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inhibit phagolysosome fusion
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immune system response to R. equi
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requires y-interferon and functional Th1 Cd4 and Cd8 lymphocytes as well as antibody. IFN activates macrophages, and activated macrophages can kill r. equi
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r. equi dx
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clinical signs, CBC- very high WBC count, elevated fibrinogen, TTW, gram positive intracellular coccobaccilli/rods. Culture: mucoid, salmon=pink colones that tend to coalesce
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r. equi tx, prevention
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macrolide + rifampin. Never use rifampin alone! . To prevent: hyperimmune plasma, early detection (fibrinogen, us)
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diseases of bordetella bronchiseptical
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tracheobronchitis and pneumona in dogs/cats. Secondary pneumonia in swine, atrophic rhinitis in swine, bronchopneumona in lab animals/guinea pig
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bordatella avium
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rhinotracheitis of turkeys (turkey coryza)
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bordatella parapertussis
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pneumonia in lambs
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bordatella bronchiseptica transmission
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gram neg coccobacillus found in URT, transmission by direct contact or aersol. Some animals may be inapparent carriers
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ITB
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infectious tracheobronchitis. Clinical signs: paraxysmal harsh, dry cough often followed by retching/gagging. Secondary pneumonia may occur. Incubation is 3-4 days. B. bronchiseptica is not only cause!
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ITB etiological agents
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b. bronchiseptica, viruses, etc.
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ITB pathogenesis
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viral inhibition of resp defense mechanisms predisposes to infection by b. bronchiseptica. BB attaches to cilia of URT epithelium via adhesions found on the outer membrane and via fimbriae. BB LPS preotects gainst complement and defensins. BB is encapsulated, enabling evasion of phagocytosis. does not invade epithelial cells ,but remains on surface and proliferates, producing toxins. bacterial growth in tracheal lumen results in attraction of PMNs to mucosal surface
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bordatella bronchiseptica toxins
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tracheal cytotoxin: induces ciliostasis and destruction of epithelial cells. Adenylyl cyclase: inhibits phagocytosis by macrophages and also inhbits the respiratory burst of neutrophils.
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main defense against ITB
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IgA - prevents bacterial attachment and neutralizes toxins. Elimination of ITB may take 6-14 weems
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ITB tx
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treat dog to help client- decrease coughing even though infection is self limiting. Antimicrobial therapy will not diminish or shorten the duration of clinical signs of ITB
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kennel cough vaccine
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parenteral with killed whole cell product -> IGG response. IN with attenuated -> IgA response (short lived response). Present recommendateion: use both in sequence
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bordatellosis in swine
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secondary pneumonia, atrophic rhinitis - colonization of nasal mucusa by strains of Bb that produce dermonecrotic toxin
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dermonecrotic toxin
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exotoxin that damages osteoblasts of nasal turbinates resulting in the regenerative atrophy of turbinates in young pigs.
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signs of turkey coryza
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decreased appetite/weight gain/feed efficienty, loss of voice, ocular/nasal disahcrge, conjunctivitis, sneezing, flicking the head, dyspnea
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name three pulmonary mycoses
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histoplasmosis, blastomycosis, coccidioidomycosis
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geography of blastomycosis
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south east
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geography of histoplasmsis
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mississipi, Ohio and missouri river valleys
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geography of coccidioidomycosis
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south west
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histoplasmosis
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histoplasma capsulatum - dimorphic fungus. Saprophytic soil fungus that grows esp well in soil enriched with bird or bat guano
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histoplasmosis pathogenesis
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inhalation of microconidia from environment. Conversion to yeast phase in vivo. organisms bind to phagocytes via adhesins. adhein-integrin binding diminshes respiraty burst. organism increases phagolysosome PH Yeast replicate in monocytic cells then lyses cell. May spread from lungs via lymphatics or blood to a variety of tissues including gi, liver, spleen, bone marrow. Characteristics lesions are granulomatous. resolution is dependent on CMI
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histoplasmosis clinical signs
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mainly in cats/dogs. pulmonary infections predominatn, disseminated infections common. Chronic dz characterized by inappetence, weight loss, fever, and poor response to antibiotic therapy. GIT involvement/diarrhea/protein losing enteropathy common in the dog. Anemia may be present.
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histoplasmosis dx
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clinical signs/ history. Serology (usefulness limited), demonstration of agent in tissue (buffy coat, LN aspirate, rectal scraping, biopsy, bone marrow aspirate)
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impression smear appearance of histoplasmosis
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small yeast cells within macrophages or neutrophils. Size = 2-4um. Round yeast with basophilic center and a clear halo.
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histoplasmosis culture
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do not culture! Send to BSL3 lab. Don’t send rectal scrapings - contaminated. Keep cool in transit
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histoplasmosis treatment and prognosis
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tx with azoles- for at least 4-6 months. Severe dz may need amphotericin B IV in combo with oral azole. Also glucocorticoides. Prognosis for dissemeinated is grave.
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blastomycosis
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blastomyces dermatitidis. Dimorphic fungus. Mainly dz of of dogs/humans. Pulmonary infections predominate but disseminated dz is common. Chronic dz characterized by depression, fever, wieght loss and poor response to ab therapy. Generalized lymphadenopathy, ulcerative skin lesions, ocular/bone involvement. likes low lying moist areas. most common clinical signs are not very specifc
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blastomycosis dz pathogenesis
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inhalation of conidia from environment. Converstion to yeast phase in vivo. Adhesion Bad1 allows phagocytosis wihout respiratory burst and downregulates TNFa. Grows intra (m0 and giant cells) and extracellulary as large budding yeasts. May spreads from lungs via lymphatics or blood to skin,eyes,bones,joints. characteristic lesions are pyogranulomatous
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common epidemiology of blastomycosis
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point sources of infection within endemic areas
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blasto dx
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clinical signs, history, demonstration of agent in tissues/sampes (LN, cutaneous lesions, TTW, BAL), serology (high specifity, lower sensitivity), culture (send to bsl3 lab)
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blasto yeast form
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8-15um, broad based, thick/double walled. Hard to ID if not budding
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blasto tx
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2-3 months of azoles / itraconazole. May need amphotericin B for severe dz. + glucocorticoids
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coccidioidomycosis
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coccidioides immitis, dimorphic fungus. Endemid to lower sonoran life zone- hot, sermi arid low lying areas of SW US. Soil organism (saprophyte) produces small arthroconidia that are inhaled. AKA san joaquin valley fever
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coccidioidomycosis pathogenesis
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inhalation of arthroconidia from soil. Development of spherule from an arthrocondium- in the resp system. Spherules matures with production of endospores that are released in vivo. Infection may be localized to foci wthin lung, may extend to LNs or may disseminate to bone/skin
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coccidioidomycosis clinical signs
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mainly in dogs/humans. Pulm infections predomiate but dissemination is common. Chronic dz characterized by fever, anorexia, weight loss and poor response to Ab therapy. Lameness, draining skin lesions, and ocular infections are signs of dissemination. lameness is common clinically presented
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coccidioidomycosis dx
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clinical signs, history, demonstration of agent in tissues/sampes (LN, exudates, biopsies), serology, culture (send to bsl3 lab)
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appearance of coccidioidomycosis on slide
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very large, round, double walled spherules
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coccidioidomycosis tx
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8-12 MO azoles, + ampthotericin B. good prognosis for resp only d
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pneumocytosis
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uncommon opportunistic dz of animals. Clinicaly seen most commonly in immunocompromised mini dachshunds <1 yr of age, and in SCID foals. Host specfic strains, so not zoonotic. Pneumocystis carinii- saprophytic fungus that responds to antiprotozoal meds.
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pasteurellaceae
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family (13 genera) of gram neg coccobacilli
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important pathogenic genera in the family pasteurellaceae
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pasteurella, mannheimia, bibersteinia
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pasteurella, mannheimia, bibersteinia
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gram neg rods/coccobacillus. Commensals on mucous membranes especially of the oropharyngeal, nasopharyngeal and tonsillar areas. Opportunistc pathogens in many species but NOT horses
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pasteurella multocida
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found in nasopharynx/oropharynx of a variety of animals- rums, swine, birds, dogs, cats. Many serogroups (ABDEF) and serotypes (1-16) exist. Can cause suppurative bronchopneumona, atrophic rhinits (swine), snuffles (Rabbits), septiciemia/fowl cholera, bite wound contaminations
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pasteurella multocida hemolysis
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non hemolytic
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Snuffles
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rabbits, assoc with stress. Major cause: mucopurulent rhinosinusitis, pneumonia, otitis media/interna, purulent infections, septicemia. Most raibbits are carriers Other lesion: head tilt, conjuntivitis, cutaneous abscess, etc
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fowl cholera
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chickens, turkeys, waterfowl, peracute dz -> sudden death. Multifocal small pale foci of hepatic necrosis or petechial hemorrhages in heart/GIT. Chornic form: resp dz manifests as chornic sinusitis, swollen wattles, snyovitis. Need to differentiate from: mycoplasma gallisepticum, infectious coryza, swollen head syndrome.
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fowl cholera - control, prevention, treatment
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best control- biosecurity and sanitation. Vaccine- live and killed. Protein is not complete. Ttreatment- last resort. Check ab sensitivity of isolates
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mannhemia haemolytica
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biotype a- arabinose fermenter. Pathogenic for ruminants. Major cause of severe, acute pneumoa and pleuropneumonia in cattle, goats, sheep. Mastitis in ewes
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bibersteinia trehalosi
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biotype T- trehalose fermenter. Pathogenic for rums only. Causes: septicemia in lambs, pneumonia in bighorn sheep. Bovine pneumonia??
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BRD complex
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severe and complex dz syndrome associated with stress combined with viral/bacterial pathogens. Enzootic (dairy calves <3 mon) or shipping fever (beef calves 6-18mon).
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the underlying pulmonary lesion in BRD
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bronchopneumona, fibrinous pneumona or fibrinous pleuropneumonia (aerosol origin, cranioventral consolidation). Lesions differ among cases.
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etiologic agents of BRD- shipping fever
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mannheimia haemolytica. Serotype 1. main lesion: fibrinous pneumonia or fibrinous pleuropneumonia. Other bacteria include: histophilus somni, P multocida, B trehalosi for acute cases. Chronic case: arcanobacterium pyogenes, subacute -> chronic: mycoplasma bovis
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BRD pathogens
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bacterial resp pathogens are part of normal nasopharyngeal flora of calves. When stressed the bacteria proliferate and are inhaled into the lung -> severe pneumonia
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m. haemolytica virulence factors
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endotoxin- damages vessel walls. Capsule- ihibits phagocytosis. Leukotoxin- toxic to RUMINA macrophages, lymphocytes and neutrophils.
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major clinical signs of acute BRD infection
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nasal discharge, dyspnea, cough, anorexia, abnormal lung sounds, fever. Body posture: depressed stance with head down, neck extended, open mouth breathing, wide stance
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major clinical signs of chronic BRD infection
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weight loss, poor doers, lethargy, depression, anorexia, chronic respiratory signs
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BRD diagnosis
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clinical signs, history, necropsy, isolation of bacteria (TTW).
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BRD tx
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early recognition and treatment are mandatoy for acute pneumonia. Most older products not efficacious, use newer strains. Isolation/Ab sensitivity testing important
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metaphylaxis definition
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the timely mass medication of a group of animals to eliminate or minimize an expected outbreak of disease.
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is there a BRD vaccine?
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yes vaccines are availaable for all the common bovine viral respiratory pathogens., reduces risk but will not prevent! Bacterial vaccines: m.haemolytica (stimulates ab to leukotoxin and surface Ag). P multocida and h. somni vaccines - no published studies
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enzootic pneumonia of dairy calves
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resp dz complex of young dairy calves. Second most common dz of dairy calves (diarrheal diseases 1st). Usually a suppurative bronchopneumonia. Stress factors play a role
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bacteria of enzootic pneumonia
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p. multocida (serogroup A), b. trehalosi, m. haemolytica (less frequent)
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enzootic pneumona vaccine?
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no good vaccines for p.multocida, No vaccines for b trehalosi at all
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pasteurellosis in sheep
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m. haemolytica- pneumonia, septicemia in lambs. Mastitis in eyes. All ages of bighorns susceptible to pneumonia. B. trehalosi- septicemias of older lambs, pneumonia in bighorn sheep. P. multocida- sporadic secondary pneumonia
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swine pasteurellosis
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p. multocida- atrophic rhinitis (serogroup D)- produce pasteurella multocida toxin. Major cause of porcine bronchopneumonia (Serogroup A)
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atrophic rhinitis
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disease of young pigs, infectually usually occurs by 3 weeks of age. Results in atrophy of the nasal turbinate bones. Clinical signs include lacrimation, sneezing and distortion of the snout.
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pathogenesis of atrophic rhinitis:
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b. bronchiseptica- colonizes the nasal mucosa and produces a txin that inhabits the osteoblasts of the nasal turbinates. Probably more importantly, Bb infection enhances colonization of toxigenic strains of P multocida-serogroup D, that produce a toxin that enhances bone resorption (increased osteoclast activity) leading to turbinate loss
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atrophic rhinitis control
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Ab to reduce levels of bacteria, maangement (imrpve air conditions), vaccination program- vaccinate sows with bacterin toxoids for both agents, vaccinate piglets at 1 and 3 weeks of age
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p. multocida zoonotic potential
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oral/pharyngeal commensal in dogs/ cats. BSL2 - potential for human infection. Bite wounds can become infected. Septicemia in neonates/immunocompromised.
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class mollicutes
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soft skin mycoplasmas, smallest free living bacteria, lack a cell wall
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class mollicutes, genera found in animals that typically colonize mucous membranes
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mycoplasma, ureaplasma, acheoleplasma, anaeroplasma
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characteristics of mycoplasmas
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have a very small genome- lack the genes to form a cell wall. Require intimate association with host cells (but are extracellular). Resistant to beta-lactam Abs. pleomorphic and filteraable. Fried egg colon morphology (umbonate). Have complex nutriional requirements for in vitro growth. Very small colony size <1mm.
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mycoplasma reservoir and transmission
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reservoir: mucous membranes of animals (URT, lower genitourinary tract). Transmission: airborne droplets; direct contact; venereal (Semen); egg transmission in poultry, mechanical transmission in mastitis. NO ZOONOSES
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mycoplasma: general dz characteristics
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usually chronic diseases with high morbid/low mortality. Economic diseases. Associated with confinement raised and intensively reard animals (cattle, swine, poultry). Diseases manifestations: respiratory, arthritis/synovitis, mastitis, keratoconjunctivitis, repro tract infection
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mycoplasma pathogenesis
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not well understood. Close assoc with resp epithelial cells. High ammonia in air enhances infection. Ciliostasis seen in some infections. Many mycoplasma spp have variable surface proteins that change antigenc structure- allowing for evasion of the immune system. release of factors such as proteases, h2o2, hemolysis, etc, may damage host cells
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mycoplasma hyopneumoniae
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enzootic pneumonia of swine
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mycoplasma hyorhinis
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polyserositis and arthritis in young pigs <10wks
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mycoplasma hyosynoviae
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arthritis in older pigs (3-6mo)
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enzootic pneumonia of swine
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mycoplasma hyopneumoniae. Very common. High morbid, almost 0 mortal. Chronic nonproductive coough, retarded growth rate, poor feed efficiency. Economic impact
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pathogenesis of m. hyopneumoniae
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infection usually occurs in young pigs from 3-8 wks. Clinical signs (dry cough) most prominent as pigs reach the feeder stage (8-12wk). Lesions are characterized by peribronchiolar and perivascular cuffing with extensive lymphoid hyperplasia
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m. hyopneumoniae gross lesions
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pneumonia, usually in cranioventral lung lobes. Plum-to-grey-colored areas that are firm on palpation.
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relationship between m hyopneumoniae and other bacterial/viral infections
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m. hyopneumoniae predisoses to infections suth as pasteurella multocida and bordatella bronchiseptica, and increase severity of viral infections
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diagnosis m. hyopneumoniae
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slaughter. Histopath to determine chracteristic lung lesions. Definitive dx: culture, Fab or IHC on affected lung tissue. Gross and histopath are essentially pathognomonic
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m. hyopneumoniae control and tx
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tx with Abs if dz is explosive in a herd- mecrolides or tetracyclines. Will decrease clinical signs. Vaccination progeams- inactivated whole cell or subunit vaccines can be used to decrease clinical signs and gross lesions. Mgmt- decrease overcrowding and enhance air quality, allin allout procedures. establish m.hyopneumoniae free herd.
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mycoplasma gallisepticum
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chronic resp dz of chickens and turkeys
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mycoplasma meleagridis
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air sacculitis in turkeys, chronic syndovitis in breeder turkeys
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mycoplasma iowae
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air sacculitis in turkeys
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mycoplasma synoviae
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infections synovitis of chickens and turkeys
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m. gallisepticum
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reportable in turkeys! High morbid, low mortality dz characterized by sinusitis, rhinitis and air sacculitis. May be complicated by other secondary bacterial infections. Transmitted by droplet or via eggs.
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mycoplasma airsacculitis agents in turkeys
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m. meleagridis - less frequent infections. Spread via droplets, eggs or venereal. Results in poor growth, airsacculitis, reduction in hatachability, osteodystrophy, poor feathering and synovitis in breeder turkeys. M iowae- widespread, spread via dropets, eggs, venearl. poor growth, airsacculitis, reduction in hatchability, osteodystrophy, poor feathering
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mycoiplasma mycoides mycoides
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small colony. Contagious bovine pleuropneumona. Foregin to US
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mycoplasma bovis
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arthrtis, mastitis, pneumoniae. Role in subacute to chronic resp dz
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mycoplasma dispar
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bovine pneumonia, but predominantly in eurap
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bovine mastitis agents
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m. californicum, m. canadense
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granular vulvovaginitis agents
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ureaplasma diversum, m. bovigenitalium
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contagious bovine pleuropneumonia
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foreign animal dz. M. mycoides mycoides- small colony. Causes acute severe necrotic fibrinous pleuropneumoniae in cattle that can become chronic. Chronically infected animals are reservoir. Grosly resembles m. haemolytica pneumonia. Also causes arthritis/synovitis in calves. eradicated from US in 1892
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m. bovis in bovine pneumonia
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commonly assoc with subacute to chronic pneuomnia in feedlot cattle. Some affected animals also have fibrinous synovitis. Contributing factor in feedlot pneumonia. Multiple small coalescing foci of caseous pneumoniae are the typical m. bovis lesion, may allso look like CBPP
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important mycoplasmas of sheep and goats
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m. agalactiae; m. conjunctivae; m. ovipneumonoae
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mycoplasms cause more important dz in ____ than in ____
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goats > sheep
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m. mycoides capri
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septicemia, arthritis, pneumonia, and keratoconjunctivits in young kids. Mastitis and keratoconjuncitivits in adults. Occurs in usa.
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m. capricolum capricolum
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septicemina which may include acute interstitial pneuomnia in kids. Occurs in USA
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m. capricolum capripnuemoniae
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FAD. Contagious caprine pleuropneumonia. Caute, highly contactious dz characterized by fever, coughing, severe resp distress, high mortality, principal lesion is fibrinous pleuropneumonia
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m cynos
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pneumonia in dogs
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m. canis
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urogenital tract dz in dogs
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m. spumans
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arthritis in dogs
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m. felis
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conjuncitivis and URIs of cats
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m. gateae
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arthritis in cats
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m. felis
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pleuritis in horses
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L- forms
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cell wall deficitentn forms of bacterial. Unlike mycoplasmas, L-forms DO nhave the genetic capability to form a cell wall. External conditions inhibhit cell wall synth while still alloiwing bacterium to survive (exposre to b lactams or lysozyme).
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porcine pleuropneumonia
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highly contagious and severe pleuropneumonia of swine. Caused by actinobacillus pleuropneumoniae- gram negative coccobacillus. Organism is V-factor (NAD_ depdendent. Requires V-factor for isolation, grows only in assoc with v factor resulting in satelliting type of grwoth
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V-factor
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can only be supplied by staph aureus
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porcine pleuropneumonia transmission and reservoir
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a. pleuropneumoniae is transmitted from one pig to another by aerosol droplet/direct contect. Carrier swine are the reservoir.
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a. pleuropneumoniae virulence factors
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capsule (polysacc, 12 serovars). Cytotoxins (toxic to phagocytic cells). Urease (increases phagolysosome ph and activates phagocytes). Endotoxin (LPS- adhesion, increased vasc permeability and vessel thrombosis in lung; edema, hemoorhage and necrosis in lung)
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a. pleuropneumoniae pathogenesis and clinical signs
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may have peracute to chronic dz depending on herd and individual immunity. Peracute- sudden death, die wtihin hours of becoming ill. Necropsy lesions- severe fibrinonecrotic and hemorrhagic pneumonia with fibrinous pleuritis. Endotoxin plays major role. acute- fever, resp distress, open mout breathing, blood stained froth from nostrils and mouth. chronic- cough, poor weight gain, sequesered lesions and pleuritis at slaughter
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a. pleurpneumoniae dx
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clinical signs, necropsy lesions (fibronecrotic and hemorrhagic pneumonia and fibrinous pleuritis). Definitive dx- culture of affected lung tissue. Serology (used on a herd basis, but canot determine carrier status of individual)
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a. pleurpneumoniae tx and control
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antimicrobials, medicate feed/water, treat early! Control difficult- recovered animals are carriers and antimicrobails don’t work. Vaccines- serovar specefic bacterins - decrease mortality rate
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trueperella pyogenes
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gram positive rod, commensal on mucous membranes of rums and swines. Involved in numerous pyogenic infections, secondary pneumonia, abscesses, repro tract infections, etc
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chamydiaceae
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gram neg obligate intracellular coccobacilli that lack peptidoglycan. Two familes- chlamydia and chlamydophila
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chlamydia trachomatis
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conjunctivits and STD in humans
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chlamydia suis
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sbclinical in swine (conjunctivits, enteritis, pneumonia)
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chlamydia muridarum
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sublicanil resp infections in mice and hamsters
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chlamydophila psittaci
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psittacosis and ornithosis in birds. Parrots/psittacines at high risk
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chlamydophila felis
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feline conjunctivis
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chlamydophila caviae
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guinea pig conjunctivitis
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chlamydophila pneumoniae
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humas mainly, resp pathogen. Also isolated from koales and horses
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chlamydophila pecorum
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koalas- resp and urogenital tract dz. Rums/swine- abortion, conjunctivit,s encephalomyeltis, (sporadic bovine encephalomyelitis), enteritis, pneumonia, and polyarthrtis (stiff lamb dz)
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chlamydophila abortus
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rum- abortion (Esp sheep/goats). Enzootic abortion of ewes
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chlamydiaeceae epidemiology
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transmission- inhalation or ingestion of elementary bodies in dried fecal material or nasal exudate. Incubation period usually 3-10 days, but can extend to years. Stress precipiates active infection.
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life cycle of chlamydiaeceae- obligate intracellular bacteria
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elementary body (small dense infections particle with rigid cell wall, extracellular form, environmentall resistant) binds to and enters host cell. Reticulate body (intracellular form, metabolically active) replicates within host cell. EB attaches to host cell and initiates endocytosis. EB within phagosome inhibits lysosome fxn with phagosome. binary fission occurs within phagosome- develop into EBs which are resleased by cell lysis or exocytosis.
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chlamydia and energy production
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chlamydia have no ability to produce energy- use ATP from host
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avian chlamydiosis or psittacosis
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c. psittaci- obligate intracellular bacterium. EB live for several months in enviro and aerosolize easily. Reportable! Aka ornithosis, damage is thought to be due to host cell lysis.
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clinical signs of generalized psittacosis
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most commonly psittacine birds, turkeys, pigeons. Lethargy, anorexia, ruffled feathers, serous to mucopurulent oculonasal discharge, greenish diarrhea, decreased egg production, may become emaciated, dehydrated and die
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lesions of psittacosis
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pneuomia, airsacculitis, hepatitis, myocarditis and fibrinous epicarditis, fibrinous periphatitis/peritonitis, enlarged spleen with white foci
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diagnosis psittacosis
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impresion smears, culture, serolgoy (need 4x increase in titer), Ag tests
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psittacosis treatment and control
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isolate, tx with tetracycline or doxy for 45 days. Avoid aersolization. Disinfection. Zoonotic!
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