25. mycoplasmas and respiratory pathogens I (bacteriology)

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37 Terms

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what is special about the structure of mollicutes (mycoplasma spp.)?

lack cell walls → have a single trilaminar membrane rich in proteins and lipids

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are mycoplasmas typically found as free-living organisms?

no → obligate parasite

  • co-evolve with their host

  • limited host range

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what classes of antibiotics are ineffective against mycoplasmas?

  • all beta lactam antibiotics

  • sulfonamides

4
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mycoplasma mycoides subsp. mycoides is the causative agent of what disease? what species does it affect?

  • contagious bovine pleuropneumonia (CBPP)

  • affects cattle and buffalo

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mycoplasma bovis sources (infection in calves)

contaminated milk, possibly aerosols, or fomites

  • almost all calves born on M. bovis infected farms end up colonized

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mycoplasma bovis reservoir

mucosal surfaces (respiratory, genital, conjunctiva, mammary gland, alimentary canal, and joints(?))

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how is mycoplasma bovis transmitted?

ingestion, possible inhalation, or direct contact

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mycoplasma bovis virulence mechanisms

  • suspect antigenic variation (variable surface lipoproteins)

  • damage host cells (phospholipases, H2O2, and superoxide radicals)

  • biofilm formation

  • can adhere to neutrophils and inhibit respiratory burst activity

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how does mycoplasma spread systemically? what are its predilection sites?

  • hematological spread

  • predilection sites:

    • nares

    • tonsils

    • eyes

    • tympanic bulla

    • meninges

    • lungs

    • udder

    • joints

    • genital area

<ul><li><p>hematological spread</p></li><li><p>predilection sites:</p><ul><li><p>nares</p></li><li><p>tonsils</p></li><li><p>eyes</p></li><li><p>tympanic bulla</p></li><li><p>meninges</p></li><li><p>lungs</p></li><li><p>udder</p></li><li><p>joints</p></li><li><p>genital area</p></li></ul></li></ul><p></p>
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what are possible outcomes of mycoplasma bovis infection in calves?

  • clear infection

  • chronic colonization of URT & intermittent shedding

  • increased replication in URT → spread from URT → clinical disease

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what are complications associated with myocplasma bovis infection in calves?

  • otitis

  • pneumonia

  • arthritis

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clinical signs of mycoplasma bovis infection in calves

progressive disease

  • fever & anorexia

  • otitis → scratching ear, head shaking, ear droop

  • head tilt ± other neurologic signs indicate otitis interna (CN VIII) ± nystagmus

  • advanced otitis media-interna → meningitis and/or other cranial nerve deficits

    • → spontaneous regurgitation, loss of pharyngeal tone, dysphagia, and aspiration pneumonia

  • unilateral or bilateral neurologic deficits

  • purulent aural discharge + ruptured tympanic membrane

  • arthritis

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mycoplasma bovis diagnosis (calves)

  • based primarily on clinical signs

  • pharyngeal swabs for culture or PCR

  • synovial fluid from calves with arthritis can be aspirated for culture or PCR

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treatment of mycoplasma bovis infection in calves

  • antimicrobials are usually unrewarding but may be beneficial in early stage disease

  • puncturing the tympanic membrane to allow for drainage may alleviate pain from trapped exudate

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what age of animal does mycoplasma bovis mastitis affect? how is it transmitted?

  • affects any age

  • type of contagious mastitis (spread easily among animals by direct contact and fomites)

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clinical signs of mycoplasma bovis mastitis

  • infection usually subclinical

  • clinical mastitis usually mild → may have some discharge; affected udders not typically painful

  • only indicator may be sudden drop in milk production

  • history of recurrent mastitis is common

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clinical/lab findings of mycoplasma bovis mastitis

  • somatic cell counts usually normal

  • milk may appear discolored

  • false negative cultures/PCRs common due to intermittent shedding (need to do repeat sampling)

  • serology testing individual cow is useless due to high number of false negatives (m. bovis is intracellular)

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mycoplasma bovis mastitis treatment

  • intramammary antimicrobial therapy not effective

  • if cow spontaneously resolves infection, she can become a carrier

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mycoplasma bovis pneumonia source

carrier animals

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mycoplasma bovis pneumonia transmission

ingestion or inhalation

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mycoplasma bovis pneumonia predisposing factors

  • all ages affected

  • stressors (shipment, parturition, weather changes) that affect innate immunity (impaired mucociliary escalator)

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what is a gross finding of mycoplasma bovis pneumonia? what is a common sequelae?

  1. lung abscesses

  2. arthritis

23
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mycoplasma bovis pneumonia clinical signs

  • fever, tachypnea, dyspnea, and decreased appetite ± nasal discharge and coughing

  • poor weight gain in chronically affected animals

  • can be accompanied by ear infection and/or arthritis

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mycoplasma bovis pneumonia diagnosis

  • presence of M. bovis in the respiratory tract of healthy animals confound diagnosis

  • diagnosis will be presumptive and depends on clinical signs and presence of organism in lesion (necropsy) or transtracheal wash

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mycoplasma bovis pneumonia treatment

antimicrobials administered early (e.g. tetracyclines) may help + supportive care → unrewarding with advanced disease

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what is an important practice to reduce mycoplasma bovis infections?

mycoplasmas are sensitive to disinfection → good farm disinfection & biosecurity practices

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rhodococcus gram stain

gram positive rods

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rhodococcus equi is the causative agent of what disease? (what age/hosts does it affect?)

  • pyogranulomatous pneumonia in foals < 6 months of age

  • uncommon infections in other animals

  • commonly causes pyogranulomatous pneumonia in immune compromised humans

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rhodococcus equi virulence factors

  • plasmid expressing virulence associated protein A (VapA) essential for intracellular survival in foal macrophages

    • helps resist phagolysosome fusion and keeps pH inside phagosome neutral

  • lipid rich cell envelope protects from desiccation in environment and supports survival within macrophage

<ul><li><p>plasmid expressing <strong>virulence associated protein A (VapA)</strong> <strong><u>essential</u></strong> for intracellular survival in foal macrophages</p><ul><li><p>helps resist phagolysosome fusion and keeps pH inside phagosome neutral</p></li></ul></li><li><p><strong>lipid rich cell envelope</strong> protects from desiccation in environment and supports survival within macrophage</p></li></ul><p></p>
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rhodococcus equi source

manure contaminated soils, hays, and sandy stalls (risk factor)

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rhodococcus equi transmission

inhalation of organisms

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predisposing factors to rhodococcus equi infection

heavy environmental contamination and inadequate colostrum

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rhodococcus equi pathogenesis

bacteria engulfed by alveolar macrophages, where it persists → foal macrophages are inefficient at killing bacteria & VapA interferes with lysosome-mediated killing → accumulation of bacteria-laden macrophages → pulmonary pyogranulomas

  • evades host immune response (i.e. no fever)

  • can cause extensive, irreversible lung damage before foal shows signs of illness

  • pyogranulomas can be found in other body sites (eyes, joints, intestines)

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rhodococcus equi clinical signs

  • subclinical until advanced disease

  • based on location of organisms

    • respiratory: coughing, crackles, tachypnea, flared nostrils

    • GI: diarrhea with ulcerative colitis and mesenteric lymphadenitis if intestines become infected

    • osteomyelitis with bone infection (bone swelling, pain/lameness)

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rhodococcus equi diagnostics

  • clinical signs

  • transtracheal or bronchiolar lavage for culture and cytology

  • PCR detection of VapA gene is definitive (plasmid only present in virulent strains)

  • nasal swabs are useless

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rhodococcus equi prognosis/treatment

  • prognosis is good if infection caught early; advanced infections have high mortality rates (40-50%)

  • sick foals should be isolated and treated with antibiotics (macrolides + rifampin) for several weeks

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what is a risk to consider when treating rhodococcus equi with antibiotics?

both mare and foal are at risk for clostridioides difficile associated diarrhea (CDAD)