Mycoplasma/Mollicutes Flashcards

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1
Q

Mollicutes-Mycoplasmas

A

“minimal cells”- highly host-dependent, don’t survive well outwith host

Small genome: 600,000bp-1.4 million BP- straddle size of obligatue intracellulars

physiologically restricted- highly fastidious in terms of growth characteristic- need rich growth media

Lack cell wall (peptidoglycan): cytoplasmic membrane is exposed to envrionment, pleomorphic

Sterols present in the cell membrane (nb: sterols are a eukaryotic characteristic)

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2
Q

Diagnosis of mycoplasma infection

A

pathology- gross and histopath

isolation and ID: not as tricky as obligate intracellular pathogens, but still tough.

serological response; Ag detection, genomic detection

Difficulties: asymptomatic carriage; similarity between pathogenic and non-pathogenic; strain heterogeneity

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3
Q

Pathogenicity of mycoplasma

A

“parasites” of animals, arthropods, plants, mucosal-associated

occurs in urogenital tracts, oral/nasal mucosa, NOT GIT

asymptomatic, chronic or acute infection

high inter-strain heterogeneity

pathogenic and non-pathogenic strains can be very similar

lack conventional virulence factors

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4
Q

Mollicute genera

A

mycoplasma: ~100 species, pathogens and commensals
ureaplasma: pathogens and commensals
spiroplasma: plant pathogens; insect commensal
anaeroplasma: rumen commensal

Acholeplasma: mainly commensal

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5
Q

Virulence mechanism of mollicutes

A

Adhesins

Competition for metabolites and degradative enzymes- physiological destruction

Cytotoxic metabolites: means by which they damage host

endotoxicity: lipogalactan (elicit inflammatory response) and lipopeptides (similar endotoxin to what outer membranes do)

antigenic variation/capsule: escape developing IRs

Intracellular survival

Assimilation of host cell antigens

lymphocyte suppression

antigen persistence

Immunomodulation and immunopathology

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6
Q

Respiratory mycoplasma infection

A

e.g. mycoplasma hypopneumonia (porcine enzootic pneumonia)

Inhalation–>adherence to ciliated epithelium–>colonisation of bronchioles/alveoli–> ciliostasis and “ciliotoxicity”

Immunomodulation/immune evasion–> alveolar and peribronchial inflammation–> mononuclear cell infiltration and hyperplasia–> LN enlargement–> catarrhal (inflamm of mucous membranes) exudation–> lung consolidation

frequently chronic infection- persists months/years

secondary consequences.

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7
Q

Secondary consequences to mycoplasma hypopneumoniae

A

immunocompromise

secondary infections:

pasturella multocida, actinobacillus pleuropneumoniae, hemophilus parasuis, bordetella bronchiseptica, streptococcus suis

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8
Q

Contagious pleuropneumonia: acute/peracute respiratory mycoplasmosis

A

Contagious bovine pleuropneumonia-CBPP and Contagious caprine pleuropneumonia- CCPP

Notifiable diseases

acute/per-acute usually, occasionally sub-acute/chronic

high mortality, highly contagious, remission and re-activation, get chronic carriers

mononuclear cell infiltration and proliferation

neutrophil infiltration–> necrosis

fluid exudation, vascular inflammation.

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9
Q

Hemotrophic mycoplasmas- hemoplasmas

A

Feline hemolytic anemia: hemobartonella felis

mycoplasma hemofelis

Porcine eperythrozoonosis: eperythrozoon suis

Mycoplasma (hemo)suis

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10
Q

General features of hemotrophic mycoplasmas

A

erthryocyte associated

unculturable

predisposed by intercurrent infection? i.e. feline infectious anemia predisposed by FeLV? and porcine eperytthrozoonosis predisposed by procine reproductive and respiratory syndrome virus?

Transmission: in utero? iatrogenic? arthropod? cuts, scratches, bites?

Detected in an increasing range of mammalian hosts

Emerging genus of RBC parasitic/pathogenic mycoplasma

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11
Q

Infection scheme of hemotrophic mycoplasma

A

mycoplasma haemx–> entry into circulation–> adhere to erthyrocytes

adherence to RBCs causes 1) indentations/rupture due to degradative enzymes or 2) autoimmunity

both 1 and 2 causes erthyrocyte lysis and consequent anemia.

cross-species tranmission suggests zoonotic potential.

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12
Q

Control of mycoplasmoses

A

test and slaughter

disease free herds/flocks

selective breeding

ABX chemotherapy: obviously don’t target cell wall synthesis (i.e. beta lactones or cyclosporins). use ABX that inhibit protein synthesis (i.e. tetracycline, chloramphenicol, macrolides, aminoglycosides) or that inhibit DNA replication (fluoroquinolones).

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