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58 Cards in this Set

  • Front
  • Back
Class Mollicutes
-"soft skin": no rigid cell wall
-pathogenic genera: Mycoplasma, Ureaplasma
Mycoplasmas general characteristics
-smallest prokaryotes
-0.12-0.5 nm
-smallest self replicating organisms
-small genome (0.6Mb)
-reduced metabolic capacity; lack many genes for biosynthesis
-slow growth
-enriched media: require exogenous cholesterol for cell membrane stability
Mycoplasmas cell make up
-no peptidoglycan in cell wall
-trilaminar plasma membrane (triple layered membrane)
-refractory to many antibiotics: can't treat with penicillin!
Mycoplasmas epidemiology
-mucus surfaces: conjunctiva, nasal cavity, oropharynx, intestinal and genital tracts of animals
-environment: fragile, don't persist for long periods in environment (because they don't have rigid cell wall)
-last for 3 days in the environment in tropical areas and up to 2 weeks in temperate zone
-host specific
Mycoplasmas pathogenesis
-no "classic" toxins
-adherence to host cells vital for virulence
-production of ROS (reactive oxygen species)
-antigenic variation of surface proteins: immune invasion
Mycoplasmas pathogenesis: adherence
-needed for colonization of epithelial surfaces
-avoids physical removal by mucociliary activity
-attachment organelle located at bacterial pole serves to localize adhesins
Mycoplasmas pathogenesis: production of ROS
-leads to tissue damage
-cell lysis, lipid peroxidation, etc.
Mycoplasmas pathogenesis: capsule
-injection of the MmmSC capsule into calves evokes pulmonary edema
pathogenic effects of mycoplasmas
Diagnosis of mycoplasmas
-fresh samples: nasal swabs and/or broncho-alveolar washings (immediate transport, refrigeration, transport medium)
-isolation of bacteria
Diagnosis of mycoplasmas: enriched media for isolation
-sterol source
-serum and yeast extract
-inhibitors (e.g. penicillin)
-37 degrees C up to 14 days
-fried egg microcolonies (very small: 0.1-0.6mm)
-sterol source
-serum and yeast extract
-inhibitors (e.g. penicillin)
-37 degrees C up to 14 days
-fried egg microcolonies (very small: 0.1-0.6mm)
Contagious bovine pleuropneumonia (CBPP)
-severe contagious disease of cattle
-claimed to have caused more cattle deaths worldwide than any other disease except rinderpest
-caused by MmmSC
-only bacterial OIE (world organisation for animal health) List A disease
-Mycoplasma mycoides subspecies mycoides Small Colony type
-identifies in 1898 by Nocard and Roux
Contagious bovine pleuropneumonia (CBPP): OIE List A disease
"potenital for a very serious and rapid spread irrespective of national borders, or serious socio-economic or public health consequence, and of major importance in the international trade of animals and animal products"
CBPP: History/evolution
-molecular analysis distinguishes 3 main lineages of MmmSC: correlates with their geographical origins
-introduced to South Africa in 1853
-bulls imported from Netherlands
-spread rapidly through cattle production
-contributed to the mid-19th century decimation of the Xhosa people
-present in Northern Africa prior to 1853
CBPP: Strains of European origin
-not able to oxidize glycerol
-glycerol metabolism linked to H2O2 production
-may account for lower pathogenicity
CBPP: distribution
USA, Canada, most of Europe
-eradication 19th century
-persistent infection parts of Italy, Spain, Portugal in 1990s
-Portugal officially free 2003
CBPP: distribution
-endemic in many sub-Saharan countries (30 countries)
-most important cattle disease in Africa
-2 billion annual losses
CBPP: distribution
Asia and South America
-problem in China and India
-Never reported in South America
CBPP transmission
-aerosol spread
-close contact
-incubation 4-6 weeks
-naive cattle populations: up to 50% mortality, close to 100% morbidity
CBPP: variation in disease expression
-acute, subacute, chronic and unapparent forms
-epidemics: acute cases predominate initially
-as epidemic progresses, sub acute and chronic presentations more frequent
-hence difficult to detect clinical cases of CBPP in endemic areas
Acute case of CBPP
-characteristic stance: elbows abducted, head extended, arched back
-respiratory distress
-15-20 litres of pleural fluid in chest cavity
-characteristic stance: elbows abducted, head extended, arched back
-respiratory distress
-15-20 litres of pleural fluid in chest cavity
CBPP port mortem
-"marbling" (thickened intralobar septa): subacute lesion
-"sequestra" (fibrotic capsule containing necrotic lung tissue/dead bacteria): chronic lesion
CBPP diagnosis
-herd serology: CFT (compliment fixation test), ELISA
-isolation of bacteria: slow
CBPP prevention and control: exotic
-control imports
-slaughter of affected and in-contact
CBPP prevention and control: endemic regions
-control animal movement (difficult sub-saharan africa)
-attenuated live vaccine available: not 100% effective, may lead to increases in subclinical infection
-antibiotic treatment not used: illegal in many countries; thought to lead to carrier/subclinical animals and accelerated sequestra development
Mycoplasma bovis
-pneumonia in calves
-one of the causative agents of "enzootic pneumonia of calves" along with a range of other viruses and bacteria (such as RSV, PI3, M. haemolytica and P. multocida)
-stress as a precipitating factor
-also a cause of mastitis and arthritis
-reservoir and transmission: respiratory tract and milk
-affected cow can shed bacteria in milk
Lung of calf with Mycoplasma bovis
Arthritic joint from calf with Mycoplasma bovis
Mycoplasma bovis diagnosis
-clinical signs and pathological lesions of M. bovis infection are not distinctive
-laboratory diagnosis necessary for identification
Mycoplasma bovis diagnosis: individual
-isolation of M. bovis: lower respiratory tract (bronchoaveolar lavage)
-immunohistochemistry against Mycoplasma antigen in infected tissue
Mycoplasma bovis diagnosis: herd
-serology: indirect ELISA
Mycoplasma bovis treatment and control
-pneumonia treatment: prolonged antibiotic therapy (2-3 weeks; tetracyclines)
-no vaccine
-mastitis: cull, no treatment, highly infectious
-pneumonia: improve management and environment
Contagious agalactia
-M. agalactiae main cause in sheep and goats
-found in Mediterranean, western Asia, North Africa
-can be asymptomatic, acute, or chronic
Contagious agalactia clinical signs
-in lambs and kids: losses due to septicemia and pneumonia
Contagious caprine plearopneumonia (CCPP)
-M. capricolum subsp capripneumoniae
-one of the most sever diseases in goats
-respiratory disease: extremely contagious and frequently fatal
-naive flocks: morbidity up to 100%, mortality up to 80%
-causes major economic losses in endemic countries (E.g. East Africa and the Middle East)
CCPP clinical signs
-coughing, labored breathing
-lesions confined to thoracic cavity
CCPP diagnosis and control
-diagnosis: culture or PCR (preferred)
-some antibiotics, such as tetracycline, can be effective if given early
-vaccine available: inactive Mccp (provides protection for over 1 year)
Atypical pneumonia
-M. ovipneumoniae
-sheep and goats
-most commonly isolated mycoplasma from the respiratory tract of normal sheep
-disease linked to intensive management: stress triggers atypical pneumoniae (through inhibition of ciliary activity)
Atypical pneumonia: clinical signs and diagnosis
-chronic cough
-co-infection with Mannheimia haemolytica produces a more severe pathology
-PCR and ELISA for detection
Ovine infectious keratoconjuntivitis
-mycoplasma conjunctivae
-lambs: conjunctivitis
-adults: keratitis and corneal ulceration
Ovine infectious keratoconjuntivitis: diagnosis and control
-PCR or immunoflourescent antibody test (IFAT) on smears
-topical oxytetracycline for treatment (3-4 times/day)
-increase trough space, treat all additions to flock
-widespread throughout UK/Ireland
Mycoplasma hypopneumoniae
-causes porcine enzootic pneumoniae
-transmission: aerosol, close contact
Mycoplasma hypopneumoniae: pathology and clinical signs
-M. hyponeumoniae attaches to cilia, causing clumping and destruction
-loss of cilia function: invasion by secondary infections
-persistent dry cough
-loss of weight gain
Mycoplasma hypopneumoniae: diagnosis and control
-PCR, FAT, serology
-improved ventilation and housing
Pig Mycoplasmas
Mycoplasma diseases of poultry: M. gallisepticum
-chronic respiratory disease in chickens
-high morbidity, low mortality
-infectious sinusitis in turkeys
-infection for life
-egg transmission
-mild disease unless secondary invasion by E.coli (increased pathology)
-chronic respiratory disease in chickens
-high morbidity, low mortality
-infectious sinusitis in turkeys
-infection for life
-egg transmission
-mild disease unless secondary invasion by E.coli (increased pathology)
Mycoplasma diseases of poultry: M. synoviae
-infectious synovitis (inflammation of synovial membrane) in chickens and turkeys
-upper respiratory infection which may become systemic and spread to joints
-infection by contact
Mycoplasma diseases of poultry: M. meleagridis
-egg transmission and AI
-reduced growth, hatchability, sinusitis, skeletal abnormalities
Mycoplasma diseases of poultry: diagnosis and treatment
-isolation of pathogen, ELISA, or PCR
-antimicrobials active against Mycoplasma and secondary invaders (e.g. macrolides)
-live vaccine available
Mycoplasma diseases of poultry: eradication
-improve hygiene and management
-treat breeder layers and eggs
-monitor for infection (seropositives) and cull positives
Haemotropic mycoplasmas (aka haemoplasmas)
-formerly known as Haemobartonella and Eperythrozoon
-small (<1nm)
-pleomorphic bacteria that attach to RBC of various mammalian species
-until 2000, classified with Rickettsia
-16S rDNA gene sequencing revealed closer relationship to the class Mollicute: reclassified as Mycoplasma
Haemotropic mycoplasmas include:
-Mycoplasma haemofelis (Haemobartonella felis)
-Mycoplasma haemocanis (Haemobartonella canis)
-Mycoplasma (Eperythrozoon) suis
-Mycoplasma (Eperythrozoon) ovis
-Mycoplasma (Eperythrozoon) wenyonii
the haemoplasmas
-parasitize erythrocytes: adhere to erythrocyte surface
-coccoidal shape, small <0.9 nm
-cannot cultivate in vitro
-stain well with Romanowsky-type stains: mixtures of methylene blue, azure, and eosin compounds (e.g Giesma)
-transmitted by arthropods
-sensitive to tetracyclines
-resistant to penicillin
Mycoplasma (Haemobartonella) haemofelis
-feline infectious anaemia (FIA)
-common infection worldwide
-large % population latent carriers
Feline infectious anaemia (FIA) tranmission
-biting, fighting (young tom cats)
-blood transfusion
-biting arthropods
Feline infectious anaemia (FIA) clinical signs
-immunosuppression/stress precipitates clinical episode
-acute: fever, jaundice, anaemia, splenomegaly
-chronic: weakness, emaciatin, anaemia
-autoimmune attack on the parasitized cells: anaemia
-25-30% mortality
-lifelong carrier status in animals that survive
Feline infectious anaemia (FIA) diagnosis and treatment
-blood smears over several days (cocci or rods on surface of erythrocytes)
-cyclical bacteremia
-haematology: anaemia
-concurrent FeLV or FIV infections: immunosupression worsen the anaemia
-treat with tetracycline