MYCOPLASMA SPECIES INTRODUCTION? Mycoplasma coming under the classMollicutes.There are 9 genera in theclass Mollicutes. Thus class Mollicutes have 3 families are Mycoplasmataceae,Acholeplasmataceae, Anaeroplasamataceae . From that 9 genera , 5 are veterinary importance (Mycoplasma, Ureaplasma,Acholeplasma,Anaerplasma,Asteroplasma) .There are 100 spp in the Mycoplasma genus .
First Mycoplasma identified in 1890 was Mycoplasma mycoides subsp mycoides .Similar types of Mycoplasmas weresubsequently identified called as Pleuro Pneumonia Like Organisms (PPLO).Mycoplasma is a genus of bacteria that lack a cellwall aroundtheir cell membrane.1 Without a cell wall, they areunaffected by many common antibiotics such as penicillin or other beta-lactam antibiotics that target cell wallsynthesis.? Generally Mycoplasma are Prokaryotes, have capable of replication. Pleomorphic organisms which will appear as spherical , filaments .They do not have cellwall so they cannot synthesizespeptidoglycan .
However they have 3 layered flexible outer membranewhich will causes the flexibility property of that organism . Flexibility: Allows to passthrough bacterial membrane filters (0.22 to 0.45µ) .Sensitive to heat , dessication, detergentsbut they resistant to penicillinHABITAT: -Mycoplasmaorganisms found on mucosal surfaces of conjunctiva ,nasal cavity, oro-pharynx,intestinal, genital tract .
Theseare extracellular organisms.Generally host specific in nature.PATHOGENESIS: -Parasiticmycoplasms tend to adhere firmly to host’ s mucous membrane (adhesin). There they producehaemolysins, proteases, nucleases, other lethal factors that leads to death of cells. Somemycoplasmal organisms have predilectionsite in mesenchymal cells – joints, serous cavities.
Respiratory tract and lungs – frequent site of the pathogenic organisms. It destroys the cilia of respiratory tract thereby causes 2° bacterial invasion .Latency can occur in that microbial pathogenecity .Stress , intercurrent infection & agepredisposes the disease .Infectionsmay be chronic or low grade and theyare exogenous or endogenousLABORATORY DIAGNOSIS:-Specimens:? Samples are fragile in nature , it should be kept at refrigerated condition and delivered to a laboratory within24 – 48 hours of collection .Samples :Mucosal scrapings, tracheal exudates, aspirates, pneumonic tissue from the edge oflesion , cavity or joint fluids, mastitis milk Isolation : -Mycoplasmaare fastidious organisms, facultative anaerobes, 5-10% CO?. It requires enriched media for growth .
Basic medium is a good quality beefinfusion with supplements pH ofthe medium – 7.2 to 7.8. Commercially available agar or broth (supplementedwith horse serum 20% and yeast extract with amino acid).
Penicillin – inhibitionof gram positive, Thallous acetate- inhibition of gram negative . Specimenshould be inoculated into 2 broths (2 agar plates 1 for mycoplasm,1 for ureaplasm).Fluidmaterial (fetal fluids , exudates)- directly inoculated into broth and agarmedium. Some specimens (semen, joint fluids, tissues) contain inhibitors ofmycoplasms. Both undiluted specimen & ten fold dilutions in mycoplasmalbroth should be culturedIDENTIFICATION: -Differentiation from bacterial L forms 😕 Some bacteria temporarily failed to form cellwalls (L forms) can produce microcolonies similar to the mycoplasms .
Staining of microcolonies with Diene ‘s stain – aids indifferentiation between L and mycoplasmal colonies .Mycoplasmal colonies retain stain L formdecolorise within 15 mins COLONIAL MORPHOLOGY:-Microscopic examination:-? Appear asfried egg colonies. Diene’s stain – recognizes microcolonies . Inoculated agar plates placed in a humid atm.
at 37°CIDENTIFICATION OF THEGENUS: -Sensitivityto digitonin 😕 Mycoplasma and urea plasma aresensitive to digitonin.Doneby digitonin disc applied on the agar media .Positive – Zone of inhibition should be 5 mm ormoreIDENTIFICATION OFSPECIES: -Fluorescent antibody staining: To identify M.dispar and Ureaplasm – bronchial epithelium of calves FA (directand indirect) for staining mycoplasmal colonies and for recognizing mixed cultures.
Commonly used in avian mycoplasms.Enzymelinked immunoperoxidase: Porcinebronchial epithelium – M.hyopneumoniae . AGID- Using known antisera to detectmycoplasmal ag .ELISA – ag identification with known antisera .Speciesspecific DNA probes areavailable.
Antibiotic susceptibility: Although it develop resistant to antimicrobial drugs .So ABST not usually performed.Tylosin, tetracyclin,tiamulin, fluroquinolones used for treatment .Specific pathogenfree (SPF ) programmes established for poultry and pig herds.There are 2phases in these programmes 1)Detection of infections and culling or isolation of affected animals.2)Followed by serological monitoringof the flocks to demonstrate continued freedom from infection CLINICAL INFECTIONSContagiousbovine pleuropnumonia caused by M.mycoides subsp.
mycoides(small colonytype),Contagious caprine pleuropneumonia caused by M.capricolumsubsp.capripneumoniae ,Contagious agalactiae of sheep and goats are caused byM.agalactiae, Enzootic pneumonia of pigs are caused by M.hyopneumoniae, Chronicrespiratory disease caused by M.
gallisepticum, Feline infectious anaemia causedby M.haemofelis.CBPP:-· CHARACTERISTIC STANCE – Head, neck, extended andelbow abducted .Postmortem lesions are marbledappearance lung . Grey , red consolidated lobulesalternate irregularly with pink emphysematous lobules. Chronic : fibrinous encapsulation ofnecrotic foci (viable mycoplasms).
Break down of capsules is major factor in the persistenceand spread of CBPP. Joints – fibrin insynovial space & articular cartilage erosion CCPP: -? Highly contagious disease.Incubation period : 6-10 days Transmission is by direct contact.Post mortem lesions are granular lung appearance and fibrinous pneumoniaCRD: -? Highly versatile and successfulpathogen . Once infected, it remains for life. Transmission is mainly Vertical transmission.
Economically significant disease. Post mortem lesions are Sinusitis,conjunctivitis, tracheitis withexcessive mucous , air sacculitis , pneumonia , synovitis, osteomyelitis