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| − | {{review}}
| + | #REDIRECT[[:Category:Mycobacterium species]] |
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| − | {{toplink
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| − | |backcolour =
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| − | |linkpage =Bacteria
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| − | |linktext =BACTERIA
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| − | |pagetype=Bugs
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| − | <br>
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| − | ===Overview===
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| − | *Mycobacterial infections are caused by bacteria belonging to the family Mycobacteriaceae, order Actinomycetales
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| − | *Includes obligate pathogens, opportunistic pathogens and saprophytes
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| − | *Cause chronic, progressive, granulomatous infections
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| − | *Cause tuberculosis, [[Intestines Proliferative Enteritis - Pathology#Paratuberculosis (Johnes disease)|Johne's disease]] and feline leprosy
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| − | *''M. bovis'', ''M. tuberculosis'' and ''M. avium'' cause [[Respiratory Bacterial Infections - Pathology#Tuberculosis|tuberculosis of cattle]], [[Respiratory Bacterial Infections - Pathology#Tuberculosis in pigs|tuberculosis of pigs]] and [[Respiratory Bacterial Infections - Pathology#Tuberculosis in dogs|tuberculosis of dogs]] respectively
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| − | *The 'classical' tuberculosis lesions are caused by the [[Mycobacterium tuberculosis complex]]
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| − | *The Johne's type lesions are caused by the [[Mycobacterium avium complex]]
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| − | *Environmental species are found in soil, vegetation and water
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| − | *''Mycobacterium leprae'' and ''M.lepraemurium'' cause human, feline and murine leprosy
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| − | *Atypical mycobacteriosis is a localized opportunistic skin and subcutaneous infection caused by saprophytic and rapidly growing atypical mycobacteria
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| − | *Granulomatous lesions in [[Muscles Inflammatory - Pathology#Tuberculosis|muscle]] and[[Bacterial skin infections - Pathology#Bacterial granulomatous dermatitis|skin]]
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| − | ===Characteristics===
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| − | *Aerobic, weakly Gram-positive acid-fast rods
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| − | *Non-motile, non-spore forming
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| − | *Cell walls contain mycolic acid
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| − | *Require egg-based media for growth
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| − | *Slow-growing colonies
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| − | *Resistant to disinfectants and environmental conditions; susceptible to pasteurisation
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| − | *Mycobacteria stain with carbol dyes and resist subsequent decolorization with inorganic acids; this characteristic which is due to the spatial arrangement of mycolic acids within the cell wall makes them acid fast
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| − | ===Identification===
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| − | *Identified by Ziehl-Neelson staining
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| − | *Differentiated by culture, biochemical tests, chromatography and molecular techniques
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| − | *Pathogenic species require at least three weeks for growth on egg-based media
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| − | ===Bovine tuberculosis===
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| − | *Epidemiology
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| − | **World-wide disease caused by ''M. bovis''
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| − | **Aerosol transmission between cattle kept in close contact
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| − | **Transmission to calves via ingestion od contaminated milk
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| − | **Wildlife reservoirs include badgers and possibly deer in the Europe
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| − | *Pathogenesis and pathogenicity
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| − | **The ability of mycobacteria to survive and multiply within macrophages determines whether disease will occur within the host
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| − | **Survival and multiplication in macrophages at primary site of infection due to prevention of phagosome-lysosome fusion
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| − | **Mycobacteria utilize several virulence factors including cord factor or trehalose dimycolate, surface glycolipid, sulfatides, lipoarabinomannan, heteropolysaccharide, heat shock protein, complement, and tubuloprotein
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| − | **The types of immune responses that are critical in responding to mycobacterial infection are cell-mediated immunity and the delayed hypersensitivity response
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| − | **Pathogenicity of mycobacteria depends on their ability to escape phagocytic killing, mostly imparted by the cell wall consitiutents:
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| − | ***Cord factor (trehalose dimycolate) – surface glycolipid responsible for serpentine growth in vitro
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| − | ***Suphatides – surface glycolipid containing sulphur which prevents fusion of phagosome with lysosome. cAMP secreted by the bacteria may also facilitate this.
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| − | ***LAM – heteropolysaccharide which inhibits macrophage activation by IFNγ and induces macrophages to secrete TNFα which induces fever and IL-10 which suppresses mycobacteria-induced T cell proliferation
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| − | ***The wax of the cell wall, peptidoglycans and other glycolipids are responsible for the adjuvant activity – attracts antigen presenting cells
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| − | ***Tubuloprotein – important antigen; purified tubuloprotein is the basis of the tuberculin test
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| − | **Mycobacteria are released from macrophages and also migrate within macrophages around the body
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| − | **Waxy cell wall contributes to the host immune response to the mycobacteria and the development of lesions
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| − | **Cell-mediated immune response with activated macrophages and sensitised T cells
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| − | **Delayed-type hypersensitivity response with granuloma formation
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| − | **Lesions contain macrophages, multinucleate giant cells and later a central area of caseous necrosis, giving a cheesy appearance
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| − | *Clinical signs
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| − | **Initially asymptomatic
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| − | **Loss of condition
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| − | **Cough and intermittent pyrexia with lung pathology
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| − | **Tuberculous mastitis with transmission via milk
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| − | *Diagnosis
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| − | **Tuberculin test - comparative intradermal test
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| − | **Avian and bovine tuberculin (purified protein derivative) is injected intradermally into two different clipped sites on the side of the neck
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| − | **Skin thickness at these sites is compared before and 72 hours after the injection of tuberculin with calipers
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| − | **Increases in skin thickness at the bovine PPD site of more than 4cm greater than the avian PPD site are seen as positive (reactor)
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| − | **Blood tests including the gamma interferon assay are being developed
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| − | **Laboratory examination of lesions, lymph nodes and milk
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| − | **Ziehl-Neelson staining of tissues
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| − | **Isolation requires Lowenstein-Jensen medium
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| − | *Control
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| − | **Eradication programs using a test and slaughter policy
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| − | **Reactors positive to the tuberculin test are slaughtered and restrictions applied to the affected herd
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| − | ===Avian tuberculosis===
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| − | *Caused by members of the ''M avium'' complex
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| − | *Depression, loss of condition and lameness in affected birds
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| − | *Granulomatous lesions in liver, spleen, bone marrow and intestines
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| − | *Diagnosis by Ziehl-Neelson staining of smears and post-mortem appearance
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| − | *Tuberculin testing of poultry
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| − | ===Feline leprosy===
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| − | *Caused by ''M. lepraemurium''
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| − | *Sporadic infections of cats via bites from infected rodents
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| − | *Subcutaneous nodules form usually on the head or limbs and can ulcerate
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| − | *Smears reveal Ziehl-Neelson-positive rods
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| − | *Diagnosis by histopathology
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| − | *Treatment includes excision of lesions
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| − | ===[[Intestines Proliferative Enteritis - Pathology#Paratuberculosis (Johnes disease)|Johne's Disease (paratuberculosis)]]===
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| − | *[[Intestines Proliferative Enteritis - Pathology#Paratuberculosis (Johnes disease)|Johne's Disease]] is a chronic, contagious enteritis of ruminants
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| − | *Caused by ''M avium'' subsp. ''paratuberculosis''
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| − | *Epidemiology
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| − | **Transmitted to young calves by ingestion of mycobacteria in faeces of infected adults
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| − | **Organisms viable in environment for long periods
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| − | **Long incubation period with clinical signs appearing in cattle over 2 years of age
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| − | **Subclinical carriers can occur, shedding organisms in their faeces
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| − | *Pathogenesis and pathogenicity
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| − | **''M avium'' subsp. ''paratuberculosis'' is an intracellular pathogen
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| − | **Mycobacteria are ingested by macrophages in the Peyer's patches
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| − | **Survival and replication of mycobacteria in macrophages initiate an immune-mediated granulomatous reaction
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| − | **Lymphocytes and macrophages accumulate in the lamina propria and submucosa, resulting in marked thickening and folding of the intestinal wall
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| − | **Mesenteric lymph nodes are enlarged
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| − | **A protein-losing enteropathy results, along with failure to absorb nutrients and water
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| − | *Clinical signs
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| − | **Diarrhoea, initially intermittent, and weight loss in cattle
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| − | **Weight loss in sheep and goats
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| − | **Rapidly fatal with weight loss and diarrhoea in some deer
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| − | *Diagnosis
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| − | **All diagnostic procedures have faults but include:
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| − | **Microscopy of rectal biopsies
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| − | **Faecal culture
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| − | **Serology of serum including complement fixation tests, agar-gel immunodiffusion test and an ELISA
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| − | **Histopathology of intestines and lymph nodes
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| − | **Isolation and identification of mycobacteria from faeces and tissues
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| − | **Ziehl-Neelson-positive smears
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| − | **Intradermal tuberculin test
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| − | **DNA probes for detection in faeces
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| − | *Control
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| − | **Slaughter of affected animals
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| − | **Detection and slaughter of subclinical shedders using faecal culture, DNA probes and ELISA
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| − | **Good hygiene to protect young calves
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| − | **Separation and isolation of calves from affected dams
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| − | **Inactivated adjuvanted vaccines are available and reduce shedding of mycobacteria but do not eliminate infection
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