Difference between revisions of "Mycobacteria spp."

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

Latest revision as of 10:44, 14 May 2010