Podcast
Questions and Answers
What is the common outcome of the nodules in the nasal form of Glanders?
What is the common outcome of the nodules in the nasal form of Glanders?
What is the primary method of diagnosis for Glanders?
What is the primary method of diagnosis for Glanders?
What is a common outcome of untreated Glanders in the lungs?
What is a common outcome of untreated Glanders in the lungs?
In which organs can nodules be seen in the Cutaneous form of Glanders?
In which organs can nodules be seen in the Cutaneous form of Glanders?
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What is the primary reason antimicrobials are not used to treat Glanders?
What is the primary reason antimicrobials are not used to treat Glanders?
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What is the significance of 'star-shaped' cicatrices in Glanders?
What is the significance of 'star-shaped' cicatrices in Glanders?
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What is the result of the Mallein test in hypersensitive horses?
What is the result of the Mallein test in hypersensitive horses?
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What is the fate of equine imports that test positive for Glanders?
What is the fate of equine imports that test positive for Glanders?
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What is the histological feature of Glanders?
What is the histological feature of Glanders?
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What is a consequence of the Pulmonary form of Glanders?
What is a consequence of the Pulmonary form of Glanders?
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Which species of Burkholderia is associated with Glanders?
Which species of Burkholderia is associated with Glanders?
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What characteristic is shared by both Burkholderia mallei and Burkholderia pseudomallei?
What characteristic is shared by both Burkholderia mallei and Burkholderia pseudomallei?
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Which of the following is the most common source of infection for Glanders in animals?
Which of the following is the most common source of infection for Glanders in animals?
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Which region is NOT mentioned as endemic for Glanders?
Which region is NOT mentioned as endemic for Glanders?
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What is the incubation period range for acute Glanders?
What is the incubation period range for acute Glanders?
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Which animals are particularly susceptible to Glanders?
Which animals are particularly susceptible to Glanders?
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Which of the following is not a clinical sign of acute Glanders?
Which of the following is not a clinical sign of acute Glanders?
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What is the primary way Burkholderia mallei enters the body?
What is the primary way Burkholderia mallei enters the body?
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What categorizes Burkholderia mallei as a bioterrorism agent?
What categorizes Burkholderia mallei as a bioterrorism agent?
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Which factor is NOT listed as influencing the manifestation of Melioidosis?
Which factor is NOT listed as influencing the manifestation of Melioidosis?
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What characteristic differentiates Burkholderia pseudomallei from Gleners in terms of host range?
What characteristic differentiates Burkholderia pseudomallei from Gleners in terms of host range?
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In which condition is Melioidosis NOT typically presented?
In which condition is Melioidosis NOT typically presented?
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What is a unique aspect of Burkholderia pseudomallei's natural habitat?
What is a unique aspect of Burkholderia pseudomallei's natural habitat?
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What route of transmission is unique to goats for Burkholderia pseudomallei?
What route of transmission is unique to goats for Burkholderia pseudomallei?
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Which typical feature of Burkholderia pseudomallei is true regarding its interaction with environment?
Which typical feature of Burkholderia pseudomallei is true regarding its interaction with environment?
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Which of the following is NOT a transmission method for Burkholderia pseudomallei?
Which of the following is NOT a transmission method for Burkholderia pseudomallei?
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Which descriptor is NOT characteristic of the type of disease caused by Burkholderia pseudomallei?
Which descriptor is NOT characteristic of the type of disease caused by Burkholderia pseudomallei?
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Which species is affected by conditions mimicking glanders?
Which species is affected by conditions mimicking glanders?
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What type of lesions are primarily observed in melioidosis pathology?
What type of lesions are primarily observed in melioidosis pathology?
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Which of the following animals can show clinical signs similar to goats in the case of melioidosis?
Which of the following animals can show clinical signs similar to goats in the case of melioidosis?
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What is characteristic about the bacteria's survival mechanism within the cell?
What is characteristic about the bacteria's survival mechanism within the cell?
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Which species has febrile and localized suppurative foci as symptoms?
Which species has febrile and localized suppurative foci as symptoms?
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Which feature is common to all members of the genus Bordetella?
Which feature is common to all members of the genus Bordetella?
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Where is melioidosis endemic in humans?
Where is melioidosis endemic in humans?
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Which mechanism allows microorganisms to move within the host cell during melioidosis?
Which mechanism allows microorganisms to move within the host cell during melioidosis?
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What is the characteristic shape of Bordetella bacteria?
What is the characteristic shape of Bordetella bacteria?
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What is the primary function of the Tracheal cytotoxin?
What is the primary function of the Tracheal cytotoxin?
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Which toxin is responsible for increasing intracellular concentration of cAMP levels?
Which toxin is responsible for increasing intracellular concentration of cAMP levels?
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Which Bordetella species is responsible for causing whooping cough in humans?
Which Bordetella species is responsible for causing whooping cough in humans?
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What is the primary method of transmission for Bordetella spp.?
What is the primary method of transmission for Bordetella spp.?
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Which virulence factor is responsible for biofilm formation in Bordetella spp.?
Which virulence factor is responsible for biofilm formation in Bordetella spp.?
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What is the primary function of the Osteo Toxin?
What is the primary function of the Osteo Toxin?
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Which toxin is responsible for hemolytic and pore-forming activity?
Which toxin is responsible for hemolytic and pore-forming activity?
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What is the significance of Multiple Iron Acquisition Systems in Bordetella spp.?
What is the significance of Multiple Iron Acquisition Systems in Bordetella spp.?
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Which virulence factor is responsible for the inhibition of differentiation of osteoblasts in bone tissues?
Which virulence factor is responsible for the inhibition of differentiation of osteoblasts in bone tissues?
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What is the primary mechanism of action of the Pertussis toxin?
What is the primary mechanism of action of the Pertussis toxin?
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Which effect is directly caused by the bacterial attachment of Bordetella to ciliated epithelial cells?
Which effect is directly caused by the bacterial attachment of Bordetella to ciliated epithelial cells?
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What is a common consequence of Bordetella interference with phagocytosis in the host?
What is a common consequence of Bordetella interference with phagocytosis in the host?
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What typically characterizes the catarrhal phase of Bordetella infection?
What typically characterizes the catarrhal phase of Bordetella infection?
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Which event in the pathogenesis of Bordetella contributes to secondary pneumonia?
Which event in the pathogenesis of Bordetella contributes to secondary pneumonia?
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What outcome is linked to the production of ciliostasis by Bordetella?
What outcome is linked to the production of ciliostasis by Bordetella?
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How does Bordetella contribute to progressive atrophic rhinitis in pigs?
How does Bordetella contribute to progressive atrophic rhinitis in pigs?
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What is the primary factor in Bordetella's ability to avoid immune clearance in the host?
What is the primary factor in Bordetella's ability to avoid immune clearance in the host?
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Which clinical sign is uncommon but may occur during the catarrhal phase of Bordetella infection?
Which clinical sign is uncommon but may occur during the catarrhal phase of Bordetella infection?
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What is the consequence of Bordetella-induced loss of iron regulation in tracheal epithelial cells?
What is the consequence of Bordetella-induced loss of iron regulation in tracheal epithelial cells?
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Which pathology phase includes rhinitis and sinusitis?
Which pathology phase includes rhinitis and sinusitis?
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What ages of piglets are most commonly affected by primary pneumonia caused by Bordetella bronchiseptica?
What ages of piglets are most commonly affected by primary pneumonia caused by Bordetella bronchiseptica?
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Which pathogen is responsible for the progressive form of atrophic rhinitis in swine?
Which pathogen is responsible for the progressive form of atrophic rhinitis in swine?
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Which of the following is NOT commonly associated with Bordetella bronchiseptica infections in young dogs?
Which of the following is NOT commonly associated with Bordetella bronchiseptica infections in young dogs?
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Which clinical sign is NOT typically associated with Bordetella bronchiseptica infection in cats?
Which clinical sign is NOT typically associated with Bordetella bronchiseptica infection in cats?
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What is a key characteristic of Bordetella bronchiseptica pneumonia in dogs?
What is a key characteristic of Bordetella bronchiseptica pneumonia in dogs?
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Which of the following is a common outcome of a Bordetella bronchiseptica infection in guinea pigs?
Which of the following is a common outcome of a Bordetella bronchiseptica infection in guinea pigs?
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What is the usual outcome for dogs recovering from canine infectious tracheobronchitis without treatment?
What is the usual outcome for dogs recovering from canine infectious tracheobronchitis without treatment?
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What is a key difference in the respiratory diseases caused by Bordetella bronchiseptica in cats compared to dogs?
What is a key difference in the respiratory diseases caused by Bordetella bronchiseptica in cats compared to dogs?
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What type of infection is Bordetella bronchiseptica in swine subcategorized as when it progresses without Pasteurella multocida involvement?
What type of infection is Bordetella bronchiseptica in swine subcategorized as when it progresses without Pasteurella multocida involvement?
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How long can cats carry Bordetella bronchiseptica asymptomatically following recovery?
How long can cats carry Bordetella bronchiseptica asymptomatically following recovery?
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Which natural habitat is NOT commonly associated with Fusobacterium necrophorum?
Which natural habitat is NOT commonly associated with Fusobacterium necrophorum?
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Which disease is primarily associated with Fusobacterium necrophorum in cattle and has significant economic impact?
Which disease is primarily associated with Fusobacterium necrophorum in cattle and has significant economic impact?
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What condition must be met for Fusobacterium necrophorum to colonize the rumen wall?
What condition must be met for Fusobacterium necrophorum to colonize the rumen wall?
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Which type of abscesses is Fusobacterium necrophorum known to cause in wild ruminants and marsupials?
Which type of abscesses is Fusobacterium necrophorum known to cause in wild ruminants and marsupials?
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Which disease is specifically referred to as 'necrobacillosis'?
Which disease is specifically referred to as 'necrobacillosis'?
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What is the initial cause of liver abscesses secondary to rumen damage in cattle?
What is the initial cause of liver abscesses secondary to rumen damage in cattle?
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Which factor does NOT directly predispose the rumen wall to colonization by Fusobacterium necrophorum?
Which factor does NOT directly predispose the rumen wall to colonization by Fusobacterium necrophorum?
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What sequence correctly describes the pathogenesis starting from the colonization of Fusobacterium necrophorum?
What sequence correctly describes the pathogenesis starting from the colonization of Fusobacterium necrophorum?
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Which type of Fusobacterium necrophorum infection is least associated with economic impacts in cattle?
Which type of Fusobacterium necrophorum infection is least associated with economic impacts in cattle?
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Which anatomical region is primarily involved when Fusobacterium necrophorum causes footrot?
Which anatomical region is primarily involved when Fusobacterium necrophorum causes footrot?
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What is a likely consequence for guinea pigs that survive a bronchiseptica infection?
What is a likely consequence for guinea pigs that survive a bronchiseptica infection?
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Which clinical sign is NOT associated with respiratory infections caused by Bordetella hinzii in birds?
Which clinical sign is NOT associated with respiratory infections caused by Bordetella hinzii in birds?
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What characteristic does Fusobacterium necrophorum share with other members of the genus Fusobacterium?
What characteristic does Fusobacterium necrophorum share with other members of the genus Fusobacterium?
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What allows anaerobic bacteria to survive initial oxygen exposure in infected tissues?
What allows anaerobic bacteria to survive initial oxygen exposure in infected tissues?
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Which species is primarily affected by 'Turkey coryza'?
Which species is primarily affected by 'Turkey coryza'?
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What type of infections can Fusobacterium canifelinum often be isolated from?
What type of infections can Fusobacterium canifelinum often be isolated from?
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Which of the following species is considered a major animal pathogen within the genus Fusobacterium?
Which of the following species is considered a major animal pathogen within the genus Fusobacterium?
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Which product of anaerobic bacteria is known for creating a putrid odor and having cytotoxic effects?
Which product of anaerobic bacteria is known for creating a putrid odor and having cytotoxic effects?
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Which disease in birds is caused by Bordetella avium?
Which disease in birds is caused by Bordetella avium?
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What condition might develop if bronchiseptica infection in guinea pigs is not treated quickly?
What condition might develop if bronchiseptica infection in guinea pigs is not treated quickly?
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What is the main feature that distinguishes Mycobacterium leprae from other species within the Mycobacterium genus?
What is the main feature that distinguishes Mycobacterium leprae from other species within the Mycobacterium genus?
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Which structural characteristic in Mycobacterium species provides resistance against chemicals and antibiotics?
Which structural characteristic in Mycobacterium species provides resistance against chemicals and antibiotics?
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What is the differentiating factor for Mycobacterium caprae within the Mycobacterium TB Complex?
What is the differentiating factor for Mycobacterium caprae within the Mycobacterium TB Complex?
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How is Mycobacterium tuberculosis primarily transmitted?
How is Mycobacterium tuberculosis primarily transmitted?
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Which mycobacterium species is NOT part of the Mycobacterium TB Complex?
Which mycobacterium species is NOT part of the Mycobacterium TB Complex?
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Which Mycobacterium species primarily causes TB-like infections in birds?
Which Mycobacterium species primarily causes TB-like infections in birds?
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What characteristic defines the members of the CMNR group?
What characteristic defines the members of the CMNR group?
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What is the primary method of zoonotic transmission for Mycobacterium bovis?
What is the primary method of zoonotic transmission for Mycobacterium bovis?
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Why is Mycobacterium canettii unique among other Mycobacterium species?
Why is Mycobacterium canettii unique among other Mycobacterium species?
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What is a significant characteristic of Mycobacterium microti?
What is a significant characteristic of Mycobacterium microti?
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What is the primary mediator for driving macrophages to mature and contain Mycobacterium infection?
What is the primary mediator for driving macrophages to mature and contain Mycobacterium infection?
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What is the role of T-helper 1 cells in immunity to mycobacterium infection?
What is the role of T-helper 1 cells in immunity to mycobacterium infection?
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Which factor is crucial for the differentiation of T-helper cells?
Which factor is crucial for the differentiation of T-helper cells?
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How do mycobacteria avoid macrophage activation and bactericidal response?
How do mycobacteria avoid macrophage activation and bactericidal response?
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Which cells form Granulomas or Tubercles during mycobacterial infection?
Which cells form Granulomas or Tubercles during mycobacterial infection?
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What outcome can caseous necrosis in tuberculose lesions lead to?
What outcome can caseous necrosis in tuberculose lesions lead to?
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Which form of Mycobacterium is associated with Crohn's disease in humans?
Which form of Mycobacterium is associated with Crohn's disease in humans?
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What is a common method of transmission for mycobacterial infections in humans?
What is a common method of transmission for mycobacterial infections in humans?
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What type of immune response is key to disease onset after mycobacterial infection?
What type of immune response is key to disease onset after mycobacterial infection?
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Which mycobacterial species is not primarily associated with human infection?
Which mycobacterial species is not primarily associated with human infection?
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What is the primary site of infection in birds infected with M.avium avium?
What is the primary site of infection in birds infected with M.avium avium?
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Which species of animals are susceptible to M.bovis, M.avium paratuberculosis, and M.avium hominissuis?
Which species of animals are susceptible to M.bovis, M.avium paratuberculosis, and M.avium hominissuis?
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What is the common sign of advanced disease in tuberculous infections?
What is the common sign of advanced disease in tuberculous infections?
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What is the primary route of infection for M.avium paratuberculosis in ruminants?
What is the primary route of infection for M.avium paratuberculosis in ruminants?
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Which species of animals are more susceptible to mammalian than to avian mycobacteria?
Which species of animals are more susceptible to mammalian than to avian mycobacteria?
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What is the primary site of infection in dogs infected with M.bovis?
What is the primary site of infection in dogs infected with M.bovis?
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What is the characteristic of lesions in dogs infected with M.bovis?
What is the characteristic of lesions in dogs infected with M.bovis?
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Which species of mycobacteria is commonly found in the environment and causes opportunistic TB-like infections?
Which species of mycobacteria is commonly found in the environment and causes opportunistic TB-like infections?
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What is the incubation period for Johne’s disease?
What is the incubation period for Johne’s disease?
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What is the primary method of transmission for Johne’s disease?
What is the primary method of transmission for Johne’s disease?
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What percentage of infected animals progress to the terminal stage of M.avium paratuberculosis?
What percentage of infected animals progress to the terminal stage of M.avium paratuberculosis?
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What is a characteristic gross appearance of intestinal mucosa in M.avium paratuberculosis?
What is a characteristic gross appearance of intestinal mucosa in M.avium paratuberculosis?
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Which of the following is NOT a cost-effective treatment for M.avium paratuberculosis?
Which of the following is NOT a cost-effective treatment for M.avium paratuberculosis?
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What is the primary role of interferon gamma in the context of TB?
What is the primary role of interferon gamma in the context of TB?
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What is a common feature of feline leprosy syndrome?
What is a common feature of feline leprosy syndrome?
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How is M. bovis typically transmitted?
How is M. bovis typically transmitted?
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What is a common location of lesions in feline leprosy syndrome?
What is a common location of lesions in feline leprosy syndrome?
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What is the result of the binding of mycobacterial cell wall to pattern recognition receptors on macrophages?
What is the result of the binding of mycobacterial cell wall to pattern recognition receptors on macrophages?
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What is a characteristic of the nodules in feline leprosy syndrome?
What is a characteristic of the nodules in feline leprosy syndrome?
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What is the characteristic of the inflammation seen in opportunistic dermal infections in small animals and paraTB in ruminants?
What is the characteristic of the inflammation seen in opportunistic dermal infections in small animals and paraTB in ruminants?
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What is a consequence of not treating feline leprosy syndrome with antimicrobials?
What is a consequence of not treating feline leprosy syndrome with antimicrobials?
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What is the fate of the bacteria in mature tubercles?
What is the fate of the bacteria in mature tubercles?
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What is a feature of M.smegmatis and M.ulcerans infections in cats and dogs?
What is a feature of M.smegmatis and M.ulcerans infections in cats and dogs?
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What is the consequence of reactivation and dissemination of latent TB?
What is the consequence of reactivation and dissemination of latent TB?
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What is a method used for identifying exposed and shedding animals in M.avium paratuberculosis?
What is a method used for identifying exposed and shedding animals in M.avium paratuberculosis?
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What is the primary mechanism by which mycobacteria inhibit the maturation of phagolysosome?
What is the primary mechanism by which mycobacteria inhibit the maturation of phagolysosome?
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What is the best approach for overall herd health in M.avium paratuberculosis?
What is the best approach for overall herd health in M.avium paratuberculosis?
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What is the role of granulomas in the context of TB?
What is the role of granulomas in the context of TB?
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What is the primary difference between M. bovis and M. avium pathogenesis?
What is the primary difference between M. bovis and M. avium pathogenesis?
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What is the outcome of the infection in animals with weak or waning immune responses?
What is the outcome of the infection in animals with weak or waning immune responses?
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Study Notes
Burkholderia Genus
- Gram-negative, aerobic, rod-shaped bacteria
- Found in acidic soil, associated with soil fungi, with over 100 species
- Two species important in veterinary medicine: Burkholderia mallei and Burkholderia pseudomallei, both producing pyogranulomatous disease and designated as category B bioterrorism agents
Glanders Disease (Burkholderia mallei)
- Contagious, acute or chronic, and usually fatal disease
- Characterized by nodule development in upper respiratory tract, lungs, and skin
- Infectious to humans, with 95% fatality rate if left untreated due to septicemia
- Commonly transmitted through contaminated food and water, less commonly through contaminated fomites and aerosols
- Affects horses (Equidae), dogs, cats, camels, goats, and sheep, with felids being particularly susceptible
- Endemic in parts of Asia, Africa, and South America
Acute Glanders Disease
- Incubation period of 3 days to 2 weeks
- Fatal in ~2 weeks, predominantly in donkeys and felids
- Clinical signs include septicemia, high fever, weight loss, thick mucopurulent nasal discharge, respiratory signs, and death
Chronic Glanders Disease
- More common in horses, with donkeys and mules being affected more severely
- Animals may live for years, disseminating the organism
- Three manifesting forms:
- Nasal Form: nodules in nasal mucosa, degenerating into deep ulcers
- Pulmonary Form: small tubercle-like nodules in lungs, with consolidation of lung tissue and pneumonia
- Cutaneous Form ("Farcy"): nodules along lymph vessels, degenerating and ulcerating
Diagnosis and Control of Glanders
- Mallein test: interpalpebral inoculation of mallein, with hypersensitive horses developing purulent conjunctivitis and eyelid swelling within 24 hours
- Treatment with antimicrobials is deemed inappropriate, as it does not reliably produce a cure and infection can remain persistent
- Equine imports from endemic regions are mallein tested, and if positive, euthanized
Burkholderia pseudomallei (Whitmore's Disease)
- Gram-negative, aerobic, rod-shaped bacteria that is facultative intracellular
- Causes pyogranulomatous disease called Melioidosis, affecting a wide host range including humans
- Superficially resembles Glanders, but has a large host range and is a saprophyte
Transmission and Habitat
- Found in soil and water in subtropical and some extratropical regions
- Can be transmitted through direct contact with contaminated soil or surface water, inhalation, ingestion, wound infections, and arthropod bites
- Can also be transmitted transplacental in goats
Melioidosis (Whitmore's Disease)
- Can be systemic or localized, acute, chronic, subclinical, latent, or fulminant
- Manifestation depends on the extent and distribution of the lesions, strain differences, and the host's innate and adaptive immune status
- Treatment is costly, prolonged, and usually unsuccessful, with no commercially available vaccines
Species Diseases
- Horses: mimics Glanders
- Cattle: acute and chronic diseases localizing in lungs, joints, and uterus
- Sheep: arthritis and lymphadenitis
- Goats: loss of condition, respiratory and CNS disturbances, arthritis, and mastitis
- Swine: similar to goats, with abortions and diarrhea
- Dogs: febrile, localized suppurative foci
Epidemiology of Melioidosis
- Clinical disease is usually sporadic
- Endemic in humans in SE Asia and Northern Australia
- Host range is virtually unlimited, with non-mammalian cases documented in birds, tropical fish, and reptiles
- Humans, especially veterinarians, can acquire infection from a wide range of animals
Mechanism of Pathogenesis
- Microorganisms are taken up via phagocytosis and survive inside the cell by being resistant to lysosomal contents and escaping phagosomes and phagolysosomes
- Bacteria gain actin-based motility and undergo 'budding' from affected and unaffected cells
- Infected cells release inflammatory cytokines and undergo apoptosis
Pathology
- Primary pyogranulomatous lesions characterized by single to multiple suppurative or caseous nodules in organs
- Commonly affects lungs, spleen, liver, and associated lymph nodes
- Small abscesses tend to coalesce into large foci
Genus Bordetella
- Gram-negative, small rods that tend to look like coccobacilli
- 16 species, with 3 species causing respiratory diseases in animals
- Found in animal respiratory tracts and has an affinity for ciliated epithelial cells
- Capable of intracellular survival, and healthy animals are carriers for B. bronchiseptica
- Environmental reservoir is amoebae
Bordetella spp. Virulence Factors
- Adhesins, biofilms, LPS, outer membrane proteins, and multiple iron acquisition systems are involved in Bordetella virulence
- Tracheal cytotoxin damages ciliated epithelial cells, interfering with DNA synthesis
- DNT (dermonecrotizing toxin) causes dermal necrosis following injection into the skin
- Exotoxins alter the actin cytoskeleton of affected cells, inhibiting differentiation of osteoblasts in bone tissues, leading to turbinate atrophy
- Adenylyl cyclase toxin has hemolytic and pore-forming activity, increasing intracellular CAMP levels and disrupting iron and fluid regulation
Transmission of Bordetella
- B. bronchiseptica can cause respiratory disease in nearly all animals, primarily through airborne transmission via aerosols
- Environmental contamination and direct transmission through contaminated water and litter are also significant factors
- B. avium is directly transmitted in turkeys via contaminated water and litter
Pathogenesis of Bordetella
- Bacterial attachment to ciliated epithelial cells leads to expression of adhesins with toxic or pro-inflammatory properties, production of ciliostasis, and initiation of inflammation
- Adherence to immune cells and release of adenyl cyclase toxin and effector proteins interferes with phagocytosis, leading to proliferation and active inflammation
- Mucus and fluid accumulation in the upper respiratory tract results in loss of control in iron and fluid regulation, leading to secondary pneumonia
Consequences of Bordetella-induced Changes
- Depression of respiratory clearance mechanisms facilitates complications
- In pigs, B. bronchiseptica causes nasal irritation, making turbinates susceptible to P. multocida toxin, leading to progressive atrophic rhinitis or non-progressive, mild, reversible turbinate hypoplasia
Pathology of Bordetella Infection
- Clinical disease caused by Bordetella is characterized by pathogen attachment, functional impairment, and destruction of ciliated respiratory epithelium
- The disease process begins with a catarrhal phase, followed by a suppurative phase, which may result in pneumonia or air sacculitis
- Compromised host clearance mechanisms in the upper respiratory tract may result in pneumonia or air sacculitis, enhanced by secondary bacterial pathogens
Bordetella Infections
-
Swine:
- Atrophic rhinitis: progressive form is a combined infection with P. multocida and B. bronchiseptica, while non-progressive form is caused by B. bronchiseptica alone
- Transient and self-limiting, affecting piglets 3-4 weeks old
- Pneumonia: usually a secondary infection, but primary pneumonia can occur in neonatal piglets (3-4 days old), causing coughing, dyspnea, high morbidity, and high mortality at times
Canine Infectious Tracheobronchitis (Kennel Cough)
- Caused by B. bronchiseptica
- Clinical disease most common in young dogs or mature dogs with a lowered immune system
- Often associated with viral infections, including canine influenza virus (CIV), canine parainfluenza virus (CPV), canine adenovirus 1 or 2 (CAV-1/2), and canine herpesvirus (CHV)
- Disease outbreaks occur rapidly in kennels and animal hospitals, with an incubation period of approximately 1 week
- Clinical symptoms:
- Acute coughing
- Gagging and retching (severe cases)
- Recovery within a few weeks without treatment, but bacteria can persist and cause a relapse infection
- Pneumonia: usually secondary and associated with other pathogens
Feline Upper Respiratory Disease
- B. bronchiseptica is becoming increasingly important in terms of feline respiratory infections
- Clinical signs:
- Mild tracheobronchitis
- Conjunctivitis
- Nasal discharge
- Sneezing
- Coughing
- Signs resolve after 10 days, but cats can carry the organism asymptomatically for up to 19 weeks following recovery
Guinea Pigs
- Extremely susceptible to B. bronchiseptica infections
- Acute development of disease associated with high mortality
- Clinical signs:
- Depression
- Ruffled fur
- Labored breathing
- Sneezing
- Anorexia
- Mucopurulent or catarrhal exudate in the nares (may be present)
- Without quick treatment, usually progresses to fatal pneumonia
- Necropsies show consolidation of cranioventral lung tissue, fibrinous suppurative pleuritis, and exudate in the airways
- Guinea pigs that survive infection will become chronic, asymptomatic carriers
Poultry and Birds
- Two species cause diseases in birds and are associated with stunted growth and tracheal collapse:
- B. avium (‘Turkey coryza’): affects young turkeys, leading to tracheobronchitis, sinusitis, and air sacculitis
- B. hinzii: commensal in poultry respiratory tract, causing clinical signs such as nasal exudate, conjunctivitis, sneezing, and dyspnea
- Morbidity can be high, mortality is generally low except for cases of secondary infections
- Recovery can begin after approximately 2 weeks, but illness can persist for 6 weeks
Gram-Negative Anaerobes
- Most anaerobes are part of normal microbiota in the mouth, GI tract, upper respiratory tract, and female urogenital tract in various species
- Genera of anaerobic bacteria associated with animal diseases include:
- Bacteriodes
- Dichelobacter
- Treponema
- Porphyromonas
- Prevotella
- Fusobacterium
General Pathogenesis of Anaerobic Bacteria
- Microenvironments:
- Process of establishing infection is dependent on the site involved
- Bacteria need to generate a local anaerobic microenvironment or be able to tolerate oxygen exposure
- Microenvironments may be created by bacterial damage to the host or because of synergistic interactions with facultative anaerobic bacteria that can utilize oxygen
- Protective enzymes:
- Many anaerobes can grow at low oxygen tension by using enzymes that protect them against oxygen, such as superoxide dismutase (SOD), catalase, and nicotinamide adenine dinucleotides (NAD) oxidase
- Bacterial products = damage:
- Tissue destruction may occur from host immune responses and inflammation that are triggered by bacterial products
- Local release of a wide variety of inflammatory cytokines
- Fermentation products create characteristic putrid odor of anaerobic infections and have inflammatory cytotoxic effects, including:
- Lactic acid
- Butyric acids
- Ammonia
Genus Fusobacterium
- Gram-negative, obligate anaerobic, non-motile, spindle-shaped (fusiform) or long filamentous bacilli
- 17 species, all producing large amounts of butyric acid as a fermentation product
- Species of relevance to veterinary medicine and public health:
- Fusobacterium necrophorum: major animal pathogen
- Fusobacterium canifelinum, nucleatum, and russi: members of normal oral microbiota in dogs and cats, frequently isolated from bite wounds in humans
- Fusobacterium equinum: normal part of oral microbiota in horses, isolated from oral-associated and respiratory diseases of horses
- Fusobacterium necrophorum:
- 2 subspecies: necrophorum and funduliforme, varying in cellular morphology, colonial characteristics, growth patterns in broth, extracellular enzymes, virulence factors, and general virulence and infrequency of occurrence in infections
- Natural habitat: mouth, gastrointestinal tract, urogenital tract, and soil, especially well-manured soil
- Fusobacterium necrophorum types of diseases and pathologic changes:
- Major bovine pathogen, causing necrobacillosis and associated with numerous necrotic disease conditions
- Hepatic necrobacillosis (liver abscesses): occurs secondarily to damage of the rumen wall epithelium, resulting in rumen acidosis and epithelial damage, which is required for F. necrophorum to colonize
Genus Mycobacterium
- 188 species, mostly saprophytic, obtaining food by absorbing dissolved organic material
- Non-flagellated, rod-shaped, and aerobic, with varying lengths
- Acid-fast, resisting decolorizing after staining, and cytochemically Gram-positive
- Characterized by a mycolic acid layer or mycomembrane, conferring high resistance to chemicals and antibiotics
Pathogenic Species: Host-Adapted Species
- Mycobacterium tuberculosis (humans): host-adapted, rarely infects other animals, and has limited environmental survival capability
- Mycobacterium bovis (cattle, humans): zoonotic, transmitted bidirectionally via aerosols and ingestion of unpasteurized milk
- Mycobacterium pinnipedii (seals): host-adapted strain
- Mycobacterium caprae (goats): host-adapted strain
- Mycobacterium mungi (banded mongoose): host-adapted strain
- Mycobacterium microti (voles, humans): host-adapted strain
- Mycobacterium canettii (unknown): host range unknown
Pathogenic Species: Environmentally Adapted Species
- Mycobacterium avium complex: found in surface water, includes distinct species, and causes TB-like infections in birds
- Mycobacterium intracellulare: opportunistic pathogen
- Mycobacterium avium: includes four subspecies, causing infections in birds, swine, humans, and ruminants
- Mycobacterium chelonae, Mycobacterium fortuitum, Mycobacterium kansasii, Mycobacterium marinum, and Mycobacterium ulcerans: all opportunistic pathogens
Pathogenesis of Mycobacterial Infections
- Transmission: inhalation of aerosols, ingestion of unpasteurized milk, and inoculation through damaged skin
- Pathogenesis: entry via mucosa or skin breach, phagocytosis by macrophages, and avoidance of macrophage activation and bactericidal response
Progression to Clinical Disease
- Clinical disease depends on the number of bacteria, infecting dose, virulence, and development of anti-mycobacterial cell-mediated immunity
- Disease onset: ~3 weeks after infection, mediated by T-helper 1 cells, IL-12, and Interferon Gamma
- Granulomas or tubercles form, containing infected macrophages, epithelioid cells, lymphocytes, and fibroblasts
- Caseous necrosis develops, dependent on disease outcome, and tubercles may enlarge and coalesce, eventually effacing large areas of tissue
General Pathogenesis of TB
- Infected animals mount both humoral and cell-mediated immune responses of varying efficacy
- Interferon gamma is key to host protection
- Granulomas are central to mycobacterial control in the body
M.bovis Pathogenesis
- Transmitted via direct aerosol and shedding into milk
- Initial uptake via alveolar macrophages and epithelial cells
- Binding of mycobacterial cell wall and pattern recognition receptors on macrophages
- Persists in macrophage phagosome and inhibits maturation of phagolysosome
- Proliferates in phagosomal vacuole
M.avium Pathogenesis
- Transmitted via fecal-oral route
- Initial uptake via M cells of intestinal Peyer's Patches
- Binding of mycobacterial cell wall and pattern recognition receptors on macrophages
- Persists in macrophage phagosome and inhibits maturation of phagolysosome
- Proliferates in phagosomal vacuole
Infection Outcomes
- Spontaneous healing
- Containment of the infection (remission)
- Reactivation and dissemination (progression)
Predilection Sites
- M.bovis: lung and lymph nodes of the head and thorax
- M.avium paratuberculosis: small intestine and mesenteric lymph nodes
Clinical Signs
- Weight loss is a common sign of advanced disease
- Respiratory symptoms (M.bovis)
- Intestinal dysfunction symptoms (M.avium paratuberculosis)
Tuberculous Infections in Animals
- Birds: naturally susceptible to primarily M.avium avium
- Ruminants:
- Cattle: M.bovis, commonly progressive with hematogenous dissemination to the liver and kidneys
- Sheep and goats: susceptible to M.bovis, M.avium paratuberculosis, and M.avium hominissuis
- Deer: susceptible to M.bovis
- Dogs and cats:
- Dogs: M.bovis, lesions resemble foreign body reaction than tubercles
- Cats: M.avium species, intestinal and abdominal localization
- Horses: rarely infected, usually with M.avium hominissuis
- Swine: infection usually via the alimentary route, M.bovis causes progressive disease with classical lesions
- Wild animals: serve as reservoir for M.bovis
Nontuberculous Infections
- Prevalent in the environment, cause opportunistic TB-like infections in animals and humans
- Infections can cause false positive test results due to cross immune reactions
- Mostly saprophytic species
- Opportunistic, granulomatous infections
- Johne's disease (Paratuberculosis) caused by M.avium paratuberculosis
Johne's Disease (Paratuberculosis)
- Chronic, irreversible wasting disease of ruminants
- Caused by M.avium paratuberculosis
- Clinically affected and asymptomatic shedders
- Main route of infection is fecal-oral
- Signs: reduced milk production, breeding problems, increased incidents of mastitis, early culling, and overall economic losses
- Lesions: characteristic gross corrugated appearance of intestinal mucosa
- No cost-effective antimicrobial treatments
- Prevention and elimination of infected animals is best for overall herd health
Feline Leprosy Syndrome
- Chronic, nodular, and ulcerative mycobacterial infection of the skin
- Several causative species, including M.lepraemurium
- Common locations of lesions suggest transmission by rodent bites or arthropods
- Disease is more common in older cats and progresses slowly
- Lesions: nodules occur in cutis or subcutis, ulceration, and lymph node involvement
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Description
Bacteriology: Burkholderia, Bordetella, Fusobacterium, Mycobacteria