5.3 Gram Positive Rods 2 Flashcards
what is a feature of the “anatomy” of the mycolata group of bacteria (i.e. corynebacterium, mycobacterium, rhodococcus)
they have a lipid rich outer membrane containing mycolic acid
all mycolata are what type of pathogens
facultative intracellular; like macrophages
all mycolata (corynebacterium, mycobacterium, rhodococcus) cause ______________ inflammation, which involves a ___________ immune response
granulomatous; type 1
what species do corynebacteria infect
humans, ruminants, other animals
what species do mycobacterium infect
humans, birds, ruminants, horses, pigs
what species do rhodococcus infect
herbivores
what is an important disease in small ruminants caused by corynebacterium, and what specific species is the bacteria
corynebacterium pseudotuberculosis causes caseous lymphadenitis
what is the causative agent of caseous lymphadenitis
corynebacterium pseudotuberculosis
what shape do corynebacterium spp. take
pleomorphic: rods, cocci, clubs
corynebacterium are commensals of (2)
skin and mm
what type of infection (appearance) do corynebacterium cause
pyogenic
what are 2 important tests to diagnose C. pseudotuberculosis
gamma interferon test and serology
what is the purpose of the gamma interferon test
checks for a type 1 cellular immunity response, characteristic of mycolata
T/F C. pseudotuberculosis is contagious and zoonotic
T
what is the typical “structure” of C. pseudotuberculosis lesions
caseous lymphadenitis with an onion ring structure
what is the consequence of in vitro vs in vivo antibiotic use against corynebacterium
in vitro effective but in vivo problematic due to intracellular nature of pathogen and poor penetration of granulomas
describe the vaccine against corynebacterium
poor efficacy and major side effects such as microabscessation
how do we control corynebacterium infection
culling based on blood test results
how does mycobacterium stain and what does this mean
weakly gram positive, requires acid-fast stain to see
mycobacterium spp. survive well or poorly in the environment
well, but slow growing
what type of infections do mycobacterium spp. cause
chronic granulomatous infections
T/F domestic animal species are susceptible to M. tuberculosis
F; only humans and primates
what species are susceptible to M. bovis
ruminants, humans, horses, pigs
what species are susceptible to M. avium subsp. paratuberculosis
ruminants
T/F M. bovis is reportable and zoonotic
T
what is the major implication of wildlife species being infected with M. bovis
wildlife reservoir
describe the pathogenesis of tuberculosis
starts with inhalation of infectious particles -> lungs -> pulmonary macrophage -> infected macrophage migrates to local LN -> from there innate control results in either healing or acute disease or containment -> from containment (i.e. granuloma) the disease becomes latent -> <10% of the time it reactivates and then can cause disease and spread
what type of cellular response is induced by tuberculosis (M. bovis for example)
TH1 response with IFN-γ
how is M. bovis usually diagnosed
at slaughter using the tuberculin test; then traced back to farm and the remaining animals are tested
if you wanted to examine a tissue sample for M. bovis, how would you stain it
using acid-fast
why is culture not a great option to diagnose bovine tuberculosis caused by M. bovis and what is a better detection method in this case
slow culture; DNA-based methods (or staining or tuberculin test)
what is the treatment for M. bovis
culling
where does M. bovis persist in Canada? what other gram-positive aerobic bacteria is also endemic to this area?
Wood Buffalo National Park (AB); Bacillus anthracis
T/F avian tuberculosis is zoonotic
T
what is the causative agent of avian tuberculosis
Mycobacterium avium subsp. avium, MAC
in what ways is avian tuberculosis similar to bovine tuberculosis
entry by air, chronic infection, granulomatous
T/F Johne’s disease is zoonotic
T
what is the causative agent of Johne’s disease
Mycobacterium avium subsp. paratuberculosis
how does M. avium subsp. paratuberculosis like to grow
on lipid rich media
how do we visualize M. avium subsp. paratuberculosis (what stain)
acid-fast stain
how is John’s spread
milk, pasture, in utero
what does M. avium subsp. paratuberculosis cause
granulomatous enteritis, cachexia, diarrhea
If you diagnose an animal with M. avium subsp. paratuberculosis (Johne’s) why would you immediately shit yourself
because if there are clinical animals in the herd there are way more (60%) subclinical animals also present in the herd that are shedding the bacteria… you’re fucked
T/F there is a genetic predisposition to Johne’s
T
how do we treat and prevent Johne’s
culling of infected and sick animals; detecting and culling subclinical shedders using serology and gamma interferon test
how do rhodococcus stain
gram positive and slightly acid-fast
T/F R. equi is zoonotic and reportable
F; zoonotic but not reportable
what does R. equi cause in foals
pyogranulomatous bronchopneumonia
what is the epidemiology of R. equi in foals
associated with heavy contamination of the environment and susceptibility is highest when maternal antibodies are waning
what is unique about the virulence of R. equi
contains virulence plasmids
how do virulent strains of R. equi influence the immune response
infect and survive in macrophages, but macrophages are required to induce a type 1 immune response to kill the bacteria; it also downregulates TH1 cells and can drive an inappropriate TH2 response
how do you treat R. equi
long term treatment with rifampin and macrolides
how do you prevent R. equi
dust control; colostrum; reduced manure load
how would a laboratory confirm a suspected case of tuberculosis
PCR, acid-fast staining of tissue, culture (slow)
how could you assess whether live animals on a farm were exposed to M. bovis
whole blood gamma interferon test
T/F if you detect caseous lymphadenitis you should treat with antibiotics
F; there will be poor penetration of the antibiotics so it is a waste
