Mechanisms of Microbial Infections Flashcards
How does rabies invade the body?
nerve endings - begins to move upward
How does listeriosis target cells of the body?
circles nerve and follows nerve to trigeminal nerve (CN V)
spoiled silage - bacterium through mouth adhesions
What target cells spread microbes locally, regionally, or systemically?
macrophages (monocytes)
lymphocytes
dendritic cells
Explain leukocyte trafficking
when leukocytes (lymphatics) come from afferent lymphatic (and also comes from circulation), go through high endothelial venules (post-capillary venules), then drains into thoracic duct back into heart
then to other organ systems in which specific target cells are infected
What are the types of epithelial target cells?
covering epithelial
lining epithelium
glandular epithelium
What does it mean by epithelia target cells - covering epithelium?
epidermis (M/C junction, cornea)
serosa (mesothelium, meninges)
What does it mean by epithelia target cells - lining epithelium?
mucosae
endothelium
What does it mean by epithelia target cells - glandular epithelium?
endocrine
salivary
gonads
What are portals of entry for the alimentary system?
tonsillar epithelium
villus epithelium
crypt epithelium
M cells (Peyer’s patches)
What are the portals of entry for the respiratory system?
inhalation
hematogenous
direct penetration
metabolic (from club cells)
What are club cells, aka Clara cells and what do they do??
discovered by German doctor who used Holocaust patients from gas chambers
metabolizes toxins
metabolize gas into something else (could be bad)
How can you tell club cells are injured? Why?
via metabolism issues
- toxin upon intake
- chemical converted into a more toxic substance
What is this?
club cell - characteristic apical bleb
What are portals of entry for the urogenital system?
ascending infection
hematogenous
metabolic (kidney PCT)
What is the most metabolically active cell in the kidney?
PCT epithelial cells
What is the most common route of infection for the urogenital system?
ascending infection
How can you tell the kidney is injured via metabolism issues?
the kidneys metabolize drugs a lot, also:
- toxin upon intake
- chemical converted into a more toxic substance and then affects perfusion
What are components of the integumentary system?
epidermis - compact
dermis - compact
subcutis - “stretchy pants” —> tent skin, loose CT in SQ
adnexa - compact
What are the portals of entry for the integumentary system?
direct contact
- abrasions
- bites
What are some non-cell microbial targets?
mucous
specific parts of a cell - cilia, microvilli
What is the morphologic diagnosis for brachyspira hyodysenteriae?
mucohemorrhagic necrofibrinous colitis and typhlitis with diphtheritic membranes
How does brachyspira hyodysenteriae cause disease in pigs?
stimulates the colonic cells to make more mucus (RTX toxin)
able to actively move through the mucus layer to gain access to mucosal epithelial and goblet cells
prefers to initially replicate in mucigen droplets within goblet cells
Describe this lesion
thick, cream to brown to black, friable (crumbly) adhered to mucosal surface of colon
if adhered, have to be attached by something like fibrous CT or fibrin
What are pathways used to cross barriers and enter MALT?
- transcytosis - M cells
- intracellular junctions
- transcytosis
- processes of dendritic cells
- leukocyte trafficking via lymphocyte
- leukocyte trafficking via monocyte/macrophage
- nerve endings
How do microbes invade?
use cell structures
transcytosis, endocytosis, exocytosis —> receptor-mediated actions
What is “normal” phagocytosis?
APC —> antigen —> MHC complex
APC —> takes in phagosome —> phagosomelysosome fusion —> degradation
How do some microbes inhibit phagosome-lysosome fusion?
phagosome-lysosome fusion is disrupted —> microbe lives, proliferates, and spreads to lymph acts
if fusion does occur, can neutralize enzymes = failure to degrade microbe
What are some examples of microbes that inhibit phagosome-lysosome fusion? What do they target?
Johne’s disease - mycobacterium avium subspecies paratuberculosis
rhodococcus equi
corynebacterium paratuberculosis
all of these are macrophages
What are virulence factors?
factors expressed genetically by microbes which enable them to cause disease
What do VF allow for?
adhesion
colonization
invasion
replication, growth
evasion, suppression of the immune system
systemic spread
Look at this VF chart
What are some virulence factors regarding attaching and binding to membranes (adhesions)?
adhesion: protein on the bacterium binds to a receptor on a target cell
pili and fimbrae are extensions of membrane that contain adhesions
T/F: Toxins are virulence factors
TRUE!
Match the term to the toxin it produces: exotoxins, endotoxins, lipoteichoicacid
a. dead gram-negative
b. live gram-positive
c. dead gram-positive
exotoxins: b. live gram-positive
endotoxins: a. dead gram-negative
lipotechoicacid: c. dead gram-positive
What is the end result of all toxins?
cell dysfunction and death
What are examples of toxins? Give an example for both
leukotoxins: mannheimiosis
neurotoxins: botulism clostridium botulinum, tetanus and tetanospasmin clostridium tetani
For manheima hemolytic, the causative agent of Shipping Fever in bovines, what specific cells do they target?
leukocytes: macrophages, neutrophils
What is epitheliogenesis imperfecta?
animal does not produce epithelial cells
absence of stratified squamous epithelium
death due to opportunistic infections
A piglet has patches of solely dermis and areas of both epidermis and dermis. His mother is known to be a carrier of the gene. What is the disease? What could potentially happen with him?
epitheliogenesis imperfecta
mutates physical barriers - death due to opportunistic infections
What is ciliary dyskinesia?
defect in cilia morphology and function in 9+2 microtubule
dysplastic or immotile cilia
What are some infectious causes of ciliary dysfunction?
bordatella bronchiseptica
mycoplasma sp.
manheimia hemolytica (also has leukotoxins)
How does mannheimia hemolytica also cause ciliary dysfunction besides targeting ruminant leukocytes?
paralyzes cilia
cranial-ventral distribution —> breathe in and have turbulence —> gets stuck and not flushed out —> stuck in mucus
What are leukocyte adhesion deficiencies?
LAD, BLAD, CLAD
defect in Beta-2 integrins
autosomal recessive trait
What are the hallmarks of leukocyte adhesion deficiencies?
leukocytosis with marked neutrophilia (neutrophils can’t get out of blood into tissues)
leukocyte adhesion cascade is important because it will grab neutrophils and slow it down as it rolls through the blood vessel until it stops —> then, it transmigrates through blood vessel walls out into tissues —> chemical mediators give directions
What happens when there is a deficiency in leukocyte adhesion deficiency?
problem with B2 integrin cascade
neutrophils cannot get out of blood vessels
Where are places in the body most susceptible to lesions from a leukocyte adhesion deficiency?
prone to infections, especially at much-cutaneous junctions due to lots of bacteria (normal flora) there
T/F: Antibiotics can solve issues with leukocyte adhesion deficiencies
FALSE - will never entirely resolve the issue
