Patterns of Disease- Synovial Joints and CNS Flashcards
Joint disease terminology
arthritis: lesions in articular cartilage in addition to inflammation of the synovial membrane
synovitis: inflammation of the synovium ONLY
even if the cause of the inflammation is cleared, if there’s irreversible damage to the cartilage or synovium, can progress to degenerative joint disease (DJD)
i.e. joint infection can progress to DJD.
Portals of entry into joints
- hematogenous
- extension from osteomyelitis (i.e. as a result of embolic osteomyelitis)
- extension rom adjacent soft tissue infection
- diagnostic or therapeutic procedures
- penetrating damage (puncture or cutting)- make sure you assess joint when assessing wounds.
Hematogenous entry
Neonatal bacteraemia secondary to omphalitis (umbilical stump infection) or oral-intestinal entry often leads to polyarthritis (joint ill)
Extension of infection (from osteomyelitis)
suppurative inflammation in distal end of femur of foal–> rupture through articular cartilage
Extension from adjacent soft tissue infection
i.e. from discospondylosis: suppurative inflammation in an intervertebral disc extends into adjacent bone in spine of dog.
Penetrating damage
penetrating injury causes bacterial infection in the skin; dorsal aspects of P1 and P2 are inflamed (osteomyelitis)
Inflammation in P2 has extended into the DIP joint
Pale area in P3 is a sequestrum- cut off from blood supply–> necrotic bone.
CNS pattern of disease case example
Dorsal funiculus of spinal cord= ascending sensory axons
vental funiculus of spinal cord= descending motor axons
lateral funiculus= mixture of ascending sensory and descending motor axons.
sensory axon cell bodies are in spinal ganglia or in the organ–> ascend to the brain
motor axon cell bodies are in the brain and descend away from the brain to the periphery.
At the point of trauma, there will be a region of axon separate from the neuronal body that degenerates (wallerian). Everything distal to the point of trauma will degenerate and be phagocytosed.
case example continued
If we’re looking at a spinal cord, where the head is to the left and the tail is towards the right, and there’s an arrow marking an area of compression, we can figure out what will be affected.
Cranial (to left of the arrow): distal part of sensory axons will degenerate because nerve cell bodies are closer to the tail
Caudal (to right of the arrow): motor axons will degenerate caudal to compression because cell bodies are in the brain
At the compression site, sensory and motor axons degenerate.
Portals of entry into CNS
- direct
- hematogenous
- leukocyte trafficking
- retrograde axonal transport.
Direct entry into CNS
penetrating trauma through calvarium
extension of a middle or inner ear infection
extension of an infection in nasal cavity or sinus through cribiform plate (i.e. aspergillus- necrotic debris filling sinus can penetrate to brain)
extensing of nasal or sinus neoplasms through cribiform plate, e.g. nasal carcinomas
from osteomyelitis or neoplasia of vertebral bodies
benign or malignant neoplasms i.e. osteochondroma (multilobar tumour of skull)
-invasion of adjacent malignant neoplasms (e.g. malignant melanoma in paravertebral LN of horse)
Hematogenous
blood stream is most common portal of entry
Neonates: bacteria can enter via umbilical vein or veins following surgical procedures e.g. castration
-capillary beds of meninges, neuropil (brain parenchyma), choroid plexus
meningitis= inflammation of leptomeninges (arachnoid and pia mater)
-bacteria e.g. e coli and strep species
usually hematogenous but can be by direct extension or leukocyte trafficking
systemic bacterial infections are a common cause in neonates.
hematogenous spread to brain in adult animals
sites of chronic inflammation i.e. chronic periodontal disease/chronic tonsilitis are sustained sources of bacteria that can enter venous system and spread to brain.
Abscesses, bacterial skin diseae, ear infections, endocarditis: abscesses usually arise in grey matter as it receives a disproportionate amount of blood flow in CNS
preferentially, they form at grey-white matter junction- blood flow there allows bacteria to attach and move through BBB
Abscesses disrupt and destory tissue and are space occupying- can have single or multiple abscesses.
Nasal/sinus infection spread to brain
can spread intracranially via veins (not just by direct extension). this occurs particularly in cattle: pasturella multocida and actinomyces (truperella) pyogenes.
In horses, strep. equi (strangles) can cause brain abscesses–> spread via bloodstream from lymphoid tissues.
TEME in cattle
thrombotic meningoencephalitis (TEME)= inflammation of meninges and brain
caused by histophilus somni (formerly hemophilus somnus), pasturella bacteria
Bacteremia following replication in resp tract- bacteria localize in BVs of the brain and other organs.
Adhere to endothelial cells, leads to vasculitis, hemorrhage and local thrombosis- seen at grey-white matter junction.
Viral hematogenous spread to brain
equine herpesvirus-1 (sometimes 4) can cause vasculitis, infarcts in spinal cord–> transferred to endothelial cells through leukocyte trafficking
eastern, western and venezuelan equine encephalomyelitis: replicate in endothelium first (vasculitis and thrombosis), infect and kill neurons.
feline infectious peritonitis (coronavirus): causes pyogranulomatous vasculitis–> surface associated meninges, periventricular white matter, eye (uvea, retina, optic nerve).
lymphocyte cuffing around BVs indicate VIRAL infection- pathognomonic lesion.
