Flashcards in Patterns of Disease: Synovial Joints and CNS Deck (26):
Lesions in the articular cartilage with inflammation of the synovial membrane.
Inflammation of the synovium only.
DEGENERATIVE JOINT DISEASE
Can be seen subsequent to arthritis/synovitis, even if the cause of inflammation is cleared.
Seen with irreversible damage to cartilage or synovium.
PORTALS OF ENTRY IN TO JOINTS
2. Extension from osteomyelitis.
3. Extension from adjacent soft tissue infection.
4. Diagnostic or therapeutic processes.
5. Penetrating damage (puncture or cutting).
HAEMATOGENOUS ENTRY IN TO JOINTS
Neonatal bacteraemia secondary to omphalitis (umbilical cord inflammation) or oral-intestinal entry often leads to POLYARTHRITIS or JOINT ILL.
EXTENSION FROM OSTEOMYELITIS
Osteomyelitis is seen as inflammation and suppuration in the metaphysis/diaphysis. This can extend in to the joint capsule after lysis of the cortex at it's weakest point (metaphyseal cut back zone).
EXTENSION FROM ADJACENT SOFT TISSUE INFECTION
Infection can extend from soft tissue in to bone.
eg. suppurative inflammation in an intervertebral disc from discospondylitis can extend in to adjacent bones in the spine.
Puncture or cutting can result in bacterial infection of skin, which can then cause osteomyelitis, which can then extend in to the joint capsule.
CENTRAL NERVOUS SYSTEM- PORTALS OF ENTRY
3. By leukocyte trafficking.
4. Retrograde axonal transport.
CNS- DIRECT EXTENSION
-Penetrating trauma through calvarium eg. antler injury, bite, gunshot.
-Penetrating trauma through vertebral body eg. bite wound.
-Extension of middle and/or inner ear infection.
-Extension of infection in nasal cavity or sinus through the cribiform plate or calvarium.
-Extension of nasal or sinus neoplasms thorugh the cribiform plate/calvarium eg. nasal carcinomas.
-From osteomyelitis or neoplasia of vertebral bodies.
-Extension through vertebrae in to vertebral canal eg. osteosarcoma invading the vertebral body from the periosteal surface, extends in to vertebral canal.
-Benign or malignant neoplasms eg. osteochondroma, multilobular tumour of skull.
-Invasion of adjacent malignant neoplasma eg. malignant melanoma in paravertebral lymph nodes in horse.
CNS- HAEMATOGENOUS ENTRY
The bloodstream is the most common portal of entry.
-Neonates- bacteria can enter the blood via the umbilical vein or via the veins following surgical procedures (eg. castration)
-Affects capillary beds of meninges, neuropil and choroid plexuses.
-Always check the ventral surface of the brain for pus- may only be seen on ventral surfaces due to effects of gravity.
-Adult animals- sites of chronic inflammation = sustained sources of bacteria that can enter the venous system and spread to the brain.
eg. abscesses, bacterial skin disease, ear infections, endocarditis.
-Nasal/sinus infections can spread intracranially by veins as well as by direct extension.
Particularly seen in cattle- P. multocida, A. pyogenes.
-Can be due to metastatic tumours eg. metastatic hemangiosarcoma, metastatic renal carcinoma.
Inflammation of the leptomeninges.
Caused by bacteria- Streptococcus and E. coli for example.
Usually haematogenous entry but can be direct extension or leukocyte trafficking.
Systemic bacterial infections are a common cause in neonates.
WHERE DO ABSCESSES USUALLY ARISE AFTER HAEMATOGENOUS ENTRY TO THE CNS?
GREY MATTER. This is because the grey matter receives a disproportionate share of the blood flow in the CNS.
At the grey-white matter junction, blood flow allows bacteria to attach and move THROUGH the Blood Brain Barrier.
This causes disruption and destruction of tissue and space occupation.
There can be single or multiple abscesses.
In horses, strangles (S. equi) can cause brain abscesses.
They are spread haematogenously via the bloodstream, from lymphoid tissues.
Thromboembolic Meningoencephalitis of cattle.
Caused by Histophilus somni.
Bacteraemis seen following replication of bacteria in respiratory tract- bacteria localise in blood vessels of the brain and other organs.
They adhere to endothelial cells, leading to vasculitis, haemorrhage and (local) thrombosis.
Seen at grey/white matter junction.
VIRAL HAEMATOGENOUS ENTRY
Equine herpesvirus (EHV-1, sometimes 4) can cause VASCULITIS, INFARCTS IN SPINAL CORD.
It is transferred to endothelial cells through leukocyte trafficking.
Eastern/Western/Venezuelan/Equine Encephalomyelitis is seen in the US/South America.
Here, the virus replicates in the endothelium FIRST, then infects and kills neurons.
In the endothelium (blood vessels) it causes vasculitis and thrombosis.
CAUSED BY TWO DIFFERENT VIRUSES!
FELINE INFECTIOUS PERITONITIS
Caused by a coronavirus.
Causes pyogranulomatous vasculitis.
SURFACE ASSOCIATED- affects meninges, periventricular white matter, eye (uvea, retina, optic nerve).
Perivascular 'cuffs' of lymphocytes- ALWAYS THINK OF VIRAL DISEASE.
Macrophages and lymphoid cells continually move in and out of capillary beds in the CNS- SENTINEL CELLS.
Some infectious agents have stages of their life cycles in the cytoplasm of lymphocytes or macrophages.
eg. feline leukaemia virus (retrovirus), Blastomyces dermatitidis.
Infected macrophages/lymphocytes moving in to capillary beds in CNS allows infection of CNS cells
Endemic to Mississippi and Ohio river valleys and vicinity of the Great Lakes.
Outbreaks are often associated with soil disruption.
The fungus makes a transition to yeast form in the lungs.
Can progress to the brain via leukocyte trafficking, where it can cause granulomas in the white matter.
RETROGARDE AXONAL TRANSPORT
Agents replicate in richly innervated tissues eg. sensory receptors and motor end plates.
RETROGRADE AXOPLASMIC FLOW is then used by these infectious agents to gain access to the CNS.
eg. Listeria monocytogenes.
-Seen mostly in domestic ruminants.
-Enters submucosa via injuries to oral mucosa.
-Travels to CNS via sensory and motor branches of the the trigeminal nerve (CN V), directly to midbrain and medulla.
Usually diagnosed on histology.
LISTERIA MONOCYTOGENES PATHOLOGY/CLINICAL SIGNS
Listeria bacteria spread to the cells- neurons, microglia, macrophages, choroid plexus epithelial cells.
Cells are damaged by inflammatory processes.
Early lesions are microglial foci.
Later, neutrophils dominate to form microabscesses.
Often, a severe meningitis is also seen, with trigeminal nerve and ganglion also inflamed.
Undergoes retrograde axonal transport.
1. Replicates in muscle after bite.
2. Enters nerve.
3. Ascends axon.
4. Dorsal root ganglion.
5. Enters spinal cord.
6. Ascends to brain via ascending (dorsal) and descending (ventral) nerve fibre tracts.
7. Enters brain.
8. Spreads to salivary glands and eye.
Inoculations to the head have a shorter incubation.
Rabies and pseudorabies cause non suppurative polioencephalomyelitis with craniospinal ganglionitis and sialoadenitis.
Pseudorabies- Aujeszky's disease of pigs (porcine herpesvirus).
Travel to brain via nasopharynx, trigeminal nerve and olfactory bulb.
Causes non suppurative meningoencephalomyelitis with trigeminal ganglioneuritis.
Inflammation of grey matter of brain, and spinal cord.
Inflammation of craniospinal ganglions.