CNS Infections- Pathogenesis & S/S Flashcards
Secondary invasion of CNS follows:
- bacteremia
- viremia
- fungemia
- parasitemia
Entry into the subarachnoid space occurs via sites of minimal resistance:
- choroid plexus
- dural venous sinuses
- cribriform plate
- cerebral capillaries
Direct entry via damage to integrity of the CNS occurs via: (4 things)
- Penetrating injuries of the skull or spinal column.
- congenital defects
* Note: for 1 and 2 of above most likely etiology is S. pneumoniae, Hib, GAS - Ventricular shunts.
- All children with cochlear implants, esp. those with implants with a positioner (rubber wedge) are at increased risk of infection for > 2 year post-implantation
Contiguous spread of infection along vascular channels from
- Nasal sinuses – Naegleria fowleri.
- Malignant otitis externa (P. aeruginosa) or otitis media.
- Mastoid.
- Sites of parameningeal infection, e.g., epidural abscess.
Infections that are spread from intra-axonal transport (retrograde flow) inside nerves:
- rabies.
- herpes.
- polioviruses.
- tetanus toxin.
Signs and symptoms of meningitis in the neonate are the same as those for neonatal sepsis and encephalitis, but are not the same as _________
the adult
Signs and symptoms of meningitis and encephalitis in the neonate are
- Fever.
- Lethargy.
- Poor feeding.
- GI disturbance (vomiting/diarrhea)/abdominal distension.
- Respiratory abnormalities (e.g., dyspnea, cyanosis)
- Cardiac abnormalities (tachycardia).
- Bulging fontanelle (indicates pressure on brain), ONLY if CNS infection.
Signs & Symptoms of any (bacterial, fungal, viral, etc.) meningitis in persons >2 y-o-age (adults too)
- Irritability – common.
- lethargy – common.
- fever – common.
- severe headache,
- nuchal rigidity,
- vomiting,
- pressure on eyeball.
- photophobia.
- Meningeal inflammation/irritation elicits a protective response (5 different signs)
Meningeal inflammation/irritation elicits a protective response (5 different signs) to prevent stretching of inflamed, hypersensitive nerve roots:
- Nuchal rigidity – meningismus, (e.g., The inability of a patient to place their chin to their chest passively without involuntary muscles spasms preventing it).
- Kernig sign - extension of the leg at the knee when patient is supine with the thigh flexed at the hip → marked pain and resistance to extension of the leg.
- Brudzinski sign - rapid flexion of the neck while patient is supine → involuntary brisk flexion of the knees.
- Opisthotonos - head drawn backward, spasm of back muscles.
- Tripod position (aka Amoss or Hoyne signs) knees and hips flexed, back arched lordotically, neck extended, and arms brought back to support the thorax
Severe S&S indicative of progression to meningoencephalitis
- decline in consciousness
- focal cerebral abnormalities (hemiparesis, monoparesis, or aphasia)
- Seizures/Convulsions
- Coma
Presence of maculopapular rash indicates infection with:
- non-polio enteroviruses (ECHOvirus, Coxsackievirus, enteroviruses),
- arboviruses
- HSV.
- S. pneumoniae.
- N. meningitidis.
- H. influenzae, type b. (Hib)
Presence of vesicular rash indicates infection with:
- HSV
- fungi
- non-polio enteroviruses
Presence of petechial/purpuric rash indicates infection with:
- S. pneumoniae.
- N. meningitidis.
- H. influenzae, type b. (Hib)
Bacteria penetration of blood-brain barrier and into CSF leads to:
- Local release of inflammatory cytokines in CSF
2. Adhesion of leukocytes to brain endothelium and diapedesis into CSF
After initial penetration of BBB, and inflammatory cytokines are released and leukocytes adhere in brain and move into CSF, the blood-brain barrier is further damaged and becomes permeable, which results in:
a. Exudation of albumin through opened intercellular junctions of meningeal venules.
b. Brain edema, increased intracranial pressure, cerebral vasculitis, altered cerebral blood flow.
c. Cranial nerve injury, seizures, hypoxic-ischemic brain damage, brain-stem herniation.
Mechanisms responsible for the encephalitic aspects of bacterial meningitis include:
a. metabolic encephalitis caused by endotoxin and TNF-α.
b. perivascular inflammation.
c. infarcts (strokes/seizures) caused by occluded blood
The greater the extent of the pathoglogy, the more devastating the manifestations in the patient and their prognosis.
Encephalitis is
inflammation of the brain parenchyma
Encephalopathy is
depressed or altered level of consciousness lasting >24 hours. Determined clinically – i.e., examination of patient
Encephalitis is encephalopathy plus 2 or more of the following:
- fever (>38oC),
- seizures,
- altered mental status,
- severe headache
- focal neurological findings (e.g., paralysis, cognitive disorders, if focal encephalitis is present),
- CSF pleocytosis (> 5 WBC/ml)
- electroencephalogram findings compatible with encephalitis,
- abnormal results on neuroimaging.
- Some manifestations of meningitis may also be present
Arbovirus causes _________ and presents as __________
causes diffuse encephalitis
fever (>38oC), seizures, altered mental status, severe headache
Polio causes __________ and presents as _________
causes focal encephalitis (Encephalomyelitis)
Acute osnet of a flaccid, ascending asymmetrical paralysis due to involvement of motor neuron in brain and spinal column with loss of superficial and deep reflexes, severe muscle aches or spasms, muscle pain, Sensory involvement - Abnormal sensations (but not loss of sensation) in an area, sensitivity to touch and paresthesia.
Rabies causes _______ and its 2 forms are ________ and ________
causes focal encephalitis
2 forms: dumb or furious
Furious rabies S&S are
Sensory sensitivity to external stimuli, hyperactivity, agitation, anxiety, insomnia, loss of natural timidity - aggressive sexual behavior, hydrophobia and foaming at the mouth arise from excruciatingly painful, laryngeal spasms → confusion, delirium → coma → death.
Paralytic/Dumb rabies S&S are
s/s are indistinguishable from viral encephalitis, then the patient manifests with paralysis starting at extremities and spreading to the trunk as areas of the brain are destroyed. Paralysis → to hypoventilation/respiratory paralysis →hypotension/cardiac failure → eventually coma and death.
Herpes causes __________ and presents as _________, treatment is _________
causes: focal encephalitis
Has distinctive clinical features due to its remarkable localization: memory defects, psychosis, slurred speech, personality changes from involvement of one temporal lobe - primarily the cerebral cortex with characteristic lesions (inflammation, focal hemorrhage, necrosis.
Treat with acyclovir.
Pathology of viral encephalitis Step 1: __________ in meningeal and perivascular spaces.
Mononuclear accumulation
Pathology of viral encephalitis Step 2:
Fragility of brain blood vessels and the occurrence of perivascular hemorrhages and infarcts allow spillage of ______ into the ________ that communicate with cerebrospinal fluid.
RBC, WBC and protein
into the Virchow-Robin spaces
Pathology of viral encephalitis Step 3:
____________ causes inflammation and severe CNS dysfunction. Few survive and those who do have serious emotional disorders and learning deficits.
Viral replication in the brain parenchyma
Neurons possess _________ that can activate a protein called _____ in neurons, which induces their death by affecting the function of ______. During a viral infection in the CNS, viral agents are recognized by at least one of the TLRs on neurons leading to _________.
toll-like receptors
SARM1
mitochondria
neuronal death in the brain
Spinal polio is the most common form of paralytic poliomyelitis; it results from viral invasion of the _________, or the___________, which are responsible for movement of the muscles, including those of the trunk, limbs and the intercostal muscles.
motor neurons of the anterior horn cells
ventral (front) gray matter section in the spinal column
Bulbar polio: The bulbar region is a white matter pathway that connects the _________. The destruction of these nerves weakens the __________, producing symptoms of encephalitis, and causes difficulty breathing, speaking and swallowing.
cerebral cortex to the brain stem
muscles supplied by the cranial nerves
Rabies virus predominates in ________ and then localizes in the _________.
predominates in the Grey matter
localizes in the limbic regions (producing focal symptoms)
Rabies also infects neurons in almost all areas of the brain.
“A variety of cells in the brain can be infected including in the _______________
cerebellum, the Purkinjes cells and also cells of the hippocampus, hypothlaamus and pontine nuclei
Signs and Symptoms of Mass Lesions
- Fever
- Headaches (elevated intracranial pressure)
- Seizures – Focal or generalized tonic-clonic seizures.
- Neurological deficits/focal signs (hemiparesis, visual loss, paraparesis).
- Altered mental status (dementia, confusions, stupor)
Mass Lesions have CT scan showing _______ that supports the diagnosis. In severe cases, a _______ may be seen, increasing risk of brain stem herniation.
ring-enhancing (mass) lesion
mid-line shift
Pathology of a mass lesion (what is it?)
An encapsulated structure grows in size (becomes visible to the naked eye) creating a mass effect – displaces brain tissue and creates intracranial pressure
Define abscess
Localized collection of purulent infectious agent material & host cell debris in a cavity formed by the disintegration of tissue.
3 potential locations of an abscess
- epidural (between vertebrae & dura).
- subdural (between dura & arachnoid).
- parenchyma (in the brain tissue).
Etiology of abscesses (Prokaryotic and Fungal)
- Procaryotic: S. aureus, anaerobic infections, L. monocytogenes.
- Fungi agents: Candida albicans.
Cystic lesions are caused by parasites. Humans may be intermediate hosts of parasites:
A helminth (flat worm) produces a tissue cyst as part of its life cycle in 2 distinct locations __________
- in the ventricles, subarachnoid space or meninges
2. parenchyma (in the brain tissue)
Parasites that cause cystic lesions in brain
- Taenia solium (Neurocysticercosis)
2. Echinococcus granulosus or multilocularis (Cystic Echinococcosis-hydatid cyst)
Etiology of pseudocyst lesions, when humans are the intermediate hosts of parasites
- a pseudocyst is formed in the brain parenchyma as a result of the human immune response to the parasitic/protozoan infection.
- Protozoan causes pseudocyst: Toxoplasma gondii (Toxoplasmosis)
S/S of Meningitis
fever, lethargy, irritability, meningimus
S/S of Encephalitis
fever, altered mental status (cognitive disorders, focal changes)
S/S of Meningoencephalitis
fever, lethargy, irritability, meningimus, altered mental status.
S/S of Mass Lesions
fever, headache, seizures.
S/S of Transverse Myelitis
fever, motor AND sensory loss at the same level
S/S of Poliomyelitis
fever, asymmetric motor deficit and NO sensory loss
