Neurologic infections



Neurologic infections





Neurologic infections can be caused by bacterial or viral infiltration into cerebral tissue. They’re an important cause of morbidity and mortality worldwide. Examples of neurologic infection include brain abscess, encephalitis, Guillain-Barré syndrome, and meningitis.


BRAIN ABSCESS

Brain abscess is usually secondary to an existing infection, especially otitis media, sinusitis, dental abscess, and mastoiditis. Other causes include subdural empyema; bacterial endocarditis; human immunodeficiency virus infection; bacteremia; pulmonary or pleural infection; pelvic, abdominal, and skin infections; and cranial trauma, such as a penetrating head wound or compound skull fracture. Brain abscess also occurs in those with congenital heart disease and congenital blood vessel abnormalities of the lungs such as Osler-Weber-Rendu disease.


Pathophysiology

Brain abscess usually begins with localized inflammatory necrosis and edema, septic thrombosis of vessels, and suppurative encephalitis. This is followed by thick encapsulation of accumulated pus and adjacent meningeal infiltration by neutrophils, lymphocytes, and plasma cells.



Complications



  • Rupture of abscess into the ventricles or subarachnoid space


  • Meningitis


  • Epilepsy


  • Recurrence of infection


  • Death


Assessment findings

Findings may vary according to cause; however, brain abscess generally produces clinical effects similar to those of a brain tumor, including:



  • constant intractable headache, worsened by straining


  • nausea and vomiting


  • confusion


  • altered level of consciousness (LOC)


  • focal or generalized seizures


  • ocular disturbances, such as nystagmus, decreased vision, and unequal pupil size.

Other findings differ with the site of the abscess:



  • temporal lobe abscess: auditory-receptive dysphasia, central facial weakness, and hemiparesis


  • cerebellar abscess: dizziness, coarse nystagmus, gaze weakness on lesion side, tremor, and ataxia


  • frontal lobe abscess: expressive dysphasia, hemiparesis with unilateral motor seizure, drowsiness, inattention, and mental function impairment.


Diagnostic test results



  • Complete blood count shows elevated white blood cell count.


  • Computed tomography (CT) scan or magnetic resonance imaging (MRI) help locate the site of the abscess.


  • Blood culture reveals any bacteria in the bloodstream.


  • Chest X-ray may reveal lung infection.


  • CT-guided stereotactic biopsy may be performed to drain and culture the abscess.



Treatment

Management of patients with brain abscess has become increasingly challenging because of the proliferation of unusual bacterial, fungal, and parasitic infections, particularly in immunocompromised patients. Therapy consists of antibiotics and antimicrobials, which may be injected directly into the abscess, to combat the underlying infection and surgical excision, aspiration, or drainage of the abscess. (CT scan or MRI can help determine the need for these procedures.) Administration of antibiotics for at least 2 weeks before surgery can reduce the risk of spreading infection.

Other treatments during the acute phase are palliative and supportive and include mechanical ventilation, administration of I.V. fluids with diuretics (urea or mannitol), and glucocorticoids (dexamethasone) to combat increased intracranial pressure (ICP) and cerebral edema. Anticonvulsants, such as phenytoin and phenobarbital, help prevent seizures.


Nursing interventions



  • Monitor neurologic status, especially LOC, speech, and sensorimotor and cranial nerve functions. Watch for signs of increased ICP (decreased LOC, vomiting, abnormal pupil response, and depressed respirations), which may lead to cerebral herniation with such signs as fixed and dilated pupils, widened pulse pressure, bradycardia or tachycardia, and absent respirations.


  • Assess and record vital signs every hour and as indicated by clinical status.


  • Monitor fluid intake and output.

If surgery is necessary, explain the procedure to the patient and answer his questions. After surgery:



  • Continue frequent neurologic assessment. Monitor vital signs and intake and output.


  • Watch for signs of meningitis, such as nuchal rigidity, headaches, chills, and sweats.



  • Provide appropriate education to the patient and his family before discharge. (See Teaching the patient with a brain abscess.)



DISCHARGE TEACHING


TEACHING THE PATIENT WITH A BRAIN ABSCESS

Before discharge, teach the patient and his family:



  • about the disorder and its implications


  • about treatment options, such as surgery


  • about prescribed medication administration, dosage, possible adverse effects, and when to notify the physician


  • the signs and symptoms of complications


  • how to prevent future brain abscesses


  • the importance of follow-up care.


ENCEPHALITIS

Encephalitis is a severe inflammation of the brain that results from infection with arboviruses specific to rural areas. In urban areas, encephalitis is most commonly caused by enteroviruses (coxsackievirus, poliovirus, and echovirus). Other causes include herpesvirus, mumps virus, adenoviruses, and demyelinating diseases after measles, varicella, rubella, or vaccination. (See Types of encephalitis, pages 248 to 251.)

Transmission by means other than arthropod bites may occur through ingestion of infected goat’s milk and accidental injection or inhalation of the virus.


Pathophysiology

Virus entry through hematogenous spread or by transmission along the neural and olfactory pathways. Intense lymphocytic infiltration of brain tissues and the leptomeninges causes cerebral edema, degeneration of the brain’s ganglion cells, and diffuse
nerve cell destruction. Resultant parenchymal damage may range from mild to severe.



TYPES OF ENCEPHALITIS

Four main virus agents cause most cases of encephalitis in the United States: eastern equine encephalitis (EEE), western equine encephalitis (WEE), St. Louis encephalitis (SLE), and La Crosse (LAC) encephalitis, all of which are transmitted by mosquitoes. Another less common cause of encephalitis is the Powassan (POW) virus; it’s transmitted by ticks in the northern United States. Most cases of arboviral encephalitis occur from June through September, when arthropods are most active. In milder parts of the country, where arthropods are active late into the year, cases can occur into the winter months.

Vaccines aren’t available for these U.S.-based diseases. However, a Japanese encephalitis (JE) vaccine is available for those who will be traveling to Japan, a tick-borne encephalitis vaccine is available for those who will be traveling to Europe, and an equine vaccine is available for EEE, WEE, and Venezuelan equine encephalitis (VEE). Public health measures often require spraying of insecticides to kill larvae and adult mosquitoes as well as controlling standing water, which is a breeding ground for mosquitoes.


Eastern equine encephalitis



  • EEE is caused by an alphavirus virus transmitted to humans and equines by the bite of an infected mosquito.


  • Incubation is 4 to 10 days.


  • Symptoms begin with a sudden onset of fever, general muscle pains, and a headache of increasing severity; it may progress to seizures and coma.


  • One-third of those afflicted will die from the disease and of those who recover, many will suffer irreversible brain damage.


  • Human cases are usually preceded by outbreaks in horses.


  • The virus occurs in natural cycles involving birds in swampy areas nearly every year during the warm months. The virus doesn’t escape from these areas, however, and this mosquito doesn’t usually bite humans or other mammals.


Western equine encephalitis



  • The alphavirus WEE is the causative agent. The virus is closely related to the EEE and VEE viruses.


  • The enzootic cycle of WEE involves passerine birds, in which the infection isn’t apparent, and culicine mosquitoes, principally Cx. tarsalis, a species associated with irrigated agriculture and stream drainages.


  • Human WEE cases are usually first seen in June or July.


  • Most WEE infections are asymptomatic or present as mild, nonspecific illness. Patients with clinically apparent illness usually have a sudden onset with fever, headache, nausea, vomiting, anorexia, and malaise, followed by altered mental status, weakness, and signs of meningeal irritation.


  • Children, especially those younger than age 1, are affected more severely
    than adults and may be left with permanent sequelae, which is seen in 5% to 30% of young patients.


  • Mortality is about 3%.


St. Louis encephalitis



  • The leading cause of SLE is flaviviral. It’s the most common mosquitotransmitted human pathogen in the United States.


  • Mosquitoes become infected by feeding on birds infected with the SLE virus. Infected mosquitoes then transmit the virus to humans and animals during the feeding process. The virus grows both in the infected mosquito and the infected bird, but doesn’t make either one sick.


  • Less than 1% of SLE viral infections are clinically apparent; the majority are undiagnosed.


  • Illness ranges in severity from a simple febrile headache to meningoencephalitis, with an overall casefatality ratio of 5% to 15%.


  • The incubation period is 5 to 15 days.


  • Mild infections present with fever and headache. More severe infection is marked by headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, occasional convulsions (especially in infants), and spastic (but rarely flaccid) paralysis.


  • The disease is generally milder in children than in adults, but in those children who do have disease, there’s a high rate of encephalitis.


  • Elderly people are at highest risk for severe disease and death.


  • During the summer season, SLE virus is maintained in a mosquito-birdmosquito cycle, with periodic amplification by peridomestic birds and Culex mosquitoes.


La Crosse encephalitis



  • The LAC virus, a Bunyavirus, is a zoonotic pathogen cycled between the daytime-biting tree hole mosquito, Aedes triseriatus, and vertebrate amplifier hosts (chipmunks, tree squirrels) in deciduous forest habitats. The virus is maintained over the winter by transmission in mosquito eggs. If the female mosquito is infected, she may lay eggs that carry the virus. Vector uses artificial containers (such as tires and buckets) in addition to tree holes.


  • LAC encephalitis initially presents as a nonspecific summertime illness with fever, headache, nausea, vomiting, and lethargy.


  • Severe disease occurs most commonly in children younger than age 16 and is characterized by seizures, coma, paralysis, and a variety of neurological sequelae after recovery.


  • Death occurs in less than 1% of clinical cases.


  • Cases are commonly reported as aseptic meningitis or viral encephalitis of unknown etiology.


  • During an average year, about 75 cases of LAC encephalitis are reported to the Centers for Disease Control and Prevention.



Powassan encephalitis



  • The POW virus is a flavivirus.


  • Recently a Powassan-like virus was isolated from the deer tick, Ixodes scapularis. The virus has been recovered from ticks (Ixodes marxi and Dermacentor andersoni) and from the tissues of a skunk (Spiligale putorius).


  • It’s a rare cause of acute viral encephalitis.


  • Patients who recover may have residual neurologic problems.


Venezuelan equine encephalitis



  • Like EEE and WEE viruses, VEE is an alphavirus that causes encephalitis in horses and humans. VEE is a significant veterinary and public health problem in Central and South America.


  • Infection of humans with the VEE virus is less severe than with EEE and WEE viruses and fatalities are rare.


  • Adults usually develop only an influenza-like illness; overt encephalitis is usually confined to children.


  • Effective VEE virus vaccines are available for equines.


Japanese encephalitis

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Jun 1, 2016 | Posted by in NEUROLOGY | Comments Off on Neurologic infections

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