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Meningitis
Definition Meningitis is inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges. The inflammation may be caused by infection with viruses, bacteria, or other microorganisms, and less commonly by certain drugs. Causes

Chemical irritation, Tumors Drug allergies Fungi, Parasites, Bacterial, Viral

Types Bacterial meningitis The types of bacteria that cause bacterial meningitis vary according to the infected individual's age group. In premature babies and newborns up to three months old, common causes are group B streptococci (subtypes III which normally inhabit the vagina and are mainly a cause during the first week of life) and bacteria that normally inhabit the digestive tract such as Escherichia coli (carrying the K1 antigen). Listeria monocytogenes (serotype IVb) may affect the newborn and occurs in epidemics. Children more commonly affected by Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) and those under five by Haemophilus influenzae type B (in countries that do not offer vaccination). In adults, Neisseria meningitidis and Streptococcus pneumoniae together cause 80% of bacterial meningitis cases. Risk of infection with Listeria monocytogenes is increased in persons over 50 years old. The introduction of pneumococcal vaccine has lowered rates of pneumococcal meningitis in both children and adults. Tuberculous meningitis, which is meningitis caused by Mycobacterium tuberculosis, is more common in people from countries where tuberculosis is endemic, but is also encountered in persons with immune problems, such as AIDS. . Viral Viruses that cause meningitis include enteroviruses, herpes simplex virus type 2 (and less commonly type 1), varicella zoster virus (known for causing chickenpox and shingles), mumps virus,HIV, and LCMV. Fungal There are a number of risk factors for fungal meningitis, including the use of immunosuppressants (such as after organ transplantation), HIV/AIDS, and the loss of immunity associated with aging.
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The most common fungal meningitis is cryptococcal meningitis due to Cryptococcus neoformans. Other common fungal agents include Histoplasma capsulatum,Coccidioides immitis, Blastomyces dermatitidis, and Candida species. Parasitic A parasitic cause is often assumed when there is a predominance of eosinophils (a type of white blood cell) in the CSF. The most common parasites implicated are Angiostrongylus cantonensis,Gnathostoma spinigerum, Schistosoma, as well as the conditions cysticercosis, toxocariasis, baylisascariasis, paragonimiasis, and a number of rarer infections and noninfective conditions. Non-infectious Meningitis may occur as the result of several non-infectious causes: spread of cancer to the meninges (malignant or neoplastic meningitis) and certain drugs (mainly NSAIDs, antibiotics and intravenous immunoglobulins). It may also be caused by several inflammatory conditions, such as sarcoidosis (which is then called neurosarcoidosis), connective tissue disorders such as systemic lupus erythematosus, and certain forms of vasculitis (inflammatory conditions of the blood vessel wall), such as Behet's disease. Epidermoid cysts and dermoid cysts may cause meningitis by releasing irritant matter into the subarachnoid space. Signs and symptoms Nuchal rigidity (the inability to flex the neck forward passively due to increased neck muscle tone and stiffness). The classic triad of diagnostic signs consists of nuchal rigidity, sudden high fever, and altered mental status Other signs photophobia(intolerance to bright light) and phonophobia (intolerance to loud noises). The fontanelle can bulge in infants aged up to 6 months. In young children are leg pain, cold extremities, and an abnormal skin color. Nuchal rigidity occurs in 70% of bacterial meningitis Kernig's sign is assessed with the person lying supine, with the hip and knee flexed to 90 degrees. In a person with a positive Kernig's sign, pain limits passive extension of the knee. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary flexion of the knee and hip. Agitation, Decreased alertness Poor feeding or irritability in children, Rapid breathing Unusual posture, with the head and neck arched backwards (opisthotonos) Another test, known as the "jolt accentuation maneuver" helps determine whether meningitis is present in those reporting fever and headache. A person is asked to rapidly
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rotate the head horizontally; if this does not make the headache worse, meningitis is unlikely. Meningitis caused by the bacterium Neisseria meningitidis (known as "meningococcal meningitis") The rash consists of numerous small, irregular purple or red spots ("petechiae") on the trunk, lower extremities, mucous membranes, conjuctiva, and (occasionally) the palms of the hands or soles of the feet. The rash is typically non-blanching; the redness does not disappear when pressed with a finger or a glass tumbler. Diagnosis CSF findings in different forms of meningitis

Type of meningitis Acute bacterial

Glucose low

Protein high

Cells PMNs, often > 300/mm

Acute viral

normal

normal or high mononuclear, < 300/mm high mononuclear and PMNs, < 300/mm < 300/mm usually mononuclear

Tuberculous

low

Fungal Malignant

low low

high high

Blood tests and imaging In someone suspected of having meningitis, blood tests are performed for markers of inflammation (e.g. C-reactive protein, complete blood count), as well as blood cultures. Analysis of the cerebrospinal fluid through lumbar puncture (LP, spinal tap).However, lumbar puncture is contraindicated if there is a mass in the brain (tumor or abscess) or the intracranial pressure(ICP) is elevated, as it may lead to brain herniation. CT or MRI scan is recommended prior to the lumbar puncture. Often, CT or MRI Management
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Treatment with wide-spectrum antibiotics should not be delayed while confirmatory tests are being conducted. benzylpenicillin be administered. Intravenous fluids should be administered if hypotension (low blood pressure) or shock are present. Mechanical ventilation may be needed if the level of consciousness is very low, or if there is evidence of respiratory failure. If there are signs of raised intracranial pressure, measures to monitor the pressure may be taken; this would allow the optimization of the cerebral perfusion pressure and various treatments to decrease the intracranial pressure with medication (e.g. mannitol). Seizures are treated with anticonvulsants. Hydrocephalus (obstructed flow of CSF) may require insertion of a temporary or long-term drainage device, such as a cerebral shunt. Bacterial meningitis Antibiotics
It

consists of a third-generation cefalosporin such as cefotaxime or ceftriaxone. In addition vancomycin is the initial treatment recommended. Chloramphenicol, either alone or in combination with ampicillin, however, appears to work equally well. Empirical therapy may be chosen on the basis of the person's age, whether the infection was preceded by a head injury, whether the person has undergone recent neurosurgery and whether or not a cerebral shunt is present. Steroids Adjuvant treatment with corticosteroids usually dexamethasone. Viral meningitis Viral meningitis typically only requires supportive therapy. Herpes simplex virus and varicella zoster virus may respond to treatment with antiviral drugs such as acyclovir. Mild cases of viral meningitis can be treated at home with conservative measures such as fluid, bed rest, and analgesics. Fungal meningitis Fungal meningitis, such as cryptococcal meningitis, is treated with long courses of high dose antifungals, such as amphotericin B and flucytosine. Raised intracranial pressure is common in fungal meningitis, and frequent (ideally daily) lumbar punctures to relieve the pressure are recommended, or alternatively a lumbar drain. Prevention Vaccination Immunization against Haemophilus vaccination schemes. influenzae type B in their routine childhood

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Immunization against mumps has led to a sharp fall in the number of cases of mumps meningitis. Childhood vaccination with Bacillus Calmette-Gurin has been reported to significantly reduce the rate of tuberculous meningitis. Antibiotics Short-term antibiotic prophylaxis is another method of prevention, particularly of meningococcal meningitis. In cases of meningococcal meningitis, prophylactic treatment of close contacts with antibiotics (e.g. rifampicin, ciprofloxacin or ceftriaxone) can reduce their risk of contracting the condition. Complications

Brain damage, Seizures, Hydrocephalus Buildup of fluid between the skull and brain (subdural effusion) Hearing loss

Encephalitis
DEFINITION Encephalitis is irritation and swelling (inflammation) of the brain, most often due to infections. Encephalitis with meningitis is known as meningoencephalitis Causes and risk factors Encephalitis is most often caused by a viral infection.

Breathing in respiratory droplets from an infected person Contaminated food or drink Mosquito, tick, and other insect bites, Skin contact Measles, Mumps, Polio, Rabies, Rubella, Varicella (chickenpox), Adenovirus, Coxsackievirus, Cytomegalovirus, Eastern Equine Encephalitis Virus, Echovirus, West Nile virus

Other causes of encephalitis may include:

An allergic reaction to vaccinations Autoimmune disease

Bacteria, such as Lyme disease,syphilis, and tuberculosis Parasites such as roundworms, cysticercosis, and toxoplasmosis in AIDS patients and other people who have a weakened immune system

The effects of cancer

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Types Viral Viral encephalitis can occur either as a direct effect of an acute infection, or as one of the sequelae of a latent infection. The most common causes of acute viral encephalitis are rabies virus,Herpes simplex, poliovirus, measles virus, and JC virus. Other causes include infection by flaviviruses such as Japanese encephalitis virus, St. Louis encephalitis virus or West Nile virus, or by Togaviridae such as Eastern equine encephalitis virus (EEE virus), Western equine encephalitis virus (WEE virus) Bacterial and other It can be caused by a bacterial infection, such as bacterial meningitis, spreading directly to the brain (primary encephalitis), or may be a complication of a current infectious disease syphilis (secondary encephalitis). Certain parasitic or protozoal infestations, such as toxoplasmosis, malaria, or primary amoebic meningoencephalitis, can also cause encephalitis in people with compromised immune systems. Lyme disease and/or Bartonella henselae may also cause encephalitis. Cryptococcus neoformans is notorious for causing fungal encephalitis in the immunocompromised. Streptococci, staphylococci and certain Gram-negative bacilli cause celebrities prior to the formation of a brain abscess. Limbic system encephalitis In a large number of cases, called limbic encephalitis, the pathogens responsible for encephalitis attack primarily the limbic system (a collection of structures at the base of the brain responsible for emotions and many other basic functions Encephalitis lethargica Encephalitis lethargica is an atypical form of encephalitis which caused an epidemic. There have been only a small number of isolated cases in the years since, though in recent years a few patients have shown very similar symptoms. The cause is now thought to be either a bacterial agent or an autoimmune response following infection. Sign and symptoms Fever that is not very high

Mild headache Low energy and a poor appetite

Other symptoms include:

Clumsiness, unsteady gait, Confusion, disorientation Drowsiness, Irritability or poor temper control Light sensitivity, Stiff neck and back (occasionally)

Vomiting

Symptoms in newborns and younger infants may not be as easy to recognize:

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Body stiffness, Vomiting Irritability and crying more often (these symptoms may get worse when the baby is picked up) Poor feeding, Soft spot on the top of the head may bulge out more

Emergency symptoms:

Loss of consciousness, poor responsiveness, stupor, coma Muscle weakness or paralysis, Severe headache Seizures Sudden change in mental functions:
o

"Flat" mood, lack of mood, or mood that is inappropriate for the situation, Impaired judgment Inflexibility, extreme self-centeredness, inability to make a decision, or withdrawal from social interaction Less interest in daily activities Memory loss (amnesia), impaired short-term or long-term memory

o o

Signs and tests An examination may show:

Abnormal reflexes, Increased intracranial pressure, Mental confusion Mouth ulcers, Muscle weakness, Neck stiffness Signs in other organs, such as the liver and lungs Skin rash, Speech problems

Tests may include:

Brain MRI CT scan of the head

Culture of cerebrospinal fluid (CSF), blood, or urine (however, this test is rarely useful)

Electroencephalogram (EEG) may show sharp waves in one or both of the temporal lobes. Lumbar puncture and CSF examination Examination of the cerebrospinal fluid obtained by a lumbar puncture procedure usually reveals increased amounts of protein and white blood cells with normal glucose, though in a significant percentage of patients, the cerebrospinal fluid may be normal. CT scan often is not
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helpful, as cerebral abscess is uncommon. Cerebral abscess is more common in patients with meningitis than encephalitis.

Tests that detect antibodies to a virus (serology tests) Test that detects tiny amounts of virus DNA (polymerase chain reaction -- PCR)

Treatment The goals of treatment are to provide supportive care (rest, nutrition, fluids) to help the body fight the infection, and to relieve symptoms. Reorientation and emotional support for confused or delirious people may be helpful. Medications may include:

Antiviral medications, such as acyclovir (Zovirax) and foscarnet (Foscavir) -- to treat herpes encephalitis or other severe viral infections (however, no specific antiviral drugs are available to fight encephalitis) Antibiotics -- if the infection is caused by certain bacteria

Anti-seizure medications (such as phenytoin) -- to prevent seizures Steroids (such as dexamethasone) -- to reduce brain swelling (in rare cases) Corticosteroids (e.g.,methylprednisolone) are used to reduce brain swelling and inflammation.

Sedatives -- to treat irritability or restlessness

Acetaminophen -- for fever and headache For Mycoplasma infection, parenteral tetracycline is given. Encephalitis due to Toxoplasma is treated by giving a combination of pyrimethamine and sulphadimidine If brain function is severely affected, interventions like physical therapy and speech therapy may be needed after the illness is controlled. Prevention An immunodeficient patient who has had contact with chicken pox virus should be given prophylaxis with hyperimmune zoster immunoglobulin Children and adults should avoid contact with anyone who has encephalitis. Controlling mosquitoes (a mosquito bite can transmit some viruses) may reduce the chance of some infections that can lead to encephalitis.

Apply an insect repellant containing the chemical, DEET when you go outside (but never use DEET products on infants younger than 2 months). Remove any sources of standing water (such as old tires, cans, gutters, and wading pools). Wear long-sleeved shirts and pants when outside, particularly at dusk.

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Vaccinate animals to prevent encephalitis caused by the rabies virus. Human vaccinations that are available include:

A vaccination to prevent a form of viral encephalitis that often affects people living in dorms or in the military

Herpes zoster Measles Complications Permanent brain damage may occur in severe cases of encephalitis. It can affect:

Hearing, Memory, Muscle control, Sensation, Speech,Vision

Neurosyphilis
Definition Neurosyphilis is an infection of the brain or spinal cord. It usually occurs in persons who have had untreated syphilis for many years. Causes, incidence, and risk factors Neurosyphilis is caused by Treponema pallidum, the bacteria that cause syphilis. It usually occurs about 10 - 20 years after a person is first infected with syphilis. There are four different forms of neurosyphilis:

Asymptomatic (most common form) General paresis

Meningovascular

Tabes dorsalis Asymptomatic neurosyphilis occurs before symptomatic syphilis. Symptoms

Abnormal walk (gait), Inability to walk Blindness, Visual disturbances There may be the sign of Argyll Robertson pupils, which are bilateral small pupils that constrict when the patient focuses on a near object, but do not constrict when exposed to bright light.

Confusion, Irritability, Headache, Dementia, Depression Incontinence Numbness in the toes, feet, or legs, Weakness Poor concentration

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Seizures, Stiff neck, Tremors

There may be no symptoms. Signs and tests Signs include:

Abnormal reflexes, Muscle atrophy, Muscle contractions

Blood tests can be done to detect substances produced by the bacteria that cause syphilis. The oldest test is the VDRL test. Other tests include:

Fluorescent treponemal antibody absorption (FTA-ABS) Rapid plasma reagin (RPR)

Treponema pallidum particle agglutination assay (TPPA)

In neurosyphilis, it is important to test the spinal fluid for signs of syphilis. Tests to look for problems with the nervous system may include:

Cerebral angiogram Head CT scan Lumbar puncture ("spinal tap") and a cerebrospinal fluid analysis (CSF fluid analysis) MRI scan of the brain, brainstem, or spinal cord Treatment Penicillin is used to treat neurosyphilis. The medicine may be given in various ways.

It may be injected into a vein several times a day for 10 - 14 days. Take probenecid by mouth 4 times a day, combined with daily muscle injections -both for 10 - 14 days. Aqueous penicillin G 3-4 million units q4h for 10-14 days. One daily intramuscular injection and oral probenecid 4 times a day, both for 10 14 days.

Brain abscess
Definition A brain abscess is a collection of pus, immune cells, and other material in the brain, usually from a bacterial or fungal infection.
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Causes, incidence, and risk factors Bacterial infections Anaerobic and microaerophilic cocci and gram-negative and grampositive anaerobic bacilli. Staphylococcus aureus, aerobic and anaerobic streptococci, Bacteroides, Prevotella, and Fusobacterium species, Enterobacteriaceae, Pseudomonas species Less common organisms include: Haemophillus influenzae, Streptococcus pneumoniae and Neisseria meningitides. Fungal and parasitic causes Fungi and parasites are especially associated with immunocompromised patients. Mycobacterium, Fungi(e.g. Aspergillus, Candida, Cryptococcus, Mucorales, Coccidioides, Histoplasma capsulatum,Blastomyces dermatitidis, Bipolaris, Exophiala dermatitidis Protozoa (e.g. Toxoplasma gondii, Entamoeba histolytica, Trypanosoma cruzi) Helminths (e.g. Taenia solium). Organisms that are most frequently associated with brain abscess in patients with AIDS are poliovirus, Toxoplasma gondii, and Cryptococcus neoformans, though in infection with the latter organism, symptoms of meningitisgenerally predominate.

These organisms are associated with certain predisposing conditions: Sinus and dental infectionsAerobic and anaerobic streptococci, anaerobic gram-negative bacilli (e.g. Prevotella, Porphyromonas, Bacteroides), Fusobacterium, S. aureus, and Enterobacteriaceae Penetrating traumaS. aureus, aerobic streptococci, Enterobacteriaceae, and Clostridium spp. Pulmonary infectionsAerobic and anaerobic streptococci, anaerobic gram-negative bacilli (e.g. Prevotella, Porphyromonas, Bacteroides), Fusobacterium, Actinomyces, and Nocardia Congenital heart diseaseAerobic and microaerophilic streptococci, and S. aureus HIV infectionT. gondii, Mycobacterium, Nocardia, Cryptococcus, and Listeria monocytogenes TransplantationAspergillus, Candida, Cryptococcus, Mucorales, Nocardia, and T. gondii NeutropeniaAerobic gram-negative bacilli, Aspergillus, Candida, and Mucorales The following raise the risk of a brain abscess:

A weakened immune system (such as in AIDS patients) Chronic disease, such as cancer Drugs that suppress the immune system (corticosteroids or chemotherapy) Right-to-left heart shunts, usually the result of congenital heart disease

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Symptoms Symptoms may develop slowly, over a period of 2 weeks, or they may develop suddenly. They may include:

Changes in mental status

o o o

Confusion, Drowsiness, Irritability Decreasing responsiveness, Slow thought processes Eventual coma Inattention

Decreased movementLoss of coordination Loss of muscle function, typically on one side Seizures, Stiff neck Language difficulties, Decreased speech (aphasia) Vision changes, Decreased sensation Fever and chills, Headache, Vomiting

Signs and tests A brain and nervous system (neurological) exam will usually show signs of increased intracranial pressure and problems with brain function. Tests to diagnose a brain abscess may include:

Blood cultures Chest x-ray Complete blood count (CBC) Head CT scan, CT with contrast agent Within 45 days the inflammation and the concomitant dead brain tissue are surrounded with a capsule, which gives the lesion the famous ring-enhancing lesion appearance on CT examination with contrast (since intravenously applied contrast material can not pass through the capsule, it is collected around the lesion and looks as a ring surrounding the relatively dark lesion). Electroencephalogram (EEG) MRI of head Testing for the presence of antibodies to organisms such as Toxoplasma gondii and Taenia solium A needle biopsy is usually performed to identify the cause of the infection.

Treatment Medication, not surgery, is recommended

Several abscesses (rare)

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A small abscess (less than 2 cm) An abscess deep in the brain

An abscess and meningitis Shunts in the brain for hydrocephalus (in some cases the shunt may need to be removed temporarily or replaced) Toxoplasma gondii infection in a person with HIV

Antibiotics will be prescribed. Antibiotics that work against a number of different bacteria (broad spectrum antibiotics) are most commonly used. Antifungal medications may also be prescribed if the infection is likely caused by a fungus. Immediate treatment may be needed if an abscess is injuring brain tissue by pressing on it, or there is a large abscess with a large amount of swelling around that it is raising pressure in the brain.

Surgery is needed if :

Increased pressure in the brain continues or gets worse The brain abscess does not get smaller after medication The brain abscess contains gas (produced by some types of bacteria) The brain abscess might break open (rupture)

Surgery consists of opening the skull, exposing the brain, and draining the abscess. Laboratory tests are often done to examine the fluid. This can help identify what is causing the infection, so that more appropriate antibiotics or antifungal drugs can be prescribed. The surgical procedure used depends on the size and depth of the abscess. The entire abscess may be removed (excised) if it is near the surface and enclosed in a sac. Needle aspiration guided by CT or MRI scan may be needed for a deep abscess. During this procedure, medications may be injected directly into the mass. Certain diuretics and steroids may also be used to reduce swelling of the brain. Complications

Brain damage, Seizures Meningitis that is severe and life threatening Recurrence of infection

Poliomyelitis
Polio; Infantile paralysis; Post-polio syndrome Definition Poliomyelitis is a viral disease that can affect nerves and can lead to partial or full paralysis.
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Causes, incidence, and risk factors Poliomyelitis is a disease caused by infection with the poliovirus. The virus spreads by:

Direct person-to-person contact Contact with infected mucus or phlegm from the nose or mouth Contact with infected feces

The virus enters through the mouth and nose, multiplies in the throat and intestinal tract, and then is absorbed and spread through the blood and lymph system. The time from being infected with the virus to developing symptoms of disease (incubation) ranges from 5 - 35 days (average 7 - 14 days). Most people do not develop symptoms. Risks include:

Lack of immunization against polio Travel to an area that has experienced a polio outbreak Immune deficiency, malnutrition, tonsillectomy, physical activity Skeletal muscle injury agents, and pregnancy. due to injection of vaccines or therapeutic

Classification Two basic patterns of polio infection are described: a minor illness which does not involve the central nervous system (CNS), sometimes called abortive poliomyelitis. A major illness involving the CNS, which may be paralytic or nonparalytic. In most people with a normal immune system, a poliovirus infection is asymptomatic. Rarely, the infection produces minor symptoms; these may include upper respiratory tract infection (sore throat and fever), gastrointestinaldisturbances (nausea, vomiting, abdominal pain, constipation or, rarely, diarrhea), and influenza-like illness. The virus enters the central nervous system in about 3% of infections. Most patients with CNS involvement develop nonparalytic aseptic meningitis, with symptoms of headache, neck, back, abdominal and extremity pain, fever, vomiting, lethargy, and irritability. About one to five in 1000 cases progress to paralytic disease, in which the muscles become weak, floppy and poorly controlled, and, finally, completely paralyzed; this condition is known as acute flaccid paralysis. Depending on the site of paralysis, paralytic classified as spinal, bulbar, or bulbospinal. Paralytic polio with symptoms Denervation of skeletal muscle tissue secondary to poliovirus infection can lead to paralysis. poliomyelitis is

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In around 1% of infections, poliovirus spreads along certain nerve fiber pathways, preferentially replicating in and destroying motor neurons within the spinal cord, brain stem, or motor cortex. This leads to the development of paralytic poliomyelitis, the various forms of which (spinal, bulbar, and bulbospinal) vary only with the amount of neuronal damage and inflammation that occurs, and the region of the CNS affected. The destruction of neuronal cells produces lesions within the spinal ganglia; these may also occur in the reticular formation, vestibular nuclei, cerebellar vermis, and deep cerebellar nuclei. Inflammation associated with nerve cell destruction often alters the color and appearance of the gray matter in thespinal column, causing it to appear reddish and swollen. Other destructive changes associated with paralytic disease occur in the forebrain region, specifically the hypothalamus and thalamus. Early symptoms of paralytic polio include high fever, headache, stiffness in the back and neck, asymmetrical weakness of various muscles, sensitivity to touch, difficulty swallowing, muscle pain, loss of superficial and deep reflexes, paresthesia (pins and needles), irritability, constipation, or difficulty urinating. Paralysis generally develops one to ten days after early symptoms begin, progresses for two to three days, and is usually complete by the time the fever breaks. Spinal polio The location of motor neurons in the anterior horn cells of the spinal column Spinal polio, the most common form of paralytic poliomyelitis, results from viral invasion of the motor neurons of the anterior horn cells, or the ventral(front) grey matter section in the spinal column, which are responsible for movement of the muscles, including those of the trunk, limbs, and the intercostal muscles. Virus invasion causes inflammation of the nerve cells, leading to damage or destruction of motor neuron ganglia. When spinal neurons die, Wallerian degeneration takes place, leading to weakness of those muscles formerly innervated by the now-dead neurons. With the destruction of nerve cells, the muscles no longer receive signals from the brain or spinal cord; without nerve stimulation, the muscles atrophy, becoming weak, floppy and poorly controlled, and finally completely paralyzed. Progression to maximum paralysis is rapid (two to four days), and is usually associated with fever and muscle pain. Deep tendon reflexes are also affected, and are usually absent or diminished; sensation (the ability to feel) in the paralyzed limbs, however, is not affected. The extent of spinal paralysis depends on the region of the cord affected, which may be cervical, thoracic, or lumbar. The virus may affect muscles on both sides of the body, but more often the paralysis is asymmetrical. Any limb or combination of limbs may be affectedone leg, one arm, or both legs and both arms. Paralysis is often more severe proximally (where the limb joins the body) than distally (the fingertips and toes).
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Bulbar polio The location and anatomy of the bulbar region (in orange) Bulbar polio occurs when poliovirus invades and destroys nerves within the bulbar region of the brain stem. The destruction of these nerves weakens the muscles supplied by the cranial nerves, producing symptoms of encephalitis, and causes difficulty breathing, speaking and swallowing. Critical nerves affected are the glossopharyngeal nerve (which partially controls swallowing and functions in the throat, tongue movement, and taste), the vagus nerve (which sends signals to the heart, intestines, and lungs), and the accessory nerve (which controls upper neck movement). Due to the effect on swallowing, secretions of mucus may build up in the airway, causing suffocation. Other signs and symptoms include facial weakness (caused by destruction of the trigeminal nerve and facial nerve, which innervate the cheeks, tear ducts, gums, and uscles of the face, among other structures),double vision, difficulty in chewing, and abnormal respiratory rate, depth, and rhythm (which may lead to respiratory arrest). Pulmonary edema andshock are also possible and may be fatal. Bulbospinal polio All paralytic polio cases have both bulbar and spinal symptoms; this subtype is called respiratory or bulbospinal polio. Here, the virus affects the upper part of the cervical spinal cord (cervical vertebrae C3 through C5), and paralysis of the diaphragm occurs. The critical nerves affected are the phrenic nerve (which drives the diaphragm to inflate the lungs) and those that drive the muscles needed for swallowing. By destroying these nerves, this form of polio affects breathing, making it difficult or impossible for the patient to breathe without the support of a ventilator. It can lead to paralysis of the arms and legs and may also affect swallowing and heart functions. Pathophysiology

A blockage of the lumbar anterior spinal cord artery due to polio (PV3) Poliovirus enters the body through the mouth, infecting the first cells with which it comes in contact the pharynx and intestinal mucosa. It gains entry by binding to an immunoglobulin-like receptor, known as the poliovirus receptor or CD155, on the cell membrane. The virus then hijacks the host cell's own machinery, and begins to replicate. Poliovirus divides within gastrointestinal cells for about a week, from where it spreads to the tonsils(specifically the follicular dendritic cells residing within the tonsilar germinal centers), the intestinal lymphoid tissue including the M cells of Peyer's patches, and the deep cervical and mesenteric lymph nodes, where it multiplies abundantly. The virus is subsequently absorbed into the bloodstream. Known as viremia, the presence of virus in the bloodstream enables it to be widely distributed throughout the body.

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This sustained replication causes a major viremia, and leads to the development of minor influenza-like symptoms. Rarely, this may progress and the virus may invade the central nervous system, provoking a local inflammatory response. In most cases, this causes a self-limiting inflammation of the meninges, the layers of tissue surrounding the brain, which is known as nonparalytic aseptic meningitis. Penetration of the CNS provides no known benefit to the virus, and is quite possibly an incidental deviation of a normal gastrointestinal infection.

Symptoms There are three basic patterns of polio infection: subclinical infections, nonparalytic, and paralytic. Most people have subclinical infection, and may not have symptoms. SUBCLINICAL INFECTION SYMPTOMS

General discomfort or uneasiness (malaise) Headache, Slight fever Red and Sore throat, Vomiting People with subclinical polio infection might not have symptoms, or mild symptoms may last 72 hours or less. Clinical poliomyelitis affects the central nervous system (brain and spinal cord), and is divided into nonparalytic and paralytic forms. It may occur after recovery from a subclinical infection. Signs and tests The health care provider may find:

Abnormal reflexes, Back stiffness Difficulty lifting the head or legs when lying flat on the back Stiff neck, Trouble bending the neck

Tests include:

Cultures of throat washings, stools, or spinal fluid

Spinal tap and examination of the spinal fluid (CSF examination ) Test for levels of antibodies to the polio virus Treatment The goal of treatment is to control symptoms while the infection runs its course. People with severe cases may need lifesaving measures, especially breathing help. Symptoms are treated based on their severity. Treatment may include:

Antibiotics for urinary tract infections

Prepared by Kawaljit Kang and Navjot Brar,MSc 2nd yr, Mai Bhago College of Nursing, Tarn Taran.

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Moist heat (heating pads, warm towels) to reduce muscle pain and spasms Painkillers to reduce headache, muscle pain, and spasms (narcotics are not usually given because they increase the risk of breathing trouble) Physical therapy, braces or corrective shoes, or orthopedic surgery to help recover muscle strength and function. There is no cure for polio. The focus of modern treatment has been on providing relief of symptoms, speeding recovery and preventing complications. Supportive measures include antibiotics to prevent infections in weakened muscles, analgesics for pain, moderate exercise and a nutritious diet. Treatment of polio often requires long-term rehabilitation, including occupational therapy, physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery. Portable ventilators may be required to support breathing. Historically, a noninvasive, negative-pressure ventilator, more commonly called an iron lung, was used to artificially maintain respiration during an acute polio infection until a person could breathe independently (generally about one to two weeks). Other historical treatments for polio include hydrotherapy, electrotherapy, massage and passive motion exercises, and surgical treatments, such as tendon lengthening and nerve grafting.

Complications

Aspiration pneumonia, Lung problems, Pulmonary edema Cor pulmonale (a form of heart failure found on the right side of the circulation system) Lack of movement, Permanent muscle paralysis, disability, deformity Myocarditis, Shock Paralytic ileus (loss of intestinal function) Urinary tract infections

Post-polio syndrome is a complication that develops in some patients, usually 30 or more years after they are first infected. Muscles that were already weak may get weaker. Weakness may also develop in muscles that were not affected before. Prevention Passive immunization

Prepared by Kawaljit Kang and Navjot Brar,MSc 2nd yr, Mai Bhago College of Nursing, Tarn Taran.

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Hammon proposed the gamma globulin, which contained antibodies to poliovirus, could be used to halt poliovirus infection, prevent disease, and reduce the severity of disease in other patients who had contracted polio. Vaccine Two types of vaccine are used throughout the world to combat polio. Both types induce immunity to polio, efficiently blocking person-to-person transmission of wild poliovirus inactivated virus vaccine Live attenuated (weakened) another live, oral polio vaccine (OPV). Post-polio syndrome Between 25% and 50% of individuals who survive paralytic polio in childhood develop additional symptoms decades after recovering from the acute infection, notably new muscle weakness and extreme fatigue. This condition is known as post-polio syndrome (PPS) or post-polio sequelae. The symptoms of PPS are thought to involve a failure of the over-sized motor units created during recovery from paralytic disease. Factors that increase the risk of PPS include the length of time since acute poliovirus infection, the presence of permanent residual impairment after recovery from the acute illness, and both overuse and disuse of neurons. Post-polio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.

List of infections of the central nervous system

There are four main causes of infections of system (CNS): bacterial, viral, fungal and protozoal. Fungal infections

the central

nervous

Cryptococcal meningitis Brain abscess Spinal epidural infection

Protozoal infections

toxoplasmosis malaria Primary amoebic meningoencephalitis

Bacterial infections

tuberculosis leprosy neurosyphilis Bacterial meningitis Late stage Lyme disease Brain abscess

Prepared by Kawaljit Kang and Navjot Brar,MSc 2nd yr, Mai Bhago College of Nursing, Tarn Taran.

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Neuroborreliosis

Viral infections

Viral meningitis Eastern equine encephalitis St Louis encephalitis Japanese encephalitis West Nile encephalitis Herpes simplex encephalitis Rabies California encephalitis virus Varicella-zoster encephalitis La Crosse encephalitis Measles encephalitis poliomyelitis slow virus infections, which include: Subacute sclerosing panencephalitis Progressive multifocal leukoencephalopathy Acquired immunodeficiency syndrome (AIDS)

Post-infectious diseases of the central nervous system

PANDAS Sydenham's chorea Acute disseminated encephalomyelitis Guillain-Barr syndrome

Prepared by Kawaljit Kang and Navjot Brar,MSc 2nd yr, Mai Bhago College of Nursing, Tarn Taran.