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Dr Charles Bryan
Emeritus Professor
University of South Carolina School of Medicine



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Bacterial meningitis
Headache and fever
Acute psychosis
Pneumococcal pneumonia


Figure 1
This ventral view of a human brain depicts a purulent basilar meningitis infection due to Streptococcus pneumoniae bacteria.
Though S. pneumoniae in a normally occurring floral inhabitant of the human upper respiratory tract, in cases where an individual’s immune system is compromised, it is responsible for causing paranasal sinusitis, middle ear infections (otitis media), and lobar pneumonia, as well as meningitis secondary to these primary respiratory infections. CDC


Figure 2
Streptococcus pneumoniae bacteria grown from a blood culture. Streptococcus pneumoniae, the bacteria responsible for pneumococcal meningitis, is very common, and normally lives in the back of the nose and throat, or the upper respiratory tract. CDC

Figure 3
Aerobic Gram-negative Neisseria meningitidis diplococcal bacteria; Mag. 1150X.
Meningococcal disease is an infection caused by a bacterium called N. meningitidis or the meningococcus. The meningococcus lives in the throat of 5-10% of healthy people. Rarely, it can cause serious illness such as meningitis or blood infection. CDC

Figure 4
Haemophilus influenzae - coccobacillus prokaryote (dividing); causes meningitis in children, pneumonia, epiglottitis, laryngitis, conjunctivitis, neonatal infection, otitis media (middle ear infection) and sinusitis in adults (SEM x 64,000)
 © Dennis Kunkel Microscopy, Inc.  Used with permission

hib patient.jpg (24392 bytes) Figure 5
This child has swollen face due to Hib infection. The tissue under the skin covering the jaw and cheek is infected. Infection is spreading into her face. She is probably very sick  Courtesy of Children's Immunization Project, St. Paul, MN


Acute Bacterial Meningitis

Acute bacterial meningitis is a medical emergency variably characterized by fever, headache, meningismus (stiff neck), nausea, vomiting, and altered mental status. In about 15% of patients and especially in young children and elderly patients, the presentation is subtle. Gastrointestinal symptoms may predominate leading to a misdiagnosis of gastroenteritis. Delayed diagnosis invites tragic consequences.

The “big 3” causes of community-acquired bacterial meningitis beyond the neonatal period of life are Streptococcus pneumoniae, Hemophilus influenzae type B, and Neisseria meningitidis. These organisms have in common the ability to colonize the nasopharynx and to elude host defenses by virtue of their polysaccharide capsules. Widespread vaccination of young children against H. influenzae type B now makes this form of meningitis uncommon. N. meningitidis is a relatively common cause in children, adolescents, and young adults (See “Meningococcemia” in the chapter on Sepsis). S. pneumoniae causes meningitis in all age groups, is the most common cause in older adults, and is frequent in persons with history of basilar skull fracture. Listeria monocytogenes is an important cause in neonates and in patients who are elderly, debilitated, or immunosuppressed (for example, patients with lymphomas or who are receiving corticosteroids). Aerobic gram-negative rods are important causes of meningitis in neonates, elderly patients, and patients who have undergone neurosurgical procedures.

The presentation is, to some extent, age-dependent. Infants may present mainly with listlessness, poor feeding, and altered breathing patterns. The frail elderly may present mainly with a decline in the level of awareness. Meningitis due to Listeria monocytogenes or to aerobic gram-negative rods usually has a less dramatic, more sub-acute onset compared to meningitis caused by S. pneumoniae, H. influenzae type B, or N. meningitidis. When any of the “big three” cause meningitis in a previously-healthy younger person, the symptoms usually prompt immediate medical attention. However, the history not infrequently suggests a nonspecific flu-like illness that gradually worsened over several days to one week. In this setting, great attention must be paid to the potential significance of any combination of headache, nausea, and vomiting.
S. pneumoniae is now the most common cause of community-acquired bacterial meningitis when all age groups are taken into account. Older patients with pneumococcal meningitis―unlike younger patients with H. influenzae or meningococcal meningitis―frequently have underlying conditions such as alcoholism or neurologic disease to which altered consciousness can be easily attributed. However, patients with pneumococcal meningitis―again, unlike younger patients with H. influenzae or meningococcal meningitis―frequently have a clinically-apparent site of infection elsewhere such as otitis media, sinusitis, pneumonia, or―rarely―endocarditis.

One should “think meningitis” when patients present with some combination of fever, headache, stiff neck, nausea or vomiting, and altered consciousness. None of these symptoms is sufficiently sensitive, however, to exclude meningitis by its absence. In adults, the overall sensitivity is about 50% for headache and about 30% for nausea and vomiting. The absence of fever, stiff neck, and altered mental status allows one to exclude meningitis with 99% to 100% confidence.

Physical examination should target the following areas:

  1. The skin, looking for the petechial rash of meningococcemia
  2. The tympanic membranes, looking for evidence of otitis media as a portal of entry for pneumococcal meningitis
  3. The optic disks, looking for evidence of papilledema as a relative contraindication to lumbar puncture (pulsations in the central retinal veins effectively exclude increased intracranial pressure)
  4. Signs of meningeal irritation

Meningeal irritation can be assessed in at least four ways, all of which can be performed briefly and are therefore recommended:

  • Anterior neck flexion. With the patient supine, ask the patient to flex the head forward (“Put your head on your chest”). Alternatively, ask the patient to put his or her head between the knees. Neck stiffness is present when the patient experiences pain on anterior flexion.
  • Kernig’s sign: With the patient supine and the hip flexed at 90 degrees, the knee is extended. Brudzinki’s sign is present when the patient experiences pain or resistance in the lower back or posterior thigh. This test can also be performed in the sitting position.
  • Brudzinski’s sign: With the patient supine and holding the patient's head, flex the head so that the chin touches the chest. Brudzinski’s sign is present when the patient flexes the knees and hips in response to this maneuver.
  • The jolt test: Ask the patient to turn his or her head from side to side at a frequency of 2 to 3 rotations per second. The jolt sign is present when this maneuver worsens the patient’s headache.

Kernig’s and Brudzinski’s signs have high specificity but low sensitivity for the diagnosis of meningitis. Jolt accentuation of headache was determined to have a 97% sensitivity and 60% specificity; in a recent review it was also concluded that the test has a positive likelihood ratio of 2.2 and a negative likelihood ratio of zero. It has been suggested that absence of the jolt sign essentially excludes meningitis. More experience is needed to establish this point with a reasonable degree of certainty.

When meningitis is suspected, lumbar puncture should be performed. Today’s frequent tendency to postpone lumbar puncture until a localized intracranial lesion has been excluded by an imaging study (CT scan or MRI scan) is unfortunate, because a delay in the institution of therapy of several hours can be crucial to the outcome. When the illness is acute and there are no localizing neurologic signs and no evidence of papilledema, the risk-benefit ratio for lumbar puncture weighs heavily in favor of proceeding with the procedure. Fluid should be obtained for leukocyte count, differential count, glucose, and protein content (collectively, these 4 parameters are known as the “CSF formula” and also for culture. The CSF formula is never diagnostic but can be extremely helpful, as follows:

  • Acute bacterial meningitis: A leukocyte count > 1000/μL with predominance of polymorphonuclear neutrophils, and with low glucose (< 40 mg/dL or <40% of the blood glucose) and high protein content (> 150 mg/dL) is highly characteristic.
  • Viral (“aseptic”) meningitis: The leukocyte count is usually < 1000/μL with < 50% polymorphonuclear neutrophils on the differential count, with normal glucose and normal or slightly elevated protein content (exceptions to these rules are discussed below under “Aseptic Meningitis”).
  • Fungal or tuberculous meningitis (chronic meningitis): The leukocyte count is usually < 500/μL with < 50% polymorphonuclear neutrophils, with low glucose and elevated protein content.
  • Parameningeal infection (such as brain abscess): The leukocyte count is usually < 1000/μL with < 50% polymorphonuclear neutrophils, normal glucose, and normal or elevated protein content.

An extra tube of CSF should always be saved, since additional studies may be indicated if the initial tests are non-diagnostic.
Untreated, meningococcal and pneumococcal meningitis are probably uniformly fatal. Survivors of H. influenzae meningitis in the pre-antibiotic era often spent the remainder of their lives in institutions for the severely retarded.

Cryptococcosis of lung in patient with AIDS. Mucicarmine stain.
Histopathology of lung shows widened alveolar septum containing a few inflammatory cells and numerous yeasts of Cryptococcus neoformans. The inner layer of the yeast capsule stains red. CDC

Aseptic Meningitis, Chronic Meningitis, and Other Causes of CSF Pleocytosis

There are numerous causes of fever, headache, focal neurologic signs and symptoms, and CSF pleocytosis. The more common ones are discussed here because of the need to distinguish these diverse syndromes and specific diseases from acute bacterial meningitis.

Aseptic Meningitis (“Viral Meningitis”)

The term “aseptic meningitis” was introduced during the 1930s to describe a self-limited condition characterized by headache, mild nuchal rigidity, and predominantly lymphocytic CSF pleocytosis. The term has been used synonymously with “viral meningitis,” but it is now recognized that there are many causes of the aseptic meningitis syndrome including drugs.
Surveillance reports suggest that aseptic meningitis affects about one in 10,000 persons each year; mild cases go unrecognized and the true incidence is unknown. Rigorous attempts to isolate or identify viruses are successful in the majority (55% to 70%) of cases. Enteroviruses are by far the most common causes in the United States (85% to 95% of cases in which a virus is identified). Aseptic meningitis caused by enteroviruses occurs mainly during the summer and fall. Infants and young children are most commonly affected. Some of the enteroviruses can cause a rash. Aseptic meningitis occurs in up to 30% of patients with mumps, often without evidence of salivary gland disease. The lymphocytic choriomeningitis virus causes aseptic meningitis with a relatively intense CSF pleocytosis. This virus is transmitted by rodents such as hamsters, mice, and rats; hence the disease occurs especially in pet owners, laboratory workers, and persons living in substandard housing. Arboviruses such as the St. Louis encephalitis virus can cause a syndrome resembling aseptic meningitis more than encephalitis (these terms are relative, since patients with meningitis usually have some brain involvement and patients with encephalitis usually have some meningeal involvement). Herpes simplex virus type 2 often causes aseptic meningitis (in contrast to HSV type 1, which more often causes encephalitis; see below). Finally, aseptic meningitis is a common manifestation of the acute retroviral syndrome due to the human immunodeficiency virus (HIV).

Aseptic meningitis can punctuate the course of many systemic bacterial, rickettsial, mycoplasmal, spirochetal, and parasitic infections. Aseptic meningitis occurs in syphilis, especially secondary syphilis. Aseptic meningitis is a prominent feature of Lyme disease (neuroborelliosis). Leptospirosis can cause an aseptic meningitis syndrome during either or both of the two phases of the disease: the acute infectious phase or the secondary phase during which manifestations are presumed due to circulating immune complexes. CSF pleocytosis can occur during the course of bacterial endocarditis as the result of emboli, immune-complex encephalitis, or possibly mycotic aneurysm. Drugs are being reported increasingly as a cause of aseptic meningitis. These include not only drugs used in chemotherapy (such as azathioprine) but also commonly-used drugs such as NSAIDs, antimicrobial agents (especially TMP/SMX and its separate components), ranitidine, and carbamazepine (in patients with underlying connective tissue diseases). Onset is usually abrupt with headache and mild nuchal rigidity but the more severe manifestations of acute bacterial meningitis such as stupor and coma do not occur.

A presumptive diagnosis of aseptic meningitis can be made when a patient with no history of recent antibiotic therapy presents with headache and mild nuchal rigidity and is found to have low-grade CSF pleocytosis, predominantly lymphocytic, with normal CSF glucose and protein levels. The diagnosis is confirmed by the clinical course, since a self-limited course distinguishes the illness from chronic meningitis (e.g., tuberculous meningitis and cryptococcal meningitis). Problems arise when either the clinical course or the CSF formula is atypical for aseptic meningitis. Some of the agents of aseptic meningitis (notably mumps and lymphocytic choriomeningitis) not infrequently cause a low CSF glucose content.
Occasional patients with aseptic meningitis present with headache, mild nuchal rigidity, and low-grade CSF pleocytosis with a predominance of polymorphonuclear neutrophils. When the history and physical examination reveal no other signs or symptoms pointing to acute bacterial meningitis and when the patient does not look especially “sick,” the clinician faces a dilemma. Should the patient be hospitalized and committed to a 7- to 10-day course of treatment for presumed acute bacterial meningitis? Or should the patient be sent home? A third option is to observe the patient closely without treatment and to repeat the lumbar puncture in 4 to 6 hours. The second lumbar puncture reveals CSF with a predominance of lymphocytes, thus pointing to non-bacterial infection. Recently, the polymerase chain reaction (PCR) has been shown to be effective for early, specific diagnosis of enterovirus infection of the CNS.

All patients with aseptic meningitis should be screened for syphilis with a VDRL on both serum and CSF. It is prudent to save an extra tube of CSF, since at the time of initial presentation there is always the possibility that the patient could have one of the causes of chronic meningitis and further studies may be necessary. Viral cultures of CSF can be attempted, but are unnecessary in daily practice.

Chronic Meningitis

The term “chronic meningitis” was introduced during the 1970s to embrace a large number of illnesses causing meningoencephalitis (fever, headache, lethargy, confusion, nausea, vomiting, stiff neck) and CSF abnormalities (predominantly lymphocytic pleocytosis, elevated protein, and often low glucose) lasting at least 4 weeks. Tuberculosis and cryptococcosis are the most common causes of chronic meningitis in the United States.

Etiologies are both infectious and non-infectious. The former include tuberculosis, fungal diseases (cryptococcosis, coccidioidomycosis, histoplasmosis, blastomycosis, candidiasis, and sporotrichosis), spirochetal diseases (syphilis and Lyme disease), brucellosis, and parasitic infections (Acanthamoeba and Angiostrongylus cantonensis). The latter include tumors, sarcoidosis, granulomatous angiitis, Behçet’s disease, and uveomeningoencephalitis. Some patients are given the diagnosis of “chronic benign lymphocytic meningitis,” and in other cases a satisfactory diagnosis is never reached. Chronic meningitis is often a component of diseases manifested mainly as encephalitis (for example, subacute sclerosing panencephalitis due to the measles virus) or as focal lesions of the CNS (for example, toxoplasmosis).

The onset is typically insidious but can be acute, mimicking bacterial meningitis or aseptic meningitis. Patients often present with a one- to several-week history of headache, fever (which can be low-grade), lethargy, and nausea. If a diagnosis is not made and treatment instituted, the illness steadily progresses although the course is sometimes characterized by remissions and exacerbations.

The key to diagnosis of chronic meningitis is early suspicion and lumbar puncture. An ample volume of CSF should be saved, since a large number of studies may be necessary. Initial studies of CSF should include cryptococcal antigen, VDRL, PCR for Mycobacterium tuberculosis, AFB and fungal cultures (each preferably on 3 to 5 mL of CSF), and cytospin cytology. All patients should also have a tuberculin skin test, chest x-ray, and imaging of the brain (CT or MRI with gadolinium enhancement). Additional studies should be targeted on the basis of a thorough history and physical examination (both of which may need to be repeated carefully) and the results of initial laboratory tests. For example, travel or residence in the southwestern United States suggests coccidioidomycosis; tick exposures in New England or elsewhere suggest Lyme disease; and eosinophilia in the CSF suggests Coccidioides, parasites, lymphoma, or chemicals.

Untreated, tuberculous and cryptococcal meningitis are nearly always fatal. In previously healthy persons, cryptococcal meningitis can cause a subtle, extremely indolent illness that culminates in dementia. Prognosis for other forms of chronic meningitis is variable.

Other Causes of CSF Pleocytosis

There are numerous causes of CSF pleocytosis, of which partially-treated bacterial meningitis is perhaps the most important to the primary care clinician. Patients who receive oral antibiotics early during the course of acute bacterial meningitis may show temporary improvement, and the CSF pleocytosis may shift from predominantly neutrophilic to predominantly lymphocytic. The CSF protein usually remains high, helping to distinguish this entity from more benign conditions. The polymerase chain reaction (PCR) may prove to be highly useful for establishing the diagnosis of partially-treated bacterial meningitis. Diagnosis of parameningeal infections, discussed further below, usually hinges on the history, physical examination, and appropriate imaging studies. Tumors not infrequently cause lymphocytic pleocytosis, sometimes with low CSF glucose. Seizures sometimes cause mild CSF pleocytosis, which tends to be predominantly neutrophilic after alcohol-related seizures and predominantly lymphocytic after seizures caused by stroke. Rare patients experience recurrent meningitis, the causes of which include leaking cyst contents from craniopharyngioma or epidermoid cyst, systemic lupus erythematosus, and an unusual condition known as Mollaret’s meningitis. Drugs are being recognized increasingly as a cause of CSF pleocytosis (as discussed in the previous section on Aseptic Meningitis).

H&E-stained micrograph depicting the histopathologic changes seen in brain tissue due to herpes encephalitis; Mag. 125x.
Characterized by headaches, fever, and altered mental state due to inflammation of the brain, herpes simplex virus, the cause of HSV encephalitis, is one of the main causes for non-epidemic, sporadic encephalitis. CDC


A case of a periorbital fungal infection known as mucormycosis, or phycomycosis.
Mucormycosis is a dangerous fungal infection usually occurring in the immunocompromised patient, affecting the regions of the eye, nose, and through its growth and destruction of the periorbital tissues, it will eventually invade the brain cavity.
CDC/Dr. Thomas F. Sellers/Emory University



Encephalitis due to Herpes simplex and Other Viruses

Viral encephalitis is a life-threatening process characterized clinically by altered consciousness and frequently by focal neurologic signs, seizures, and other abnormalities. Herpes simplex virus, type 1 (HSV-1) is the most important cause of sporadic viral encephalitis in the United States, although it accounts for only about 10% to 20% of the estimated 20,000 cases of encephalitis that occur each year. Prompt diagnosis is crucial since, in contrast to most of the other forms of viral encephalitis, specific treatment is available.

The major causes of viral encephalitis are the herpes simplex viruses, the arboviruses, mumps, measles, and varicella-zoster virus.

Encephalitis due herpes simplex virus

About 95% of cases of encephalitis due to herpes simplex virus are caused by HSV-1, and the remainder by HSV-2. About 70% of these cases result from reactivation of latent infection and about 30% result from primary infection. Why occasional patients infected by this common virus develop encephalitis remains a mystery. Most severely-affected patients are immunologically normal; indeed an intact immune system may be required for full expression of the disease since immunocompromised patients tend to have a milder course. There is little or no evidence for person-to-person transmission or influence by environmental factors. By contrast, arboviral infections causing encephalitis are mosquito borne and tickborne.

Viral encephalitis including HSV encephalitis affects persons of all age groups. Symptoms and signs of HSV encephalitis usually begins suddenly in contrast to the usual subacute onset of the other forms of viral encephalitis. The first symptoms sometimes consist of behavioral abnormalities such as hypomania, elevated mood, and the Kluver-Bucy syndrome (loss of normal emotional responses such as anger and fear with hypersexuality). Lethargy progresses rapidly to confusion, stupor, and coma. Fever is usually present and may be high. Herpes labialis is present in fewer than 10% of cases and its presence or absence has no diagnostic significance.

Kluver-Bucy Syndrome

The most characteristic symptoms and signs of encephalitis due to HSV-1 are attributed to the affinity of the virus for the medial temporal and inferior frontal lobes. This is manifested by some combination of impairment of speech, bizarre behavior, and olfactory and gustatory hallucinations. Some patients develop other localizing neurologic symptoms and signs such as hemiparesis, ataxia, or cranial nerve palsies. Focal seizures also occur.

Temporal lobe involvement can be demonstrated by imaging procedures (CT or MRI scan) or by electroencephalography (EEG). MRI scans are more sensitive than and specific than CT scans especially during the early phases of the disease. The EEG shows focal abnormalities in more than 80% of cases. Lumbar puncture usually discloses red blood cells in the CSF, which reflects the necrotizing nature of the disease. The white cell count, glucose, and protein content in CSF are variable and occasionally all of these parameters are within normal limits. The most important specific test on CSF is the polymerase chain reaction (PCR for HSV-1 DNA). Reported to be up to 98% sensitive and 100% specific, PCR has replaced brain biopsy as the diagnostic procedure of choice.

Many diseases can mimic herpes simplex encephalitis. These include vascular disease, brain abscess or subdural empyema, toxic encephalopathy, tuberculosis, fungal infections (especially cryptococcosis and mucormycosis), tumor, subdural hematoma, and connective tissue diseases.

The natural history of encephalitis due to HSV-1 was well characterized prior to the introduction of effective antiviral therapy. Coma developed in about 85% of patients, seizures in up to 60% of patients, and aphasia in about 20% of patients. Mortality was about 70% and there was a high prevalence of neurologic residua among survivors.

West Nile virus infection

West Nile virus, a mosquito-born infection, is probably the best-documented example of the introduction of a new, vector-borne human infection into the United States during the twentieth century. The virus is transmitted by at least 29 North American species of mosquitoes that bite both humans and birds—notably corvids (in North America, crows, jays, and ravens; other corvids in Europe are rooks and magpies). About 20% of humans infected with the West Nile virus develop a febrile illness, but only about one-half of these patients seek medical attention. Approximately one in every 150 infected persons develops meningitis, encephalitis, or both. Advanced age is by far the greatest risk factor for severe neurologic disease and long-term morbidity. About one-half of hospitalized patients have severe muscle weakness. Up to 10% of patients have flaccid paralysis, sometimes suggesting Guillain-Barré syndrome. The most efficient method of diagnosis consists of an IgM antibody ELISA testing of CSF or serum.

Guillain-Barrè syndrome


Brain Abscess, Subdural Empyema, and Intracranial Epidural Abscess

The term parameningeal infection (literally, “beside the meninges”) encompasses several syndromes that require prompt diagnosis and, usually, surgical drainage. Examples include brain abscess, subdural empyema, septic thrombosis of the dural sinuses, and epidural abscess (both intracranial and spinal). Newer imaging studies (CT scan and MRI) simplify the diagnosis.

Brain Abscess

Brain abscess is usually due to spread from a contiguous focus of infection or hematogenous spread from a distant site of infection. Examples of the former include sinusitis (mainly frontal and ethmoid), otitis media or mastoiditis, dental sepsis, and penetrating injury or neurosurgery; examples of the latter include congenital heart disease with a right-to-left shunt, hereditary hemorrhagic telangiectasia with pulmonary arteriovenous fistulas, suppurative pulmonary infection, endocarditis, and opportunistic infections arising in patients who are immunocompromised. Brain abscess can also complicate head trauma. Streptococci, both aerobic and anaerobic, are the usual isolates but other aerobic and anaerobic bacteria are often present. Unusual microorganisms such as fungi and Toxoplasma gondii cause brain abscess mainly in the severely immunocompromised.

Brain abscess usually presents with some combination of headache, fever, focal neurologic deficit, nausea or vomiting, seizures, nuchal rigidity, and papilledema. However, the presenting symptoms often evolve slowly and are non-specific. Headache is the most common symptom (70% of patients) and can be localized or generalized. Fever is present in slightly less than one-half of adults. Altered mental status and hemiparesis are the most common focal neurologic signs. Neurologic signs frequently predict the site of disease: for example, bizarre behavior with frontal lobe abscess; speech abnormalities with temporal lobe abscess; ataxia, nausea, and nystagmus with cerebellar abscess; and visual field cuts with temporal, parietal, or occipital lobe abscess. Symptoms and signs of the predisposing disease such as sinusitis, otitis media, dental sepsis, or pulmonary disease are often but not always present.

Subdural Empyema

Subdural empyema, which is less common than brain abscess, arises most often (60% to 70%) as an extension from sinusitis, especially frontal sinusitis. Otitis media with or without mastoiditis is the other major cause. Cases also result from trauma or surgery. Streptococci and especially anaerobic streptococci are again the most common isolates, but staphylococci (notably, S. aureus) and aerobic gram-negative rods are also encountered. Intracranial epidural abscess, which is rare, has similar predisposing causes and a similar microbiology.

Subdural empyema usually evolves more rapidly than does brain abscess. Typically, symptoms suggestive of sinusitis or of otitis media are followed within days to several weeks by fever, severe headache, neck pain (meningismus) and then by altered mental status and focal neurologic signs, sometimes with seizures. Intracranial epidural abscess, on the other hand, usually develops slowly over weeks or even months. Nonspecific symptoms give way to symptoms of increased intracranial pressure (nausea, vomiting, headache, altered mental status) and focal neurologic signs.

The reported mortality for brain abscess now ranges between 0% and 30% and the mortality for subdural empyema from 6% to 20%. Many patients, and especially those with subdural empyema, are often left with a neurologic deficit.

Methicillin-resistant Staphylococcus aureus bacteria, commonly referred to by the acronym, MRSA; Magnified 9560x

Spherical (cocci) Gram-positive Staphylococcus aureus bacteria magnified 320X

Mycobacterium tuberculosis bacteria stained using acid-fast Ziehl-Neelsen stain; Magnified 1000X.

Septic Cavernous Sinus Thrombosis

Septic thrombosis of the large dural sinuses that provide venous drainage to the brain is a rare but life-threatening cause of severe headache. Diagnosis is usually delayed. There are 3 major syndromes: cavernous sinus thrombosis, lateral sinus thrombosis, and superior sagittal sinus thrombosis. Here we will focus on the most common of these syndromes, septic cavernous sinus thrombosis.

Facial infections, most often nasal furuncles, precede about one-half of all cases of cavernous sinus thrombosis. Sphenoid sinusitis accounts for about 30% of cases, dental infections about 10% of cases, and the remainder of cases are originate from otitis media, mastoiditis, or other localized infections. Staphylococcus aureus is the most common etiologic agent and the usual cause of cavernous sinus thrombosis due to facial infections or sphenoid sinusitis. S. pneumoniae and other streptococci explain some cases, and anaerobic bacteria sometimes cause the condition especially when it is due to dental infection or other forms of sinusitis. Diabetes mellitus is possibly a risk factor.

Most patients with cavernous sinus thrombosis present with severe, progressive, unilateral, retroorbital and frontal headache. The illness usually evolves over several days but in some cases the headache can be subacute or chronic. Migraine is a common misdiagnosis. Subsequent symptoms include unilateral swelling of the orbit, diplopia, and drowsiness. Rapid progression of the disease leads to proptosis, chemosis, papilledema, and ophthalmoplegia (inability to move the eyeball). Close examination often reveals decreased sensation over the forehead, nose, upper cheek and lip, and cornea and, on ophthalmoscopic examination, papilledema or dilated and tortuous retinal veins.

Severe unilateral headache with orbital swelling suggests the possibility of septic cavernous thrombosis, which then needs to be distinguished from other conditions. Orbital cellulitis is the most common problem in differential diagnosis. Other possibilities include blepharitis, intraorbital abscess, trauma, tumors (meningioma and nasopharyngeal carcinoma), and several rare vascular diseases. The CSF is usually but not always abnormal. CSF pleocytosis is present in about two-thirds of cases and in about one-third of cases the CSF formula suggests bacterial meningitis (see above). Neurodiagnostic imaging―currently high resolution CT scan with enhancement or MRI scan with enhancement―is now the diagnostic procedure of choice.

Untreated, septic cavernous sinus thrombosis is nearly uniformly fatal.

Spinal Epidural Abscess

Spinal epidural abscess classically presents initially with fever and back pain and progresses to weakness of the lower extremities with impaired bowel or bladder function and then to paralysis. The correct diagnosis is seldom made at the first patient encounter.

As seen in primary care practice, spinal epidural abscess is usually a complication of vertebral osteomyelitis or diskitis. Bacteria gain access to the spine through hematogenous dissemination. Most abscesses are located posterior to the spinal cord, although below the level of the L1 some of them are anterior to the cord. S. aureus is the most common microorganism, being found in more than 60% of cases (>90% of cases in some series), but aerobic gram-negative rods, streptococci, M. tuberculosis, and other organisms are major causes of the disease. Spinal epidural abscess also occurs as a complication of spinal surgery, trauma, drug use, or spinal anesthesia.

Many patients first experience a flu-like illness with fever, malaise, and―especially if S. aureus is the causative organism―myalgias. As the abscess expands, patients develop severe, localized back pain often accompanied by nerve root pain. Weakness in the extremities then develops along with sensory changes and impairment of bladder or bowel function or both.

Untreated, spinal epidural abscess progresses to complete compression of the spinal cord with permanent paralysis.


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