Infective and inflammatory disease Medical Assignment Help

MENINGITIS

Meningitis (inflammation of the meninges) may becaused by:
• Bacteria
• Viruses
• Fungi
• Other organisms
• Malignant cells
• Drugs and contrast media
• Blood (following SAH)
The term is usually restricted to inflammation due to infective agents (Table 18.41). Microorganisms reach the

Bacteria
Neisseria meningitidis”
Haemophilus irdluenzse:
Streptococcus pneumoniee”
Staphylococcus aureus
Listeria monocytogenes
Gram·negative bacilli
Mycobacterium tuberculosis
Treponema pallidum
Viruses
Enteroviruses
Echo
Coxsackie
Polio
Mumps
Herpes simplex
HIV
Epstein-Barr virus
Fungi
Cryptococcus neoformans
Candida
(Coccidioides immitis, Histoplasma capsulatum, Blastomyces dermatitidis in USA)

PATHOLOGY
In acute bacterial meningitis the pia-arachnoid is congested with polymorphs. A layer of pus forms that may organize to form adhesions, causing cranial nerve palsies and hydrocephalus. In tuberculous infection the brain is covered in a viscous grey-green exudate; numerous
tubercles are found on the meninges. Cerebral oedema is common in bacterial meningitis. In viral meningitis there is a predominantly lymphocytic inflammatory reaction in the CSF without the formation of pus or adhesions. There is no cerebral oedema unless viral encephalitis develops.

CLINICAL FEATURES

Meningitic syndrome
There is intense malaise, fever, rigors, severe headache, photophobia and vomiting. The patient is irritable and often prefers to lie still.
Neck stiffness and a positive Kernig’s sign appear within a few hours. In milder cases (and many viral meningitides) there are few other signs, but it is most  unreliable to rely on the clinical impression alone whenassessing the severity of the infection. In uncomplicated meni ngitis, consciousness is not impaired, although the patient may be delirious with a high fever. Papilloedema may occur. The appearance of drowsiness, lateralizing signs and cranial nerve lesionsindicate a complication such as a venous sinus thrombosis  (see p. 912), severe cerebral oedema or hydrocephalus, or an alternative diagnosis such as a cerebral abscess (see p. 930) or encephalitis

Specific varieties of meningitis Particular attention should be paid to rashes and associated clinical features (see Table 18.42), and a search
should be made for infected foci.
ACUTE BACTERIAL MENI GITIS. The onset is sudden, with rigors and a high fever. A petechial rash, often sparse, is strong evidence of meningococcal meningitis. Septicaemia may present with acute septicaemic shock.
TUBERCULOUS MENINGITIS. Tuberculosis causes a chronic meningitis commencing with vague headache, lassitude, anorexia and vomiting. Meningitic signs may appear only after some weeks. Drowsiness, focal signs and seizures may occur. A similar picture occurs in cryptococcal meningitis, the commonest fungal meningitis in Europe. MALIGNANT MENINGITIS. Malignant cells sometimescause a subacute or chronic meningitic process. Meningitis,  cranial nerve palsies, paraparesis and root lesions are seen, often in complex patterns. The CSF shows increased cells and protein and often a low glucose. Treatment is with intrathecal cytotoxic agents. The prognosis is poor.

DIFFERENTIAL DIAGNOSIS

Acute meningitis may resemble SAH, severe migraine and  ther causes of a sudden severe headache. Meningitis  hould be considered in all patients who have headache and fever.

MANAGEMENT
Meningitis is an emergency that has a high mortality even in countries with highly developed systems of health care. Although viral meningitis is a self-limiting condition, untreated bacterial meningitis is lethal; in most series the death rate is around 15% even with treatment. f meningococcal (or other acute bacterial) meningitis is diagnosed clinically, particularly in children, immediate treatment with intravenous benzylpenicillin should be started with subsequent urgent investigations. In this acute illness, minutes count.

If there is no suggestion of an intracranial mass lesion (when CT scanning should be performed), immediate lumbar puncture should be carried out. Typical changes in the CSF are shown in Table 18.43. CSF pressure is characteristically elevated. Blood should be taken for culture
and glucose levels as well as for routine tests. Chest and skull films should be taken if possible. Gram-staining of the CSF may demonstrate organisms (e.g. Gram-positive intracellular diplococci-pneumococcus;
Gram-nega tive cocci-meningococcus). Ziehl- Nielsen stain demonstrates acid-fast bacilli (tuberculosis), though these organisms are rarely numerous. Indian ink stains fungi.
Many serological tests are now available for CSF. Syphilitic serology should always be carried out. The clinical picture and CSF examination should allow at least a presumptive diagnosis of the cause of the meningitis to be made within several hours of presentation.
Patients with impaired consciousness should be nursed as described on p. 903. General management includes diazepam for convulsions and analgesics for headache. Treatment of bacterial meningitis
It is often possible to distinguish between viral, pyogenic, tuberculous and other organisms from the clinical setting and immediate examination of the CSF. If bacterial meningitis is suspected, high doses of antibiotics are started immediately. There should be close liaison with   microbiologist. In children, dexamethasone should also be given as this reduces the frequency of complications particularly deafness.
In a pyogenic meningitis in an adult (where the organism is unknown), intravenous benzylpenicillin 2 g 2- hourly and intravenous chloramphenicol 75 mg kg:” have been given. Because of resistant organisms it is now recommended that immediate i.v. cefotaxime is used instead. If the diagnosis of pneumococcal or meningococcal infectionhas been made, penicillin alone or cefotaxime are  used. Chloramphenicol alone or third-generation cephalosporins should be used in Haemophilus infections. Tuberculous meningitis is treated for at least 9 months with antituberculous drugs; rifampicin, isoniazid and pyrazinamide is the usual combination (see p. 686).
It is no longer necessary to use intrathecal antibiotics. Local infection (e.g. an infected paranasal sinus) should also be treated, surgically if necessary. Surgical repair of depressed skull fracture or meningeal tear may be necessary.
Polyvalent vaccines are available against recurrent pneumococcal meningitis (e.g. when there is a CSP leak following skull fracture) and against some strains of meningococci (see p.23). In meningococcal outbreaks rifampicin prophylaxis should be given to contacts and family members as well as to the patient.

Differential diagnosis of (SF pleocytosis Difficulties occur in meningitis when a raised, often mixed (lymphocyte and polymorph, i.e. pleocytic) picture is found but no infecting organism. This is sometimescalled ‘aseptic meningitis’. The conditions listed in Table  18.44 should be considered.

ENCEPHALITIS

Encephalitis’ is inflammation of brain parenchyma. It iscaused by a wide variety of viruses and may also occur  in bacterial and other infections.
Acute viral encephalitis In many cases a viral aetiology is presumed but not confirmed serologically or by culture. The usual organisms cultured from cases of viral encephalitis in adults in the UK are Echo, Coxsackie, mumps and herpes simplex viruses, Adenovirus, varicella zoster, influenza, measles and other viruses are rarer causes.

CLINICAL FEATURES

Many of these infections cause a mild self-limiting illness with headache and drowsiness. In a minority there is a more serious illness accompanied by focal signs, seizures and coma. Herpes simplex virus (HSV-1) accounts for many of these severe infections in Britain and has a mortality of around 20% even with treatment. In the Far East the Japanese B arbovirus is a more usual, and epidemic, cause of severe encephalitis, with a high mortality. depressed skull fracture or meningeal tear may be necessary.

Polyvalent vaccines are available against recurrentpneumococcal meningitis (e.g. when there is a CSP leak  following skull fracture) and against some strains of meningococci (see p.23). In meningococcal outbreaks rifampicin prophylaxis should be given to contacts and family members as well as to the patient. Differential diagnosis of (SF pleocytosis Difficulties occur in meningitis when a raised, oftenmixed (lymphocyte and polymorph, i.e. pleocytic) picture is found but no infecting organism. This is sometimes called ‘aseptic meningitis’. The conditions listed in Table 18.44 should be considered.

ENCEPHALITIS

Encephalitis’ is inflammation of brain parenchyma. It iscaused by a wide variety of viruses and may also occur in bacterial and other infections.
Acute viral encephalitis  In many cases a viral aetiology is presumed but not confirmed serologically or by culture. The usual organismscultured from cases of viral encephalitis in adults in the  UK are Echo, Coxsackie, mumps and herpes simplex viruses,
Adenovirus, varicella zoster, influenza, measles and other viruses are rarer causes.

CLINICAL FEATURES

Many of these infections cause a mild self-limiting illnesswith headache and drowsiness. In a minority there is a  more serious illness accompanied by focal signs, seizures and coma. Herpes simplex virus (HSV-1) accounts for many of these severe infections in Britain and has a mortality of around 20% even with treatment. In the Far East the Japanese B arbovirus is a more usual, and epidemic, cause of severe encephalitis, with a high mortality. Partially treated bacterial meningitis
Viral meningitis

Tuberculosis or fungi
Neoplastic meningitis
Para meningeal foci (e.g. paranasal sinus)
Syphilis
Intracranial abscess
Cerebral venous or arterial infection
Following subarachnoid haemorrhage
Encephalitis, including AIDS
Rare causes (e.g. cerebral malaria, sarcoidosis, Behcet’s
syndrome, Lyme disease

DIFFERENTIAL DIAGNOSIS
This includes:
• Bacterial meningitis complicated by cerebral oedema and/or cerebral venous thrombosis
• Cerebral abscess
• Acute disseminated encephalomyelitis
• Toxic confusional states in febrile illnesses and III septicaemia
INVESTIGATION
Investigation in severe cases includes CT scanning (which characteristically shows areas of oedema), EEG (which shows slow-wave changes and/or ‘periodic complexes’) and viral serology of blood and CSP. Brain biopsy is now seldom performed in the UK.
TREATMENT
Suspected herpes simplex encephalitis is immediately treated with intravenous acyclovir, the active form of which inhibits DNA synthesis. Phosphorylation of. this drug is dependent upon the presence of viral thymidine kinase; thus the drug is specific for herpesvirus infections. If the patient is in coma the outlook is poor whether or not drugs are given.
Supportive measures are required for comatose patients. Seizures are treated with anticonvulsants. Prophylactic immunization is possible against Japanese B encephalitis and sometimes advised particularly for travellers to the Far East in endemic areas.
Acute disseminated
encephalomyelitis (ADE)
This follows many common viral infections (e.g. measles, varicella zoster, mumps and rubella) and rarely after immunization against rabies, influenza or pertussis. The  clinical syndrome is often similar to acute viral encephalitis, with added focal brain stem and/or spinal cord
lesions due to demyelination, but in which viral particles are not usually present. The prognosis is variable. Mild cases recover completely but in severe cases (those in coma) mortality is around 25% and the survivors often have permanent brain damage. Treatment is supportive, with steroids and anticonvulsants.

MYELITIS

Myelitis means inflammation of the spinal cord causing paraparesis or tetra paresis. It occurs with varicella zoster or as part of a postinfective encephalomyelitis. Poliomyelitis is a specific enterovirus infection of anterior horn cells .
.
HERPES ZOSTER (SHINGLES)

This is a recrudescence of infection with varicella zoster virus within the dorsal root ganglia, the original infection having been acquired in an attack of chickenpox many years previously. The viruses causing chickenpox and shingles are identical.

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