MENINGITIS

Definition
In meningitis, the brain and the spinal cord meninges become inflamed. Such
inflammation may involve all three meningeal membranes the dura mater, arachnoid membrane
and pia mater.
Aseptic viral meningitis is a benign syndrome characterized by headache, fever, vomiting,
and meningeal symptoms. It results from some of viral infection including enteroviruses and
arboviruses.

Etiology
Bacterial meningitis:
In neonates: E. cole, Klebsiella, Haemophilus influenzae
In children : Haemophilus influenza, Pneumococcus ( Strep. pneumonia), Meningococcus
(Neisseria meningitides)
In adults : Pneumococcus, Menigococcus
Other bacteria : Listeria monocytogenes, Streptococcus pyogenes and Staphylococcus aureus are
occasionally reponsible

Viral Meningitis
 Enteroviruses
 Arboviruses
 Herpes simplex virus
 Mumps virus
 Lymphocytic choriomeningitis virus

Epidemiology
 Incidence is between 4.6 and 10 cases per 100,000 persons per year.
 H. influenze is the most frequent cases, followed by N. meningitis and S. pneuomonia
 Males are affected by H. influenza and meningococcal infections during fall, winter and
spring
 H. influenza meningitis ia frequent in children between 2 months and 3 years of age.
 While meningococcal infections occur most often in children and adolescents,
 Pneumococcal meningitis predominates in adults over 40 years of age.

Pathophysiology
The presence of the blood-brain barrier limits host defence mechanisms and enables
multiplication of organisms. A purulent exudates most evident in the basal cisterns extends
throughout the subarachnoid space. The underlying brain, although not invaded by bacteria,
becomes congested, oedematous and ischaemic. The integrity of the pia mater normally protects
against brain abcess formation.
The cytokines, interleukin, tumor necrosis factor, and prostaglandin E2 are released as
part of an acute inflammatory response. They increase vascular permeability, cause a loss of
cerebrovascular autoregulation and exacerbate neuronal injury. The inflammatory exudate may
also affect vascular structures crossing the subarachnoid space producing an arteritis or venous
thrombophlebitis with resultant infarction. Similarly, cranial nerves may suffer direct damage.

Clinical Manifestations
The classical clinical triad is fever, headache, and stiffness.
Prodromal features variable
 Respiratory infection otitis media or pneumonia associated with muscle pain
 Meningitic symptoms
Severe frontal or occipital headache, stiff neck, photophobia
Systemic signs
 High fever. Transient purpuric or ptechial skin rash in meningococcal meningitis.
Meningitic signs
 Neck stiffness – gentle flexion of the neck is met with boardlike stiffness
 (+) Brudzinksi’s sign
 (+) Kernig’s sign
 Stretching the lumbar roots produces pain
Associated Neurological Signs
 Impaired conscious level
 Focal or generalized seizures are frequent

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  Cranial nerve sign occur in 15% of patients
 Sensorineural deafness (not due to concurrent otitis media but to direct cochlear
involvement) – 20%
Focal neurologic signs
 Hemiparesis, dysphasia, hemianopia, papilloedema – 10%
Non-neurological complications
 Shock, inappropriate secretion of ADH, Arthritis, Acute bacterial endocarditis
Coagulation disorders:
Thrombocytopenia- disseminated intravascular coagulation
Features Specific to causative bacteria

Haemophilus meningitis Meningococcal meningitis Pneumococcal meningitis

Generally occurs in small Often occurs in epidemics Predominantly an adult
children. where the organism is carried disorder. Often associated with
Preceding upper respiratory in the nasopharynx. debilitation, e.g. alcoholism.
tract infection. Septicaemia can occur with May result from pneumonia,
Onset abrupt with a brief arthralgia; purpuric skin rash. middle ear, sinus infection or
prodrome. When overwhelming, confluent follow splenectomy.
haemorhhages appear in the Onset may be explosive,
skin due to disseminated progressive to death within a
intravascular coagulation. few hours.
Outcome Gradual onset – good Mortality – 20%
Generally good prognosis Poor prognostic signs- coma,
Less than 5% mortality Sudden onset with septicaemia seizures, increased protein in
– poor outcome CSF
Overall mortality – 10%

Viral Meningitis:
 Fever up to 104°F  Abdominal pain
 Alteration of consciousness  Poorly defines chest pain
 Neck or spine stiffness  Sore throat
 Headache
 Nausea
 Vomiting

Diagnosis
The cardinal signs of meningitis are those of infection and increased intracranial pressure
(ICP). Lumbar puncture shows typical cerebrospinal fluid findings associated with meningitis
(elevated CSF pressure, cloudy or milky white CSF, high protein level, positive Gram stain and
culture that usually identifies the infecting organism unless it’s a virus, and depressed CSF glucose
concentration).
Chest X-rays are especially important because they may reveal pneumonitis or lung abscess,
tubercular lesions or granulomas secondary to fungal infection.
White blood cell count usually indicates leukocytosis, and serum electrolyte levels often
are abnormal. Computed tomography scanning can rule out cerebral hematoma, hemorrhage, or
tumor.

1.If patient has altered consciousness, focal signs, papilloedema, a recent seizure or is
immunocompromised a CT brain should be done before LP. However, do not delay treatment –
take blood cultures and commence antibiotic prior to scanning.
2. If above signs are absent or CT scan excludes a mass lesion → confirm diagnosis with a lumbar
puncture and identify the organism.
CSF examination – moderate increase in pressure <300 mm CSF
Grams stain of spun-down sediment
Gram + ve paired cocci Gram – ve bacilli Gram – ve intra and
extracellular cocci
= pneumococcus = haemophilus = meningococcus

 cell count is elevated, 100-10 000 cells/mmᵌ (80-90% polymorphonuclear leucocytes)

 glucose is depressed
 enzyme lactic dehydrogenase is elevated
 culture CSF
Serological/Immunological tests

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The latex particle agglutination (LA) test, for the detection of bacteria antigen is CSF, has a
sensitivity 80% for haemophilus and pneuomococcus and 50% for meningococcus (100%
specificity). The polymerase chain reaction (PCR), for the detection of bacteria nuecleic acid in
CSF, is available for all the suspected organism. The specificity and sensitivity of PCR is unknown
and the delay (3 to 5 days) to process results, makes the test less helpful than the combination of
Gram’s stain, culture, and the LA test.

Blood cultures
 organism isolated in 80% of cases of Haemophilus meningitis
 Pneumococcus and meningococcus in less than 50% of patients
3. Check serum electrolytes
 important in view of the frequency of inappropriate antidiuretic hormone secretion
4. Detect the source of infection
 Chest X-ray – pneumonia
 Sinus X-ray – sinusitis
 Skull X-ray – fracture
 Petrous views – mastoiditis
Differential Diagnosis
 Viral encephalitis
 Inebriation
 Delirium tremens
 Hepatic encephalitis
Prognosis
The prognosis is good and complications are rare, especially if the disease is recognized
early and the infecting organism responds to antibiotics. Mortality in untreated meningitis is 70% to
100%. The prognosis is poorer for infants and elderly people.

Complications
Potential complications of meningitis include visual impairment, optic neuritis, cranial
nerve palsies, deafness, personality change, headache, paresis or paralysis, endocarditis, coma,
vasculitis, and cerebral infarction, Children may develop sensory hearing loss, epilepsy, mental
retardation, hydrocephalus, or subdural effusions.

Medical/ Pharmacological Management

Once meningitis is suspected, treatment must commence immediately, often before
identification of the causative organism. Antibiotics must penetrate CSF, be in appropriate
bactericidal dosage and be sensitive to causal organism once identified.

Initial therapy (before organism identification)

Neonates (above 1 month) – ampicillin _ aminoglycoside and cephalosporin
Children ( under 5 years) – vancomycin _ 3rd generation cephalosporin
Adults – vancomycin + 3rd generation cephalosporin
Immunocompromised patient – vancomycin + ampicillin _ cephalosporin

Steroids
A four-day regimen of dexamethasone, starting before or with the first dose of antibiotics, is now
recommended in children with haemophilus and adults with bacterial meningitis likely to be
pneumococcal. Meta-analysis found a risk-reduction of neurological sequelae and mortality of
about 30% in pneumococcal meningitis, with no clear difference with other organisms.

Therapy after organism identification

ORGANISM ANTIBIOTIC ALTERNATIVE THERAPY
rd
Haemophilus Ampicillin or 3 generation Chloramphenicol
cephalosporin according to Fluoroquinolone
sensitivities Cefepime
rd
Pneumococcus Benzylpenicillin or 3 generation Chloramphenicol
cephalosporin according to Fluoroquinolone
sensitivities Meropenem
rd
Meningococcus Benzylpenicillin or 3 generation Chloramphenicol
cephalosporin according to Fluoroquinolone
sensitivities Meropenem
rd
E. coli 3 generation cephalosporin Aztreonam
Fluoroquinolone
Meropenem
Ampicillin

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Listeria Ampicillin Chloramphenicol
±Gentamicin Cotrimoxazole

rd
3 generation cephalosporin = Ceftriaxone or cefotaxime

Meningococcus and Haemophilus – continue for at least 1 week after afebrile

Pneumococcus –continue for 10-14 days after afebrile

Monitoring
in a deteriorating patient, CT scan will exclude the development of hydrocephalus, abscess or
subdural empyema. In suspected sinus thrombosis MR venography or sinus clearance.

PT Management
Objective of care
 The patient will maintain adequate ventilation.
 The patient will exhibit temperature within normal range
 The patient will express feelings of comfort and relief of pain
 The patient will maintain fluid volume within normal range
 The patient’s skin integrity will remain intact

Appropriate interventions /Rationale of each action

 Maintain respiratory isolation for 24 hours after the start of antibiotic therapy. Discharges
from the nose and the mouth are considered infectious. Follow strict aseptic technique
when treating patients with head wounds or skull fractures.
 Continually assess the patient’s clinical status, including neurologic function and vital
signs. Mointor for changes in LOC and signs of increased ICP. Also watch for signs of
cranial nerve involvement (ptosis, strabismus, diplopia).
 Watch for signs of deterioration. Be especially alert for a temperature increase,
deteriorating LOC, onset of seizures, and altered respirations, all of which may signal an
impending crisis.
 Monitor fluid balance. Maintain adequate fluid intake to avoid dehydration, but avoid fluid
overload.
 Position the patient carefully to prevent joint stiffness and neck pain. Turn him often,
according to a planned positioning schedule. Assist with range of motion exercises.
 Maintain adequate nutrition.
 Provide reassurance an support.

Relevant health teaching/s to patient and family

 Inform the patient and family members of the contagion risks, and tell them to notify
anyone who comes into close contact with the patient. Such people require antimicrobial
prophylaxis and immediate medical attention if fever or other signs of meningitis develop.

 To help prevent the development of meningitis, teach patients with chronic sinusitis or
other chronic infections the importance of proper medical treatment.

LEPROSY

Definition
Leprosy is a nonfatal, chronic infectious disease caused by Mycobacterium lepra, whose
clinical manifestations are largely confines to the skin, peripheral nervous system, upper respiratory
tract, eyes, and testes.

Etiology
Leprosy is caused by Mycobacterium leprae, an acid-fast bacillus that attacks cutaneous
tissue and peripheral nerves, especially the ulnar, radial, posteropopliteal, anterotibial, and facial
nerves. The central nervous system appears highly resistant. Susceptibility is highest during
childhood and seems to decrease with age. Presumably, transmission occurs through airborne
respiratory droplets that contain M. leprae or by inoculation through skin breaks (from a
contaminated hypodermic or tattoo needle, for example).

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Epidemiology
 Affects Asia, Africa, Latin America, and the Pacific.
 Africa: highest prevalence; Asia: most cases
 Leprosy is largely absent from the United States, ~4000 persons have leprosy and 100-
200 new cases are reported annually in California, Texas, New York and Hawaii among
immigrants from Mexico, Southeast Asia, Philippines, and the Caribbean.
 0.6 to 8 million affected individuals
 Twice more common in men than women
 In India and Africa, 90% of cases are tuberculoid
 Southeast Asia, 50% are tuberculoid and 50% lepromatous
 Mexico, 90% are lepromatous

Pathophysiology
1. Mycobacterium leprae attacks the peripheral nerves, especially the ulnar, radial, posterior-
popliteal, anterior-tibial and facial nerves.
2. When the bacilli damage the skin’s fine nerves, they cause anesthesia, anhidrosis and
dryness.
3. If they attack a large nerve trunk, motor nerve damage, weakness and pain occur,
followed by peripheral anesthesia, muscle paralysis and atrophy.

Clinical Manifestations
Tuberculoid Leprosy
 Begins with localized skin lesions that are at first flat and red but enlarge and develop
irregular shapes with indurated, elevated, hyperpigmented margins and depressed pale
centers (central healing).
 Neuronal involvement dominate
 As nerves becomes enclosed within granulomatous inflammatory reactions and, if small
enough, are destroyed.
 Nerve degeneration causes skin anesthesias and skin and muscle atrophy that render the
patient liable to trauma of the affected part
 Development of indolent skin ulcers
 Contractures, paralyses, and autoamputation of fingers or toes may ensue.
 Facial nerve involvement can lead to paralysis of lids, with keratitis and corneal
ulcerations.
Lepromatous (Anergic) Leprosy
 Lepromatous Leprosy involves the skin, peripheral nerves, anterior eye, upper airways
(down to the larynx), testes, hands, and feet
 vital organs and central nervous system are rarely affected because the core temperature
is too high for growth of M. leprae.
 contain large aggregates of lipid-laden with masses of acid-fast bacilli.
 Macular, popular, or nodular lesions form on tha face, ears, wrists, elbows, and knees.
 With progression, the nodular lesions coalesce to yield a distinctive leonine facie.
 Most skin lesions are hypoesthetic or anesthetic.
 Lesions in the nose may cause persistent inflammation and bacilli-laden discharge. T
 he peripheral nerves, particularly the ulnar and peroneal nerves where they approach the
skin surface, are symmetrically invaded with mycobacteria, with minimal inflammation.
 Loss of sensation and trophic changes in the hands and feet follow the nerve lesions.
Lymph nodes show aggregation of foamy histiocytes in the paracortical area, with
enlargement of germinal centers.

Diagnosis
Identification of acid-fast bacilli in skin and nasal mucosa scrapings confirms a diagnosis
of leprosy. A skin biopsy shows the typical histologic pattern of nerve changes. The skin biopsy and
scraping also are evaluated to determine the percentage of fully intact cells (morphologic index)
and to measure the amount of bacteria present (bacterial index).

Differential Diagnosis
 Sarcoidosis
 Leishmaniasis
 Lupus Vulgaris
 Deratofibroma
 Lymphoma
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  Syphilis
 Yaws
 Granuloma annulare
Prognosis/Complications
Erythema nodosum leprosum, seen in lepromatous leprosy, may produce fever, malaise,
lymphadenopathy, and painful, red skin nodules, usually during antimicrobial treatment, although
the skin lesion may occur in untreated people.

In Mexico and other Central American countries, some patients with lepromatous disease
develop Lucio’s phenomenon; generalized reddened lesions with necrotic centers. These ulcers
may extend into muscle and fascia.

Leprosy also may be complicated by secondary bacterial infection of skin ulcers,

amyloidosis, deformity contractures, ocular disorders that can result in blindness and, rarely,
hepatitis and exfoliative dermatitis.

Medical/ Pharmacological Management

1. Sulfone (Dapsone)
 50-100 mg/dl
 Mainstay of therapy for leprosy
 It is used with rifampin as the primary method of treating leprosy
 it appears to exert its antibacterial effects in a manner similar to that of the sulfonamide
drugs
 Adverse effects are: peripheral motor weakness, hypersensitivity reactions (skin
rashes,itching), fever and blood dyscresias
2.Rifampin
 600 mg daily or monthly
 alternative if Sulfone fails to respond in leprosy
 bactericidal
 Impairs DNA replication in susceptible bacteria
 Adverse effects: GI distress
3.Clofazimine
 50-100 mg/dl or 100 mg three times weekly or 300 mg monthly
 It is used primarily as an adjunct in the treatment of leprosy
 It prevents replication of the bacteria from undergoing mitosis
 Adverse effects: causes red-black skin discoloration, abdominal pain, nausea, vomiting

PT Management
Objective of care
 The patient will communicate feelings about changed body image
 The patient will express positive feelings about self
 The patient will exhibit improved or healed lesions or wounds
 The patient will interact with family or friends
 The patient will perform self-care activities independently
Appropriate interventions
 Provide supportive patient care, taking steps to control acute infection, prevent
complications, speed recovery and rehabilitation, and provide emotional encouragement.
 Plan care to promote adequate rest and optimal nutrition.
 Give patient and family opportunities to express their feelings.
 Inspect the patient’s skin and report observed changes. Assist with general hygiene and
comfort measures.

Rationale of each action

 For plantar ulcers – can be prevented by a rigid-soled footwear or walking plaster cast
 For prevention of contractures of hand- stretching exercise and cast is appropriate
 Nerve and tendon transplant and release of contracture

Relevant health teaching/s to patient and family

 Instruct the patient to be careful not to injure an anesthesized leg by putting too much
weight on it. Advise him to carefully test bath water to avoid scalding. To prevent
ulcerations, suggest wearing sturdy footwear and soaking feet in warm water after any
kind of exercise, event a short walk. Advise rubbing the feet with petrolatum oil, or lanolin.

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  Recommend that the patient use a tear substitute twice a day and protect his eyes,
especially if he experiences decreased corneal sensation and lacrimation. Tell him to
avoid rubbing his eyes and to wear sunglasses. Explain that these measures help prevent
the corneal irritation and ulceration that lead to blindness.
 Tell the patient to take antimicrobial medications exactly as prescribed for the entire length
of time prescribed—in some cases, for life.

POTT’S DISEASE

Definition
Pott’s disease is a chronic epidural infection that follows tuberculous osteomylitis of the
vertebral bodies. This arises in the lower thoracic region, can extend over several segments and
may spread through the intervertebral foramen into pleura, peritoneum or psoas muscle (psoas
abscess).

Etiology
It is caused by mycobacterium tuberculosis, the tubercle bacillus. The tuberculous
granulomas first produce caseous necrosis of the bone marrow, and effect that leads to slow
resorption of bony trabeculae and, occasionally, to cystic spaces in the bone. Because there is little
or no reactive bone formation, collapse of the affected vertebra is usual, after which kyphosis and
scoliosis ensue. The IV disk is crushed and destroyed by the compression fracture, rather than by
invasion of organisms.
If the infection ruptures into the soft tissue anteriorly, pus and necrotic debris drain along
the spinal ligaments and form a cold abscess, a term that signifies the absence of acute
inflammation. A psoas abscess forms near the lower lumbar vertebrae and dissects along the
pelvis, to emerge through the skin of the inguinal region as a draining sinus. Such a process may
occur without any prior symptoms and may be the first manifestation of the tuberculous spondylitis.

Epidemiology
 In developing countries, spinal TB is mostly a disease of childhood or adolescence.
 In Britain, it usually affects the middle aged and is particularly prevalent in immigrant
populations.
 The incidence is now increasing probably due to development of antibiotic resistance.

Pathophysiology

Tuberculosis infiltrates the spine via Hematogenous spread through the densce
vasculature of cancellous bone of the anterior vertebral bodies then there is Lymphatic spread from
para-aortic lymph nodes, it is possible but rare. Up to 75% of infected individuals develop a soft
tissue infection and it commonly occurs in the psoas muscle “cold abscess”, because it forms
slowly and does not normally present with heat, inflammation or pain and there is paraspinal fistula
which may form a communication with the chest wall on in the pelvic floor. If left untreated, there is
degeneration and inflammation of the vertebrae that causes herniation into the cord space resulting
to a compression in the spinal cord and cauda equina.

Clinical Manifestations
 Weight loss
 Night fever
 Cachexia is absent
 Pain occurs over the affected area and made made worse by weight bearing
 Kyphosis develops

Diagnosis
 MRI with gadolinium shows an epidural mass with paraspinal soft tissue swelling.
 Anterior superior or inferior angle of the vertebral body is initially involved.
 Infective process spreads throughtout the vertebral body and may involve the pedicles or
facet joints
 The disc space collapses as the vertebral plate is destroyed.

Differential Diagnosis

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  Pyogenic infections
 Typhoid spine
 Brucella spondylities
 Mycotic spondylitis
 Tumorous condition
Prognosis/Complications
Less favorable when there is joint involvement

Medical/ Pharmacological Management

 A needle biopsy is often sufficient, but occasionally an exploratory operation
(costotransversectomy) is required. Long term antituberculous therapy is commenced. If
signs of compression develop, decompression is necessary.
 Posterior decompression remove the remaining unaffected bone, likely to cause instability.
An anterior posterolateral approach is therefore required.
 Posterolateral approach: one or more ribs resected ,edially, along with the transverse
processes.
 Anterior Transthoracic Decompression with strut graft fusion is sometimes performed. This
permits clearance of pus and caseous debris without retracting the spinal cord.

PT Management
1. Period of recumbency, usually treated as SCI patients –gentle PROM and AROM exercise,
breathing exercise
2 .Healing consolidation phase-muscle strengthening, mobilization, breathing exercise and AROM
3. Bed rest
4.Immobilization before the collapse of more than one vertebral body
5. Bracing even for mild kyphosis

References
th
Fauci, AS, MD, et al. Harrison’s Principle of Internal Medicine, 11 Ed. Mc-Graw Hill
Companies, Inc.1998.

Kumar, Abbas & Fausto. Pathologic Basis of Disease, 7th Ed. 2005.

Moreau,D., Editor. Diseases.Springhouse Corporation, 2001.

th
Rowland, LP. Merritt’s textbook of neurology, 9 Ed. William & Wilkins, 1994.
st
Young, M.G., et. al. Concepts: basic and clinical notes for Physical therapy, 1 ed.

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