neuro infectious diseases

1. NEUROLOGICAL INFECTIONS
By,
Mr. Anish Ghosh
M.Sc. Nursing 2nd Year

2. INTRODUCTION-
Name of most common neurological infectious disease are Meningitis, Encephalitis, Poliomyelitis, Parasitic
Infections, Bacterial Infections, Neurosyphilis, HIV & AIDS, Brain Abscess etc.

3. DEFINITION
Meningitis is an acute inflammation of the pia mater and the arachnoid
membrane surrounding the brain and spinal cord. Therefore, meningitis is
always cerebrospinal infection.

4. ETIOLOGY
• Meningitis may result from the invasion of
bacteria, viruses, fungi, parasites, or other
toxins. Bacterial meningitis occurs most
frequently and can result in death if not
treated promptly.
• The organisms most frequently responsible
for bacterial meningitis include Neisseria
meningitidis, Streptococcus pneumoniae,
and Haemophilus influenzae.
• Viral meningitis (aseptic meningitis) usually
occurs after a variety of viral illnesses and
usually is self-limiting with full recovery

5. ROUTE OF ENTRY
• Bloodstream
• Direct Extension from a Primary Site
• Cerebrospinal Fluid
• Extension Along Cranial and Spinal
Nerves
• Mouth and Nasopharynx
• In Utero

6. TYPES OF MENINGITIS-
1. Bacterial Meningitis- it is a pyogenic (purulent) infection that involves the pia-arachnoid
layers of the meninges and the subarachnoid space including CSF.
Causes- Pneumococci, meningococci, streptococci, staphylococci. The most common causes
of bacterial meningitis depend on the age of the patient:
1. In new born: Streptococcus agalactiae, gram-negative bacilli and Listeria monocytogenes.
2. In children: Haemophilus influenzae, Neisseria meningitidis, streptococcus.
3. Adults: Streptococcus pneumoniae.

7. SIGNS AND SYMPTOMS
Headache and fever
Changes in LOC
Signs of meningeal irritation-
 Stiff neck or neck rigidity
 Kernig’s sign
 Brudzinski's sign
Generalized convulsions
Increase ICP
Endocrine disorders

8. 2. Viral Meningitis (Aseptic Meningitis)- Viral meningitis is a self-limited illness, seen most
frequently in children and young adults. The presentation is similar to bacterial meningitis
except that neurological dysfunction (e.g. change in mental status, neurological deficits) does
not occur and the overall prognosis is good.

9. 3. Chronic Meningitis (Tuberculosis Meningitis)- Tuberculosis meningitis is caused by Mycobacterium tuberculosis, which is a severe
infection that carries a high morbidity and mortality. The onset of this disease is much less acute. The patient may have been vaguely
unwell for weeks with gradually increasing headache and listlessness. This is the common and treatable disease in India.
Clinical Manifestations- Signs and symptoms are like in the case of meningitis.
1. Staging system was introduced in 1947.
- Stage I Non-specific manifestations of infection without neurological symptoms and signs. No clouding of consciousness.
- Stage II: Signs and symptoms of meningeal irritation with cranial nerve palsies, but no other neurological defects and no clouding of
consciousness. Lethargy or alteration in behavior.
- Stage III: Cross neurological deficit, stupor or coma
Focal neurological sign- unilateral or bilateral cranial nerve palsy.
Most frequently affected is VI cranial nerve
2. Neurological deficit: Hemiparesis,
3. Fundus: Optic fundus may occasionally offer specific clues to the presence of tuberculosis meningitis:
a. Visible tubercles in choroids.
b. Retinal lesions near optic disk.
c. Papilledema.
4. Hydrocephalus.

10. PATHOPHYSIOLOGY-
• Microorganisms and viruses reach the nervous system by many routes
• Invasion of bacteria into the meninges (pia-arachnoid layers of the meninges, the subarachnoid space, and the
ventricular system)
• results in an inflammatory response
• Neutrophils migrate into the subarachnoid space to engulf the bacteria, producing exudate in the subarachnoid
space
• This purulent exudate causes the cerebrospinal fluid to thicken, interfering with the normal flow of the fluid
around the brain and spinal cord and potentially obstructing the arachnoid villi,
• Hydrocephalus
• further inflammatory response, leading to increased intracranial pressure (ICP)
• Exudate accumulates over the brain and can extend to the cranial and peripheral nerves
• blood vessels in the meninges become engorged as the pressure increases in the area, disrupting blood flow
through vessels and possibly causing thrombosis or rupture of vessel walls
• Secondary infection of the brain tissue can occur, resulting in encephalitis. Furthermore, persistent elevated
intracranial pressure can cause cerebral infarction.

13. DIAGNOSTIC EVALUATION

14. MANAGEMENT-
• Meningitis can cause a medical emergency. When meningitis is suspected antibiotic
therapy (penicillin, ampicillin, ceftriaxone and cefotaxime) is instituted after the
collection of specimens for culture, even before the diagnosis is confirmed.
• Diagnostic measures include lumbar puncture (LP) and analysis of CSF. The fundus
of the eye should be examined via ophthalmoscope for papilledema before LP for
identification of possibly increased ICP.
• General treatment measures include suggestive care to control and reduce fever,
balance fluids and electrolytes and promote comfort
For Bacterial meningitis- Antibacterial therapy: Most adults are treated with ampicillin
200 mg/k/day IV and ceftriaxone 200 mg/kg/day. Injection dexamethasone 10 mg IV
every 6th hourly for 4 days may be given in severe cases to reduce the severity of
residual neurological and CN damage.

15. For Viral meningitis- Treatment is symptomatic and supportive; no drug therapy is effective
against the virus.
For Chronic Meningitis (Tuberculosis Meningitis)-
Until antibiotic sensitivity is known, treatment with four drugs is recommended for the first 2
months. A full course of treatment requires 9-12 months. Options include: .
1. Isoniazid 300 mg/day (also give pyridoxine 50 mg/ day).
2. Rifampin 600 mg/day.
3. Pyrazinamide 15-30 mg/kg/day.
4. Ethambutol 15-20 mg/kg/day, streptomycin 15 mg/ kg/day TM.
5. Ciprofloxacin 750 mg two times a day.
6. Cotreatment with dexamethasone 10 mg IV every 6 hours may also be used in severe cases
(with depressed LOC, focal deficits or multiple cranial nerve palsies) to inhibit the
response and limit damage.
Surgical treatment: Surgical intervention in tuberculosis meningitis is primarily directed at relief
of hydrocephalus. Ventricular drainage may be done to relieve pressure.

16. ENCEPHELITIS
Encephalitis is an inflammation of the brain tissue and meninges.
• Morbidity and mortality rates vary significantly with the
causative agent. The prognosis ranges from complete recovery
to death.
• According to the Centers for Disease Control and Prevention
(CDC), USA, encephalitis occurs in approximately 0.5 in every
1,000,000 individuals, most of them children, elderly people and
individuals with weakened immune system.
• The National Health Service (NHS), UK places the figure at 1.5
cases per 100,000 people.

17. ETIOLOGY
• Primary (Infectious) Encephalitis- According to the NHS (UK), there are three
main categories of viruses:
1. Common viruses, such as herpes simplex virus (HSV) or Epstein-Barr virus
(EBV).
2. Childhood viruses, such as measles and mumps.
3. Arboviruses, which are spread by mosquitoes, ticks and other insects, and
include Japanese encephalitis, West Nile encephalitis and tick-borne encephalitis.
• Secondary (Postinfectious) Encephalitis-
- Secondary postinfectious encephalitis could be caused by the complication of a
viral infection.

18. CLINICAL MANIFESTATIONS-
Symptoms of encephalitis are highly variable. Differences in the invading
organisms and area of the affected brain account for this variability.
- The onset of viral encephalitis may be acute or gradual, with fever, headache,
nuchal rigidity, irritability, lethargy, nausea, and vomiting.
- Over the course of several days, the patient may begin to show a rapidly
deteriorating level of consciousness, motor weakness, tremors, seizures,
aphasia, and Babinski’s sign.
- Herpes simplex encephalitis (herpes simplex virus type 1) is associated with
temporal lobe—limbic system deficits: olfactory and gustatory
hallucinations, bizarre behavior, temporal lobe seizures, and anosmia.

19. DIAGNOSTIC EVALUATION

20. MANAGEMENT
• Treatment focuses on alleviating symptoms.
• There are only a limited number of reliably tested specific antiviral agents, such as acyclovir; success is limited for most infections except herpes simplex
encephalitis.
• Corticosteroids may be administered to bring down the brain inflammation, especially in cases of postinfectious (secondary) encephalitis.
• Mechanical ventilation and other supportive treatment may be needed in case if the patient has severe symptoms.
• If patients have seizures they may be given anticonvulsants. Sedatives may be effective for seizures, restlessness and irritability.
• For patients with mild symptoms, the best treatment is rest, plenty of fluids and Tylenol (paracetamol) for fever and/or headaches.
• Collaborative and nursing management is symptomatic and supportive. Cerebral edema is a major problem and diuretics (mannitol) and corticosteroids
(dexamethasone) are used to control it.
• Acyclovir and vidarabine are used to treat encephalitis caused by HIV infection. For maximal benefit, antiviral agents should be started before the onset of
coma.
• Specific Protocol Patient with meningitis is hypersensitive to the environmental stimuli:
1. So provide a quiet environment in a darkroom where the patient is kept in strict bed rest, control environmental noise, control direct light.
2. Observe for increased intracranial pressure and incorporate nursing protocol to manage the increased intracranial pressure.

21. POLIOMYELITIS
A viral disease which may affect the spinal cord causing muscle weakness and paralysis. The
words polio (grey) and myelin (marrow, indicating the spinal cord) are derived from the Greek.
Poliomyelitis is a disease of the anterior horn motor neurons of the spinal cord and brain stem
caused by poliovirus I, II, III. Poliomyelitis, literally meaning “grey spinal cord inflammation.
Also called polio, infantile paralysis. It is an acute viral infectious disease caused by enterovirus.

22. EPIDEMIOLOGY-
• Usually attacks the children below 5 years.
• Infection increases in dirty, overcrowded place, where personal health is neglected.
• Polio virus remains in the throat secretions, stools of infected persons which can infect water,
milk, food, & other substances.
• flies play an important role in spreading the disease.
• Can occur more in rainy season.

23. Mode of transmission-
• Feco-oral route
• In early stage of disease, through inhalation or entry through conjunctiva of droplets of
respiratory secretions of patient.
CAUSES-
• Caused by polio virus
• Colonizes in the gastrointestinal tract (specifically) in intestine
Spread through-
• fecal-oral route,
• Oral-oral route,
• Intake of contaminated food/ water

24. RESISTANCE
• In feces: - for months at 4oC & years at 20oC
• Inactivated by heat and chlorination.
• Host range: - natural infection occurs only in humans.
• Period of communicability- 7-10 years before & after the onset of symptoms.
• Age: - most vulnerable from 6 months to 3 years.
• Seasonal: - most common during rainy season, peak season from July to September.
• Environmental source of infection: - Contaminated water and food, Flies, Overcrowding and
poor sanitation.

25. PATHOPHYSIOLOGY

26. CLINICAL FEATURES/ TYPES
Infection may occur in two forms: -
1. Inapparent/ asymptomatic (90-95%)
• Accounts for approximately 95% of cases
• Virus stays in intestinal tract and does not
attack the nerves
• Virus is shed in the stool so infected individual
is still able to infect others
2. Apparent/ symptomatic (5-10%)
• Non-paralytic aseptic meningitis
• Paralytic poliomyelitis
• Polio encephalitis
• Abortive polio-
- 4-8% infections
- Does not lead to paralysis
- Minor illness Symptoms: - Low grade fever,
Sore throat, Vomiting, Abdominal pain, Loss of
appetite, Malaise, Recovery: - complete, most
recover in <1 week, no paralysis.
• Non-paralytic aseptic meningitis-
- Occurs in 1-2% of polio infections
- Symptoms: - Headache, Nausea, Vomiting, Pain
and stiffness of neck, back and legs.
- Complete recovery after 2-10 days of
symptoms.

27. Signs-
• Tripod sign
• Signs Kiss the knee test
• Head drop sign
• Neck rigidity Method
• Paralytic poliomyelitis- 0.5-1% of of those infected develop this type. 2 phases-
- Minor- same as abortive polio
- Major- muscle pain, spasm and return of fever, followed by rapid onset flaccid
complete within 72hrs. It is of three types: - 1. Spinal paralytic poliomyelitis
2. Bulbar poliomyelitis 3. Bulbo-spinal poliomyelitis

28. DIAGNOSTIC EVALUATION-
1. History,
2. Clinical examination,
3. Stool examination,
4. CSF examination,
5. Serological tests

29. TREATMENT
The goal of the treatment is to control symptoms while the infection runs its course as there is no specific treatment for the viral
infection. Treatment may include :
- Hospitalization (may be required for those individuals who develop paralytic poliomyelitis). If the respiratory is involved, LONG-
TERM VENTILATION is necessary.
- Catheterization of distended bladder may be necessary.
- Antibiotic for urinary tract infection.
- Moist heat to reduce pain and muscle spasm
- Pain killer to reduce muscle pain, headache (such as acetaminophen).
- Physical therapy, braces or corrective shoes, or orthopedic surgery to help recover muscle strength & function
- Bed rest Essential during acute phase:- physical activity and trauma increases risk of paralytic polio, Posture to be changed every
2-3hrs.
- But it is a preventable disease by vaccination- Two types of vaccine are available: an inactivated poliovirus vaccine (IPV) and a live
attenuated OPV

30. BRAIN ABSCESS
A brain abscess is a suppurative infection consisting of a collection of pus within the
parenchyma of the brain.
ETIOLOGY-
• Direct extension from ear, tooth and mastoid or sinus infection is the primary cause.
• Other causes for brain abscess formation include septic venous thrombosis from a pulmonary
infection, bacterial endocarditis, skull fracture and non-sterile neurological procedure.
• Streptococci and staphylococci are the primary infective organisms.

31. CLINICAL MANIFESTATIONS-
• Manifestations are similar to those of meningitis and
encephalitis and include headache and fever.
• Signs of increased intracranial pressure (ICP) may include
drowsiness, confusion and seizures.
• Focal symptoms may be present and reflect the local area of
the abscess.
• For example, visual field defects or psychomotor seizures are
common with temporal lobe abscess, whereas an occipital
abscess may be accompanied by visual impairment and
hallucinations.

32. MANAGEMENT
Antibiotics- A number of drugs can be chosen depending upon the likely origin of the
abscess and the probable pathogen(s) involved. The following are the antibiotics,
• Penicillin G
• Metronidazole
• Ceftriaxone-
• Ceftazidime/Cefepime/Meropenem
• Oxacillin/Nafcillin/Vancomycin

33. AIDS-
Acquired immunodeficiency syndrome (AIDS) is characterized by a severe deficiency in cell-
mediated immunity, caused by the retrovirus known as the human immunodeficiency virus
(HIV). The deficiency in cell-mediated immunity predisposes individuals infected with HIV to a
wide Variety of opportunistic infections and malignant tumors.
SOURCE-
1. Blood.
2. Vaginal and cervical secretion.
3. Semen.
4. Cerebrospinal fluid (CSF).
5. Synovial: Pleural fluids, peritoneal, pericardial and secreted from wounds.

34. HIV TRANSMISSION

35. PATHOPHYSIOLOGY
• Virus enters into body through any route
• Infects cells that have CD, antigen
• Virus sheds its protein coat and converts RNA to DNA in presence of enzyme reverse
transcriptase
• Viral DNA integrate to host DNA and duplicate it during normal division
• Virus remains latent and become activated to produce new RNA
• Disrupt all membrane and cells of host person. Hyper T or CD, cells are primary cells
infected by HIV. It also infects macrophages, lymphocytes, monocytes & astrocytes

36. STAGES OF HIV INFECTION
• The Incubation Phase
• Acute HIV Infection
• Latency Stage
• AIDS

37. CLINICAL MANIFESTATIONS
Most individuals are asymptomatic following infection.
Approximately 20% of them develop fever, myalgia, lethargy,
rash, enlarged lymph nodes, sore throat, nausea after 2~4
weeks of infection. Common symptoms-
• Cyclical fever.
• Night sweats.
• Diarrhea, fatigue.
• Anorexia, weight loss.
• Oral hairy leukoplakia.
• AIDS dementia complex.

38. NEUROLOGICAL DISORDERS AND STAGES OF HIV
DISEASE-
Early HIV Disease- (CD4 cell levels above 500 cells/mm)
- Aseptic meningitis
- Acute encephalopathy with seizures and
confusion
- Inflammatory demyelinating
polyneuropathy (Guiljain-Barré
syndrome)
- Cranial nerve palsies (e.g. Bell’s palsy)
- Herpes zoster (shingles)
Moderate to Severe Immunodeficiency-
(200-500 CD4 cells/mm’)
- Cognitive impairment
- Distal sensory polyneuropathy (may also
appear in early HIV disease)
- Myelopathy
- Myopathy
Late-Stage HIV Disease- (less than 200 CD4
cells/mm)
- HIV encephalopathy (dementia)
- CNS toxoplasmosis
- Cytomegalovirus (CMV) infection
- Primary CNS lymphoma

39. DIAGNOSTIC EVALUATION-
• Antibody ELISA (enzyme-linked immunosorbent as say)
• Western blot
• Antigen
• Cell culture
• Lymphocyte number
• T4-T8 lymphocyte counts.

40. MANAGEMENT-
• Asymptomatic HIV positive individuals need close medical supervision. The T4 cells are
usually monitored every 3-4 months
• There is no cure for HIV/AIDS, but a variety of drugs can be used in combination to
control the virus. But these medicines only restrict further growth of HIV virus and
keep the health of immune system stable, but that is not an exact cure.
• Combinations of medication urges up a method of treatments for HIV virus known as
Highly Active Anti-Retroviral Therapy (HAART).

41. CLASSES OF HIV/AIDS ANTIRETROVIRAL
DRUGS-
1. Nucleoside reverse transcriptase inhibitors (NRTIs): NRTIs are faulty versions of building blocks that HIV needs to make copies of
itself. Examples include Abacavir (Ziagen) and the combination drugs emtricitabine, tenofovir (Truvada), lamivudine and zidovudine
(Combivir).
2. non-nucleoside reverse transcriptase inhibitors (NNRTIs): NNRTIs are common used in combination with NRTIs to help keep the
virus from multiplying. Examples include efavirenz, etravirine and nevirapine.
3. Protease inhibitors (Pls): Protease Inhibitors interfere with the protease enzyme that HIV uses to produce infectious viral particles.
Example include atazanavir, darunavir (Prezista), fosamprenavir (Lexiva) and ritonavir (Norvir).
4. Entry or fusion inhibitors: These drugs block HIV’s entry into CD4 cells. Fusion/Entry inhibitors interfere with the virus’ ability to
fuse with the cellular membrane, thereby blocking entry into the host cell. Examples include enfuvirtide (Fuzeon) and maraviroc
(Selzentry).
5. Integrase inhibitors: Integrase Inhibitors block integrase, the enzyme HIV uses to integrate genetic material of the virus into its
target host cell. Raltegravir (Isentress) works by disabling integrase, a protein that HIV uses to insert its genetic material into CD4
cells.

42. BACTERIAL INFECTIONS-
 Neurosyphilis- Neurosyphilis is an infection of any part of the nervous system
resulting from infection by spirochete Treponema pallidum.
Causes-
• It develops after inadequate treatment of early syphilis.
• Primary infection of syphilis is characterized by a chancre (firm painless genital ulcer).
• A secondary bacteremic stage may occur 2-12 weeks later and these results in generalized mucocutaneous lesions
(Palmar Plantar Rash) and lymphadenopathy.
• 2% of patients with secondary infection experience acute meningovascular syphilis.

43. CLINICAL MANIFESTATIONS
This condition produces three main diseases. The classic manifestations include:
1. Meningovascular syphilis- sudden paralysis of one of the cranial nerves or a limb, Cerebrospinal fluid (CSF)
shows slightly raised lymphocyte count and the blood Wassermann reaction (WR) will usually be positives.
Many parts of the nervous system can be involved.
2. Tabes dorsalis- Lightning pains. Girdle pains, Loss of position sense, Tendon reflex will be absent, so no
bladder control will be present, Ulcers on the feet due to loss of sensation
3. General paralysis of the insane (GPI)- In this type of neurosyphilis the nerve cells of the brain are involved.
Many of them die and the brain atrophies or shrinks
Symptoms are:
1. Slow mental deterioration leading to dementia.
2. Prominent psychiatric features. Patient may have grandiose delusions, emotional changes.
3 Fits.

44. DIAGNOSTIC EVALUATION-
Some have collected clinical and laboratory features and entered them into templates; six such
diagnostic categories, as derived could be outlined as follows:
1. Category 1: Neuropsychiatric (most common manifestations) disorders (psychosis, delirium
and dementia).
2. Category 2: Cerebrovascular accident (acute, focal neurological deficit compatible with a
cerebrovascular accident or radiological evidence of stroke).
3. Category 3: Ocular (presentation with uveitis, visual loss or optic nerve dysfunction).
4. Category 4: Myelopathy (acute, subacute or chronic dysfunction of the spinal cord).
5. Category 5: Seizure (presentation with partial seizures with or without secondary
generalization).
6. Category 6: Brainstem/cranial nerve (signs restricted to the brainstem and cranial nerves).

45. MANAGEMENT-
• Primary and secondary syphilis can be treated with benzathine penicillin 24 million
units IM weekly for 3 weeks.
• Neurosyphilis whether latent or active is treated with penicillin G 2 to 4 million units
IV every 4th hours for 10 days.

46. INTRACRANIAL TUBERCULOSIS
It is comprising a variety of neurological syndromes with a relatively high mortality and morbidity caused by
Mycobacterium tuberculosis. The most common presentation of CNS-TB is meningitis, followed by
tuberculoma, tuberculous brain abscess, and Pott's disease.
INCIDENCE-
• Risk increased with age across racial and ethnic groups
• In populations with a low prevalence of TB, most cases of TBM occur in adults.
• TBM is more common in children than in adults, especially in the first 5 years of life.

47. CLINICAL FEATURES
• Cerebral- In infants and young children, the earliest symptoms are fever, anorexia, irritability, apathy, change of
temperature, a later symptoms like meningeal irritation appear with headache, neck stiffness, photophobia and vomiting. As
the disease progresses, the cerebral manifestation such as hemiplegia, convulsion and cranial nerve palsies manifest
themselves, abdominal pin or constipation; in adults, they may present with pyrexia and headache.
In the terminal stage, the patient may become deeply comatose with fixed dilatation of pupil and evidence of
decerebration or decortication.
• Spinal Meningitis- In the acute phase, fever, pain in the back, radiating in radicular distribution accompanied by rapid
onset of paresis and a sensory loss up to a level in the trunk and bladder disturbances suggesting a picture of acute transverse
myelitis.
• Tuberculoma- Large tuberculomas usually present as intracranial space occupying lesions with convulsion or focal
neurological deficit and evidence of increasing intracranial tension. In the course of typical TBM, the CT scan may
demonstrate multiple small tuberculoma: pyelonephritis, pericarditis, epididymitis, salpingitis, arthritis, peritonitis, bowel
infection, meningitis and miliary tuberculosis.

48. DIAGNOSTIC ASSESSMENT-
• Tuberculin Test
• identifying susceptible groups
• Epidemiological Surveys
• Chest Radiograph

49. MANAGEMENT-
Chemotherapy- Active tuberculosis is usually treated with simultaneous
administration of a combination of drugs to which the organisms are susceptible;
such therapy is continued until the diseases are brought under control. Multiple drug
regimens are used to destroy as many viable microbial organisms as possible, as
quickly as possible and to minimize the emergence of organisms resistant to the
various antituberculosis drugs.

50. CEREBRAL MALARIA-
Cerebral malaria is an acute febrile and mainly diffuse encephalopathy, occurring in a
patient infected with P. falciparum. The World Health Organization Malaria Action Program
proposed three criteria for the diagnosis of cerebral malaria:
1. Unarousable coma
2. Exclusion of other encephalopathies.
3. Confirmation of Plasmodium infection.

51. ETIOLOGY-
Cerebral malaria is caused by the parasite P. falciparum. It is one of the five species of the Plasmodium parasite that causes
malaria.
Hypotheses for Origin of Cerebral Malaria- Specific cause of cerebral malaria has not been understood yet, but there
are two hypotheses for its origination. They are called the mechanical and humoral hypotheses.
 Mechanical Hypothesis- According to the mechanical hypothesis, the P. falciparum protein causes a decrease in oxygen
supply to the blood and brings about what is known as hypoxia. This is supposed to be a good explanation of the
characteristic coma condition of CM. This hypothesis for the cause of CM does not explain why there are no significant
neurological damages to a patient even after many days of unconsciousness.
 Humoral Hypothesis- Humoral hypothesis puts forward that a malarial toxin leads to uncontrolled overproduction of
nitric oxide in the body. Nitric oxide can cause similar effect to the neurological function as high ethanal or general
anaesthetics do, i.e., reduced consciousness. The biochemical reactions of this hypothesis can explain the reversibility
of CM induced coma.
• Both the proposed causes of cerebral malaria are are yet to be confirmed.

52. CLINICAL MANIFESTATIONS-
Stages of Malarial Infection The three initial stages are:
1. Cold stage: It ranges from chills to extreme shaking for 1—2 hours.
2. Hot stage: It is characterized by a high fever up to 107°F (41.7°C) for 3—4 hours.
3. Wet stage: It is characterized by profuse sweating for 2—4 hours.
Symptoms-
Primary there are three symptoms of CM, which are common in both adults and children:
1. Impaired consciousness with non-specific fever.
2. Generalized convulsions and neurological abnormalities.
3. Coma that lasts for 24-72 hours, initially rousable and then unrousable.
If not treated on time, it can lead to complications like jaundice, haemoglobinuria, a tender and enlarged spleen, acute renal
failure and uraemia and is fatal in about 20% of patients. Further, it will manifest with signs of increased intracranial pressure,
hemiplegia, encephalopathy, delirium, seizures and coma.

53. Signs- Common signs of cerebral malaria include:
• Mild jaundice
• Anaemia
• Enlargement of liver and spleen
• Kidney failure
• Blood in urine
• Rise in intracranial pressure
• Delirium and seizures

54. MANAGEMENT-
• Chemotherapy- Chemotherapy for CM mainly involves the use of quinine for a patient having chloroquine
resistance. It is the only drug, which has remained highly effective over a long period of time for treating this
disease. Quinine functions similar to chloroquine and interferes with the parasite’s enzymatic digestion.
• Adjunctive Measures-
 Antipyretics such as paracetamol
 Microcirculatory flow such as pentoxifylline
 Anticonvulsants such as phenobarbital sodium
 Desferrioxamine is an iron chelating

55. NURSING MANAGEMENT
• Altered cerebral tissue perfusion related to CNS infection, cerebral edema, increased :
intracranial pressure, : hydrocephalus
• Potential for infection related to bacterial/viral invasion of the meninges
• Hyperthermia related to infection
• a Potential for injury related to onset of seizure activity
• Pain related to headache, nuchal rigidity, photophobia, and a generalized irritability
• Altered thought processes related to HIV infection of CNS, opportunistic ; CNS infections,
CNS neoplasms, and side effects of medications
• Self-care deficit related to impaired mental status, motor and sensory loss, and
generalized faatigue
• Altered nutrition less than body requirements related to diarrhea, oral/ esophageal/
pharyngeal lesions, anorexia, vomiting, diarrhea, depression, and side effects of
medications