a short lecture on encephalitis

1. Encephalitis

6. • Encephalitis is defined as clinical evidence of
neurologic dysfunction in the presence of an
inflammatory process of the brain.
• Encephalopathy is defined as clinical evidence
of neurologic dysfunction in the absence of a
direct inflammatory process of the brain.

8. Causes of viral encephalitis
• Herpes simplex virus
• Japanese encephalitis
• Arbo virus
• Entero virus
• Varicella zooster virus VZV
• EBV
• HIV
• INFUENZA
• RABIES
• NIPAH

9. Causes of encephalopathy
• secondary to metabolic disturbances ( liver
failure, renal failure, respiratory failure)
• hypoxia,
• ischemia,
• drugs,
• intoxications,
• organ dysfunction, or
• systemic
• infections),

10. Features of acute encephalitis
a. Acute onset of fever AND
• b. Evidence of acute brain dysfunction as
manifested by
• i. Altered mental status OR
• ii. New onset of seizure OR
• iii. Any other neurological deficit
(aphasia/hemiplegia/visualfielddefect)

11. • In most cases, there is some concomitant
meningeal inflammation, in addition to the
encephalitic component—a condition
commonly referred to as
“meningoencephalitis.”

12. • Viral encephalitis presents with acute onset of
headache, fever,
• focal neurological signs (aphasia and/or
hemiplegia, visual field defects) and seizures.
• Disturbance of consciousness ranging from
drowsiness to deep coma supervenes early
and may advance dramatically.
Meningism occurs in many patients.

13. Differential diagnosis
• Encephalopathy
• Post encephalitis syndrome (ADEM)
• Non infectious CNS disease eg.
Vasculitis,collagen vuscular disease,
paraneoplastic syndrome

14. Herpes simplex encephalitis
• HSE is the most common acute encephalitis in
the world
• It affects all ages and both sexes equally,
without significant seasonal variation.
• Most cases of HSE are caused by oral herpes
(herpes simplex virus [HSV] type 1); however,
genital herpes (HSV-2) is more common
among neonates with disseminated disease.

19. Investigations
• General
• CBC with CRP- Leucopenia and lymphocytosis,
thrombocytopenia
• Blood film for Malarial Parasite (MP) or RDT for
P. Falciparum malaria
• Chest X-ray: Diffuse infiltrates, consolidation
• Blood glucose
• Serum bilirubin and SGPT
• S. creatinine
• S. electrolytes

21. CSF sudy
• CSF study- mild pleocytosis (,250/mm3 ).
• Normal or slightly raised protein and normal sugar
level; mainly done for exclusion of other causes..
• the presence of virus-specific IgM in CSF specimens
may be indicative of CNS disease caused by that
pathogenic. IgM for anti HSV.
• Nucleic acid amplification tests (such as PCR) should be
performed on CSF specimens to identify certain
etiologic agents in patients with encephalitis . PCR for
HSV, nipah

22. Neuro image
• MRI of brain- diffuse, confluent high signal
lesions involving mainly the cortical grey matter
and to a lesser extent sub-cortical and deep white
matter on T2W and FLAIR sequences
• CT, with and without contrast enhancement,
should be used to evaluate patients with
encephalitis if MRI is unavailable, impractical, or
cannot be performed

26. PROGNOSIS
• Before the availability of intravenous (IV) acyclovir,
mortality from HSE was approximately 70%. If one is able to
initiate antiviral therapy within the first 24 hours of
symptom onset, the prognosis is much better for long-term
outlook if the patient is fully treated for 21 days.
• This approach has reduced both mortality and morbidity
substantially. Overall, although morbidity remains high,
with 60–70% of patients having significant neurologic
deficits, the mortality is now 10–20%.

28. • Electroencephalogram: The
electroencephalogram (EEG) shows
continuous diffuse slow waves with or without
periodic bitemporal independent sharp wave
discharges.

29. Treatment
• Supportive/General Management
• a. Isolation (preferably in a separate unit)
• b. Barrier nursing e.g. personal protection using masks, gloves, gowns, shoe covers
• c. Hand washing with soap & water before and after handling/visiting patients
• d. Resuscitation (if needed): ABC (Annex 2):
• Airway
• Breathing
• Circulation
• e. Care of unconscious patient: posture change, care of eye, bladder, bowel and
mouth

30. • f. O2 inhalation if there is respiratory difficulty
•
• g. Nutritional support: oral/NG tube feeding according to the condition of
the patient
• h. Maintain fluid and electrolyte balance (Adults: 5% DNS, Children: 5%
DNS, half or quarter strength saline)
• i. Fluid restriction: 30% restriction particularly in children. 2/3 of the daily
maintenance can be given in children if the child is not in shock
• j. Maintain intake output chart
• k. Bronchodilators may be given through large spacers

31. Symptomatic Treatment
• a. Treatment of fever:
• Paracetamol -15mg/kg/dose or 500 mg for adult if temperature ≥101.3oF
(≥38.5°C). (Not more than 4 times in 24 hours)
• b. Treatment of convulsion:
• i. If patient present with convulsion:
• Adult: IV Diazepam 10mg stat
• Children: per rectal diazepam: 0.5mg/ kg (maximum 10mg) as stat dose
• It can be repeated once again after 10 min
• ii. If seizure persists despite above measures, treat as status epilepticus
(Annex 3)
• iii. If presents with history of convulsion(s): Give maintenance treatment
with phenobarbiton (Adult: 60 mg BD; Children: 5 mg/ kg/ day BD)

32. • c. Treatment of raised intracranial pressure (i.e.,
bradycardia, hypertension, papilloedema and deterioration
of consciousness)
• i. Elevation of head to 30⁰ with straight head
• ii. Mannitol
Adult: 200ml IV running stat and 8 hourly until features of
raised ICP resolved or not beyond eight doses of mannitol.
Children: 2.5 – 5 ml/kg over 20 minutes as bolus dose stat
and 6 hourly, not beyond eight doses of mannitol

33. • d. Treatment of hypoglycemia (<40 mg/dl or
<2.2 mmol/L)
• Adult: 25% glucose-40 ml IV
• Children: 10% glucose 5 ml/kg bolus and can
be repeated if necessary

34. • e. Treatment of Shock:
• i. 0.9% Normal Saline
• Adult: 1 litre in 1st hour
• Children: 20ml/kg over 20 mins
• ii. Dopamine (when needed):
• Adult: 05-20 microgram/kg/min)
• Children: 5-10 microgram/ kg/ min

35. • Other treatment
• The following may be given if indicated.
• i. Antibiotic e.g. IV ceftriaxon (Children: 100mg/ kg once daily,
Adult: 2gm BD for 10 days in suspected case of bacterial meningitis
• ii. IV Acyclovir 10mg/ kg 8 hourly as infusion over 20 min for 10 days
• iii. Broad spectrum antibiotics + Metronidazole/Clindamycin (for
aspiration pneumonia/secondary bacterial infection)
• iv. Anti-malarials according to national guideline

36. • In the approach to the patient with encephalitis, an
• attempt should be made to establish an etiologic
diagnosis.
• Although there are no definitive effective treatments
• in many cases of encephalitis, identification of
• a specific agent may be important for
• prognosis,
• Potential prophylaxis,
• counseling of patients and family members, and
• public health interventions.

37. • Epidemiologic clues that may help in directing the
investigation for an etiologic diagnosis include
• season of the year,
• geographic locale,
• prevalence of disease in the local community,
• travel history,
• recreational activities,
• occupational exposure,
• insect contact, animal contact,
• vaccination history, and immune status of the patient.
• Various clinical clues may also be helpful to physicians in considering
specific etiologies.

38. • Despite the wide range of viruses that have been
reported to cause encephalitis, specific antiviral
therapy is generally limited to infections caused by
the herpesviruses—specifically, herpes simplex
virus—and HIV.
• Acyclovir treatment should be initiated in all patients
with suspected encephalitis, pending results of
diagnostic studies.

39. • During the appropriate season, patients who present
with clinical clues suggestive of rickettsial or ehrlichial
infection should be treated empirically with
doxycycline.
• Empirical therapy for acute bacterial meningitis should
also be initiated if clinically indicated.
• In patients with acute disseminated encephalomyelitis,
corticosteroids are recommended; plasma exchange
should be considered in patients who do not respond
to this treatment.

44. Japanese encephalitis
• is a common mosquito borne viral encephalitis found in
Asia.
• It is numerically one of the most important causes of viral
encephalitis not only in Asia but also all over the world.
• About one third of patients die, and half of the survivors
have severe neuropsychiatric sequelae suffering from the
disease.
• The disease was confound mostly to rural areas of Asia but
now it is spreading at an alarming rate.

45. • Japanese encephalitis virus is transmitted
between animals by Culex mosquitoes, and
occurs across eastern and southern Asia and
the Pacific rim.
• Its rserviour is pig and wandering birds

47. The classic description of Japanese
encephalitis
• includes a
• dull flat mask-like facies
with
• wide unblinking eyes,
• tremor,
• generalized hypertonia,
• and cogwheel rigidity.

48. ADEM (post infectious encephalitis)
• Measles, varicella,
rubella,mumps ….may
cause immune
mediatedpost infectious
encephalitis

49. • Subacute sclerosing panencephalitis (SSPE) is
a rare chronic, progressive encephalitis that
affects primarily children and young adults,
caused by a persistent infection measles virus
(which can be a result of a mutation of the
virus itself).
• No cure for SSPE exists

50. • Characterized by a history
of primary measles
infection usually before the
age of 2 years, followed by
several asymptomatic years
(6–15 on average), and then
gradual, progressive psycho
neurological deterioration,
consisting of personality
change, seizures,
myoclonus, ataxia,
photosensitivity, ocular
abnormalities, spasticity,
and coma.

51. Introduction
• Human Nipah virus (NiV) infection, an
emerging zoonotic disease, was first
recognized in a large outbreak of 276
reported cases in Malaysia and Singapore
from September 1998 through May
1999.

52. Reservoir
• Large fruit bats of
Pteropus genus are
the natural reservoir
of NiV

53. Transmission

57. • In Bangladesh, NiV was first identified as the
cause of an outbreak of encephalitis in 2001 .
• Since then, 11 Nipah outbreaks have been
identified in Bangladesh, involving 20 districts,
all occurring between December and May ;

62. the Nipah outbreaks have been
identified in
• Meherpur (2001),
• Noagoan (2003),
• Rajbari (2004),
• Faridpur (2004) ,
• Tangail (2005),
• Thakurgaon (2007),
• Kushtia (2007),
• Manikgonj and Rajbari
(2008),
• Faridpur (2010) and
• Lalmonirhat (2011).

63. • Till April 30, 2011, a total of 197 human cases
of Nipah infection in Bangladesh were
recognized; 151 (77%) died, indicating a very
high mortality [10].

64. • Respiratory involvement including pneumonia
has been found to be considerably more
among patients in Bangladesh than Malaysia
[18, 19].
• This may be due to genetic diversity of the
viral strains. The prominent respiratory
involvement probably is responsible for
human to human transmission [19, 20].

65. • all confirmed Nipah outbreaks have occurred in the
same central and northwestern regions
• One hypothesis that would explain this geographic
concentration of human cases is that the bats are
attracted to specific foods available in these areas
during the winter and spring;
• people living in these communities are occasionally
exposed to foods contaminated with bat urine or saliva
that contains Nipah virus.

66. Transmission
• Outbreak investigations in Bangladesh have
identified two routes of transmission of Nipah
virus from its natural reservoir to human:
• 1. drinking of raw date palm sap (khejurer
rosh) contaminated with NiV and
• 2.close physical contact with Nipah infected
patients.

67. • NiV is a highly
pathogenic
paramyxovirus
belonging to genus
Henipavirus . It is an
enveloped RNA virus

68. Case Management of Nipah
encephalitis
• Suspected case
• A person fulfilling both of the following criteria is defined as a
suspected case:
• 1. Features of acute encephalitis as demonstrated by
• a. Acute onset of fever AND
• b. Evidence of acute brain dysfunction as manifested by
• i. Altered mental status OR
• ii. New onset of seizure OR
• iii. Any other neurological deficit
• 2. Epidemiological linkage
• a. Drinking raw date palm sap OR
• b. Occurring during Nipah season OR ( December to May)
• c. Patient from Nipah endemic area

69. • The outbreaks were reported during date
palm sap harvesting season of Bangladesh
between December to May

70. • Pteropid fruit bats drink the sap and,
occasionally, spoil the contents of the sap
collection pot with urine or feces . Therefore,
human might be infected by drinking NiV
contaminated raw/fresh date palm sap .
• Infected bats shed the virus in their excretion
and secretions such as saliva, urine, semen
and excreta, but they are symptomless
carriers.

71. • The person-to person transmission may occur
from close physical contact, specially by contact
with body fluids.
• Infected bat often bite fruits and few partially-
eaten fruits are left by the bats. When man or
animals consumes those partially eaten fruits,
may transmit NiV to man or other animals.
• From the pig, virus may be transmitted to human
when comes in close contact .

72. • Given the distribution of the locally abundant
fruit bats in South Asia, NiV outbreaks are
likely to continue to occur in affected
countries. The bats are migratory and they
migrate within the Asia-Pacific Region

73. • The NiV is highly contagious amongst pigs, spread
by droplet infection. Pigs acquire NiV and act as
an intermediate and possibly amplifying host
after contact with infected bats or their
secretions.
• Direct human contact with infected pigs was
identified as the predominant mode of
transmission in humans when it was first
recognized in a large outbreak in Malaysia in
1999.

74. • There were focal outbreaks of NiV in
Bangladesh and India in 2001 during the
winter. Drinking of fresh date palm sap,
possibly contaminated by fruit bats (P.
giganteus) during the winter season, may have
been responsible for indirect transmission of
Nipah virus to humans

75. • Date palm sap is consumed as a drink in Asia.
• The sap can then either be consumed in the raw form
as a sweet drink, fermented to form an alcohol
beverage or boiled to form date palm molasses
• Fruit bats also consume date palm sap and can
contaminate it with saliva, urine and faeces. This is the
means by which NiV is thought to be transmitted from
infected fruit bats to humans.
• Subsequent person-to-person transmission occurs from
close physical contact, especially contact with body
fluid.

76. Agent
• In Bangladesh recurrent Nipah outbreaks have
been recognized since 2001 and the strains of
Nipah isolates show substantial heterogeneity
in their nucleotide sequences.
• This heterogeneity suggests repeated
introductions of Nipah virus from its host
reservoir into the human population in
Bangladesh

77. Why Nipah started to spread from bat
• As the flying fox habitat is destroyed by
human activity the bats become stressed,
their immune system weakens, their viral load
increases and more virus is shed in the urine
and saliva

78. Which season Nipah occurs?
• Seasonality was strongly implicated in NiV
outbreaks in Bangladesh and India. All of the
outbreaks occurred during the months of
winter to spring (December-May).
• This could be associated with several factors
like the breeding season of the bats, increased
shedding of virus by the bats and the date
palm sap harvesting season.

79. Incubation period
• The median incubation period following single
intake of raw date palm sap to onset of illness
is 7 days (range: 2-12 days) in Bangladesh.

81. • Virus induced vasculitis causing thrombosis
and infarction in multiple areas of the brain is
the main cause of illness.
• It also causes alveolar hemorrhage in the lung.

82. Suspected case
• A person fulfilling both of the following criteria is defined as a suspected
case:
• 1. Features of acute encephalitis as demonstrated by
• a. Acute onset of fever AND
• b. Evidence of acute brain dysfunction as manifested by
• i. Altered mental status OR
• ii. New onset of seizure OR
• iii. Any other neurological deficit
• 2. Epidemiological linkage
• a. Drinking raw date palm sap OR
• b. Occurring during Nipah season OR
• c. Patient from Nipah endemic area

83. Confirmed case
• A suspected or probable case with laboratory
confirmation of Nipah virus infection either
by:
• IgM antibody against Nipah virus by ELISA in
serum or cerebrospinal fluid
• Nipah virus RNA identified by PCR from
respiratory secretions, urine, or cerebrospinal
fluid

84. Features of pulmonary involvement
• The patient might present with respiratory
features with or without encephalitis. The
respiratory features are
• Illness < 7 days duration AND
• Acute onset of fever AND
• Severe shortness of breath, cough AND
• Chest radiograph showing diffuse infiltrates

85. CLINICAL FEATURES

86. Clinical features
• Symptoms
• The following symptoms were observed (in order of frequency in
Bangladeshi cases)
• 1. Fever
• 2. Altered mental status
• 3. Severe weakness
• 4. Headache
• 5. Respiratory distress
• 6. Cough
• 7. Vomiting
• 8. Muscle pain
• 9. Convulsion
• 10. Diarrhoea

87. Symptom
• The following symptoms were observed (in order of
frequency in Bangladeshi cases)
• 1. Fever
• 2. Altered mental status
• 3. Severe weakness
• 4. Headache
• 5. Respiratory distress
• 6. Cough
• 7. Vomiting
• 8. Muscle pain
• 9. Convulsion
• 10. Diarrhoea

88. General Signs
• Reduced GCS score
• Raised temperature
• Increased respiratory rate (Adult: ≥25/min;
children of ≥ 12 months: ≥ 40/min)
• Increased heart rate (Adult: ≥100/min;
children of ≥ 12 months: ≥ 140/min)
• Crepitations in lung
• Hypertension/Hypotension

89. Neurological signs
• i. Oculoparesis
• ii. Pupillary abnormality
• iii. Facial weakness
• iv. Bulbar weakness
• v. Limb weakness
• vi. Reduced deep tendon reflexes
• vii. Plantar-absent/extensor

90. DIFFERENTIAL DIAGNOSIS
• 1. Other viral encephalitides e.g. Herpes
simplex encephalitis, Japanese B Encephalitis
(JBE)
• 2. Bacterial meningitis
• 3. Cerebral Malaria

92. General
• CBC with CRP- Leucopenia and lymphocytosis,
thrombocytopenia
• Blood film for Malarial Parasite (MP) or RDT for P.
Falciparum malaria
• Chest X-ray: Diffuse infiltrates, consolidation
• Blood glucose
• Serum bilirubin and SGPT
• S. creatinine
• S. electrolytes
• ]

93. • CSF study- mild pleocytosis. Normal or slightly raised
protein and normal sugar level; mainly done for exclusion
of other causes
• MRI of brain- diffuse, confluent high signal lesions
involving mainly the cortical grey matter and to a lesser
extent sub-cortical and deep white matter on T2W and
FLAIR sequences
• Electroencephalogram: The electroencephalogram (EEG)
shows continuous diffuse slow waves with or without
periodic bitemporal independent sharp wave discharges. It
is important especially to differentiate from HSV
encephalitis [periodic lateralized epileptiform discharges
(PLED) mainly from temporal lobe

94. Specific
• Enzyme-linked immunoassay
The diagnosis of Nipah virus infection can be established by
enzyme-linked immunoassay (ELISA) in serum or CSF. Nipah
IgM capture ELISA and an indirect IgG ELISA have high
specificity for the diagnosis.
• Polymerase chain reaction (PCR)
• RT PCRs can be used for detection of viral sequences in CSF,
throat swab or urine specimens.

95. Indication of specific testing for Nipah
• Since treatment does not depend totally on
confirmation of the cases, testing can be
requested to IEDCR selectively only in
clusters and highly suspected cases in Nipha
season and in Nipah endemic areas.

96. Supportive/General Management
• a. Isolation (preferably in a separate unit)
• b. Barrier nursing e.g. personal protection using masks,
gloves, gowns, shoe covers
• c. Hand washing with soap & water before and after
handling/visiting patients
• d. Resuscitation (if needed): ABC
• Airway
• Breathing
• Circulation
• e. Care of unconscious patient: posture change, care of eye,
bladder, bowel and mouth

97. • f. O2 inhalation if there is respiratory difficulty
• g. Nutritional support: oral/NG tube feeding according to
the condition of the patient
• h. Maintain fluid and electrolyte balance (Adults: 5%
DNS, Children: 5% DNS, half or quarter strength saline)
• i. Maintain intake output chart
• j. Bronchodilators may be given through large spacers

98. Symptomatic treatment
• a. Treatment of fever:
• Paracetamol -15mg/kg/dose or 500 mg for adult if temperature ≥101.3oF
(≥38.5°C). (Not more than 4 times in 24 hours)
• b. Treatment of convulsion:
• i. If patient present with convulsion:
• Adult: IV Diazepam 10mg stat
• Children: per rectal diazepam: 0.5mg/ kg (maximum 10mg) as stat dose
• It can be repeated once again after 10 min
• ii. If seizure persists despite above measures, treat as status epilepticus
• iii. If presents with history of convulsion(s): Give maintenance treatment
with phenobarbiton (Adult: 60 mg BD; Children: 5 mg/ kg/ day BD)

99. • c. Treatment of raised intracranial pressure (i.e., bradycardia,
hypertension, papilloedema and deterioration of consciousness)
• i. Elevation of head to 30⁰ with straight head
• ii. Mannitol
• Adult: 200ml IV running stat and 8 hourly until features of raised
ICP resolved or not beyond eight doses of mannitol.
• Children: 2.5 – 5 ml/kg over 20 minutes as bolus dose stat and 6
hourly, not beyond eight doses of mannitol
• d. Treatment of Shock:
• 0.9% Normal Saline

100. Other treatment
• The following may be given if indicated.
• i. Antibiotic e.g. IV ceftriaxon (Children: 100mg/
kg once daily, Adult: 2gm BD for 10 days in
suspected case of bacterial meningitis
• ii. IV Acyclovir 10mg/ kg 8 hourly as infusion over
20 min for 10 days
• iii. Broad spectrum antibiotics +
Metronidazole/Clindamycin (for aspiration
pneumonia/secondary bacterial infection)
• iv. Anti-malarials according to national guideline

101. Prevention

106. Reporting of suspected cases
• Patient with Nipah infection may attend at OPD/ IPD of UHC
or district general hospital or in the medical college hospital.
•
• The attending doctor will examine the patient and if the
doctor finds that the patient’s signs and symptoms have
similarity to Nipah encephalitis s/he will treat the case as
suspected Nipah encephalitis.
• As soon as the patient would be managed as Nipah
encephalitis, the hospital authority must inform IEDCR
(instantly by telephone/ mobile/ e-mail and later by official
letter) without any delay.

107. HOTLINE NUMBER , IEDCR
•01937000011
•01937110011

108. • Clinical examination:
• – Review hospital documents for clinical findings,
laboratory investigation and treatment.
• – Collect clinical information from survived
patients
• – Collect information from laboratory
investigations done
• – Collect blood, CSF and throat swab samples at
the time of recruitment, and follow up serum
samples 2 week after onset of illness.

109. Sample collection, storage and transportation of specimens for laboratory
diagnosis
• Blood: 5 ml blood
• CSF: 3 ml extra CSF
• Throat swab
• Urine

112. • Nipah Infection in 2013
• Update on 15 May, 2013
• Situation Update:
• As of 15May 2013, 24 cases of Nipah virus infection have been reported in Bangladesh since the beginning of 2013, of which 21 cases have died.
These cases are from 13 different districts (Gaibandha, Jhinaidaha, Kurigram, Kushtia, Magura, Manikgonj, Mymenshingh, Naogaon, Natore,
Nilphamari, Pabna, Rajbari, Rajshahi). The age distribution of cases is from 8 months to 60 years. Sixteen cases are male and eight are females.
•
• Nipah
• Human Nipah virus (NiV) infection, an emerging zoonotic disease, was first recognized in a large outbreak of 276 reported cases in Malaysia and
Singapore from September 1998 through May 1999.
• Agent
• NiV is a highly pathogenic paramyxovirus belonging to genus Henipavirus. It is an enveloped RNA virus.
• Incubation period
• The median incubation period of the secondary cases who had a single exposure to Nipah case was nine days (range 6–11 days) but exposure to
onset of illness varies from 6-16 days. The median incubation period following single intake of raw date palm sap to onset of illness is 7 days (range:
2-12 days) in Bangladesh.
• Transmission:
• Drinking of raw date palm sap (kancha khejurer rosh) contaminated with NiV
•
Close physical contact with Nipah infected patients
• Surveillance
• Nipah surveillance began in 2006, Institute of Epidemiology, Disease Control and Research (IEDCR) in collaboration with ICDDR,B established Nipah
surveillance in 10 District level Government hospitals of the country where Nipah outbreaks had been identified. Presently surveillance system is
functioning in five hospitals of Nipah Belt.
• Description of Nipah Patients in 2013
• Age in year Sex Address Outcome 24 Male Rajbari Death 11 Male Jhenaidah Death 8 Male Naogaon Death 35 Female Nator
Death 0.7 Male Natore Alive 9 Male Gaibandha Death 8 Male Mymensingh Death 41 Male Mymensingh Death 3 Female Pabna Alive 43 Male Pabna
Death 30 Female Rajshahi Death 48 Male Nilphamari Death 7 Male Kurigram Death 55 Male Nilphamari Death 45 Female Nilphamari Death 5 Female
Kushtia Death 32 Male Naogaon Death 40 Male Naogaon Death 1.8 Male Magura Death 53 Male Manikganj Death 39 Female Manikganj Death 7
Female Manikganj Alive 60 Female Manikganj Death 30 Male Manikganj Death

113. • Nipah virus
• Fact sheet N°262
Revised July 2009
• KEY FACTS
• Nipah virus causes severe illness characterized by inflammation of the brain (encephalitis) or respiratory diseases.
• Nipah virus can be transmitted to humans from animals, and can also be transmitted directly from human-to-human; in Bangladesh, half of reported cases between 2001 and 2008 were
due to human-to-human transmission.
• Nipah virus can cause severe disease in domestic animals such as pigs.
• There is no treatment or vaccine available for either people or animals.
• Fruit bats of the Pteropodidae family are the natural host of Nipah virus.
• Nipah virus (NiV) is an emerging zoonotic virus (a virus transmitted to humans from animals). In infected people, Nipah virus causes severe illness characterized by inflammation of the
brain (encephalitis) or respiratory diseases. It can also cause severe disease in animals such as pigs, resulting in significant economic losses for farmers.
• Nipah virus is closely related to Hendra virus. Both are members of the genus Henipavirus, a new class of virus in the Paramyxoviridae family.
• Although Nipah virus has caused only a few outbreaks, it infects a wide range of animals and causes severe disease and death in people, making it a public health concern.
• Outbreaks
• Nipah virus was first recognized in 1999 during an outbreak among pig farmers in Malaysia. Since then, there have been another 12 outbreaks, all in South Asia.
• Transmission
• During the initial outbreaks in Malaysia and Singapore, most human infections resulted from direct contact with sick pigs or their contaminated tissues. Transmission is thought to have
occurred via respiratory droplets, contact with throat or nasal secretions from the pigs, or contact with the tissue of a sick animal.
• In the Bangladesh and India outbreaks, consumption of fruits or fruit products (e.g. raw date palm juice) contaminated with urine or saliva from infected fruit bats was the most likely
source of infection.
• During the later outbreaks in Bangladesh and India, Nipah virus spread directly from human-to-human through close contact with people's secretions and excretions. In Siliguri, India,
transmission of the virus was also reported within a health-care setting, where 75% of cases occurred among hospital staff or visitors. From 2001 to 2008, around half of reported cases in
Bangladesh were due to human-to-human transmission.
• Signs and symptoms
• Human infections range from asymptomatic infection to fatal encephalitis. Infected people initially develop influenza-like symptoms of fever, headaches, myalgia (muscle pain), vomiting
and sore throat. This can be followed by dizziness, drowsiness, altered consciousness, and neurological signs that indicate acute encephalitis. Some people can also experience atypical
pneumonia and severe respiratory problems, including acute respiratory distress. Encephalitis and seizures occur in severe cases, progressing to coma within 24 to 48 hours.
• The incubation period (interval from infection to onset of symptoms) varies from four to 45 days.
• Most people who survive acute encephalitis make a full recovery, but around 20% are left with residual neurological consequences such as persistent convulsions and personality
changes. A small number of people who recover subsequently relapse or develop delayed onset encephalitis. In the long term, persistent neurological dysfunctions are observed in more
than 15% of people.
• The case fatality rate is estimated at 40% to 75%; however, this rate can vary by outbreak depending on local capabilities for surveillance investigations.
• Diagnosis
• Nipah virus infection can be diagnosed by a number of different tests:
• serum neutralization
• enzyme-linked immunosorbent assay (ELISA)
• polymerase chain reaction (PCR) assay
• immunofluorescence assay
• virus isolation by cell culture.

114. • In Bangladesh, by contrast, recurrent Nipah outbreaks have been
recognized since 2001 (13–17), and the strains of Nipah isolates show
substantial heterogeneity in their nucleotide sequences (11). This
heterogeneity suggests repeated introductions of Nipah virus from its host
reservoir into the human population in Bangladesh.
• A single species of fruit bats of the genus Pteropus, P. giganteus, lives in
Bangladesh and is widely distributed throughout the country (18). Blood
samples from P. giganteus bats in Bangladesh and neighboring India
commonly have antibodies to Nipah virus (13,19). The conditions that
permit recurrent introduction of Nipah virus from fruit bats to persons in
Bangladesh are unknown. Besides the tendency for Nipah virus outbreaks
to reoccur in Bangladesh, a second notable difference in Nipah virus
epidemiology in Bangladesh is that, in contrast to Malaysia, where person-
to-person transmission of Nipah virus was not confirmed (20), person-to-
person transmission has been repeatedly observed in Bangladesh (15,16).

115. person-to-person transmission is much more apparent
and common in Bangladesh.
• Three factors likely contributed to the higher
frequency of person-to-person transmission of
Nipah virus in Bangladesh than was observed
in Malaysia.
• First, respiratory disease associated with
Nipah infection was more common and more
severe in Bangladesh compared with that in
Malaysia and Singapore

116. • The personal care typically provided to ill and
dying relatives in Bangladesh is likely a second
important contributor to person-to-person
transmission. This care is characterized by
close physical interaction, frequent contact
with a patient’s saliva, and a lack of basic
infection control practices because the
paradigm of communicable disease is
inconsistent with the prevailing cultural
interpretation of illness

117. • Third, all Nipah virus strains from human cases
in Malaysia were genetically similar, in
contrast to the marked diversity of the strains
in Bangladesh (11). Some strains possibly
possess genetic characteristics that facilitate
person-to-person transmission.

118. • Treatment
• There are currently no drugs or vaccines available to treat Nipah virus infection. Intensive supportive care with treatment of symptoms is the main approach to managing the infection in
people.
• Natural host: fruit bats
• Fruit bats of the family Pteropodidae – particularly species belonging to the Pteropus genus – are the natural hosts for Nipah virus. There is no apparent disease in fruit bats.
• It is assumed that the geographic distribution of Henipaviruses overlaps with that of Pteropus category. This hypothesis was reinforced with the evidence of Henipavirus infection in
Pteropus bats from Australia, Bangladesh, Cambodia, China, India, Indonesia, Madagascar, Malaysia, Papua New Guinea, Thailand and Timor-Leste.
• Recently, African fruit bats of the genus Eidolon, family Pteropodidae, were found positive for antibodies against Nipah and Hendra viruses, indicating that these viruses might be present
within the geographic distribution of Pteropodidae bats in Africa.
• Nipah virus in domestic animals
• Nipah outbreaks in pigs and other domestic animals (horses, goats, sheep, cats and dogs) were first reported during the initial Malaysian outbreak in 1999. Many pigs had no symptoms,
but others developed acute feverish illness, laboured breathing, and neurological symptoms such as trembling, twitching and muscle spasms. Generally, mortality was low except in
young piglets.
• These symptoms are not dramatically different from other respiratory and neurological illnesses of pigs. Nipah should be suspected if pigs also have an unusual barking cough or if human
cases of encephalitis are present.
• Nipah virus is highly contagious in pigs. Pigs are infectious during the incubation period, which lasts from 4 to 14 days.
• Prevention
• Controlling Nipah virus in domestic animals
• There is no vaccine against Nipah virus. Routine cleaning and disinfection of pig farms (with sodium hypochorite or other detergents) is expected to be effective in preventing infection.
• If an outbreak is suspected, the animal premises should be quarantined immediately. Culling of infected animals – with close supervision of burial or incineration of carcasses – may be
necessary to reduce the risk of transmission to people. Restricting or banning the movement of animals from infected farms to other areas can reduce the spread of the disease.
• As Nipah virus outbreaks in domestic animals have preceded human cases, establishing an animal health surveillance system to detect new cases is essential in providing early warning
for veterinary and human public health authorities.
• Reducing the risk of infection in people
• In the absence of a vaccine, the only way to reduce infection in people is by raising awareness of the risk factors and educating people about the measures they can take to reduce
exposure to the virus.
• Public health educational messages should focus on the following.
• Reducing the risk of bat-to-human transmission. Efforts to prevent transmission should first focus on decreasing bat access to date palm sap. Freshly collected date palm juice should also
be boiled and fruits should be thoroughly washed and peeled before consumption.
• Reducing the risk of human-to-human transmission. Close physical contact with Nipah virus-infected people should be avoided. Gloves and protective equipment should be worn when
taking care of ill people. Regular hand washing should be carried out after caring for or visiting sick people.
• Reducing the risk of animal-to-human transmission. Gloves and other protective clothing should be worn while handling sick animals or their tissues, and during slaughtering and culling
procedures.
• Controlling infection in health-care settings
• Health-care workers caring for patients with suspected or confirmed Nipah virus infection, or handling specimens from them, should implement standard infection control precautions.
• Samples taken from people and animals with suspected Nipah virus infection should be handled by trained staff working in suitably equipped laboratories.