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Section 9: Central Nervous System Infections

Infective Syndromes of Central Nervous System

ESSAY
(Nil)
SHORT ESSAYS
(Nil)
CNS

SHORT ANSWERS
(Nil)

OBJECTIVE TYPE QUESTIONS

(July 2022)
1. A CSF sample, collected in the ward by lumbar puncture, does not reach the laboratory
for processing for bacterial culture. Discuss the correct decision and the appropriate
action to be taken.
Ans:
CSF should never be refrigerated as delicate pathogens such as H. influenzae, pneumococci or
meningococci may die
If a delay is expected, it may be kept in an incubator at 37°C

(July 2023)
2. A CSF sample was received in microbiology lab for culture. The label in the specimen
container was not matching with the specimen referral form. How will you manage the
situation
Ans: Ask to Resend the sample properly.

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Bacterial Meningitis
Bacterial Meningi�s
ESSAY
ESSAY
(February 2020)
1. A 4 years old child presented with history of fever, neck rigidity and altered sensorium for the
last 48 hours. He was admi�ed in the hospital for evalua�on. CSF was collected and examined for
cell morphology, protein, and sugar. Answer the following.
a) What is the probable diagnosis ?
b) Name the bacterial e�ologic agents causing this condi�on
CNS

c) How will you proceed with lab diagnosis?

d) What are the virulence factors associated with this and describe the pathogenesis ?
e) What measures can you take to preven�on this condi�on?

Ans:
a) What is the probable diagnosis?
 Acute Meningi�s can be due to bacterial, viral, tubercular in origin

b) Name the bacterial e�ologic agents causing this condi�on

 Streptococcus pneumoniae
 Neisseria meningi�dis
 Streptococcus agalac�ae
 Haemophilus influenzae
 Listeria monocytogenes
 Escherichia coli
 Klebsiella
 Pseudomonas
 Acinetobacter

c) How will you proceed with lab diagnosis?

Laboratory diagnosis
 CSF collec�on:
 CSF is obtained by lumbar puncture under strict asep�c precau�ons.
 Divided into 3 sterile containers :
 Cell count.
 Biochemical analysis
 Bacteriological examina�on
 Transport : for culture, the sample should never be refrigerated.
 CSF analysis

Characteris�cs Normal Individual Pyogenic Tuberculous Viral meningi�s

meningi�s/bacterial meningi�s
meningi�s
CSF pressure Normal (50 - 150) Highly elevated Moderately Slightly
elevated elevated/Normal
Total WBC 0-5 100-1000 10-500 25-500
count (/mm3)
Predominant Lymphocytes Neutrophils Lymphocytes Lymphocytes
cell type
Glucose (%mg) 40-70 < 40 20-40 Normal
Protein 15-45 >45 100-500 20-80

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*In suspected acute pyogenic meningi�s, CSF shows leukocytosis (except in listeria, where
lymphocytes increase predominantly), total protein content is elevated pressure is highly elevated.

 CSF microscopy
 Gram staining of heaped smear is done to appreciate the morphology of bacteria causing
meningi�s.
 Streptococcus pneumoniae – gram posi�ve, flame shaped diplococci.
 Neisseria menigni�dis – gram nega�ve diplococci, capsulated with adjacent sides fla�ened.
CNS

 Haemophilus influenzae - Pleomorphic gram-nega�ve capsulated coccobacilli

 Escherichia Coli- gram nega�ve bacilli arranged singly.
 Listeria monocytogenes – Gram posi�ve short bacilli, o�en confused with diptheroids.

 Direct an�gen detec�on

 From CSF – a�er centrifuga�on of CSF, supernatant can be used for an�gen detec�on. Latex
agglu�na�on test is performed using latex beads coated with an�-capsular an�bodies.
 From urine – an�gen detec�on in urine is useful for pneumococcal an�gens.

 Culture
 Blood culture - blood agar, chocolate agar , MacConkey agar,
 Use BHI broth or automated blood culture bo�les

 Iden�fica�on
 Biochemical reac�ons, MALDI-TOF,VITEK
 An�microbial suscep�bility test
 Disk diffusion method / MIC based methods – VITEK

d) What are the virulence factors associated with this and describe the pathogenesis

 Virulence factors
 Capsular Polysaccharide-
 Outer membrane proteins - porin proteins
 LPS and endotoxin - induces the release of various inflammatory mediators
 IgA proteases
 Transferrin binding proteins
 Adhesins

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Pathogenesis

Nasopharyngeal carriers

Droplet inhala�on

Entry through the nasopharynx

CNS

Reach the meninges via i)Hematogenous route

ii)Cribriform
iii)Plate conjunc�va.

Release of various inflammatory mediators

Damage the vascular endothelium

Fever
Vomi�ng
Headache
Neck s�ffness
Non-blanching rash
Loss of fluid and shock
Intravascular thrombosis
DIC
Myocardial dysfunc�on

e) What measures can you take to preven�on this condi�on?

Chemoprophylaxis Vaccine Prophylaxis

 Ce�riaxone (single dose, IM)  Meningococcal polysaccharide vaccines
 Rifampicin - Bivalent(A,C)/ quadrivalent
 Ciprofloxacin (A,C,Y,W135)
 Close contacts of primary cases, regardless of  Two doses, 3 months apart to children of 3–
their vaccina�on status 18 months of age
 Single dose to older children or adult
for high-risk people
 MenB Vaccine
 Two doses - IM route 1 month apart
 For 16–25 years age

(February 2022)
2. A 5-year-old girl was brought in by her mother with the symptoms of fever, vomi�ng (7-8
episodes) and altered sensorium for the last 24 h. Central nervous system examina�on
showed that she was drowsy, had signs of meningeal irrita�on, neck rigidity.
Examina�on of CSF showed neutrophilic predominance.
(a) What is the clinical diagnosis?
(b) Name SIX common probable causes of this clinical condi�on.
(c) Name two rapid tests to detect these causes.
(d) What are the confirmatory tests that can be done in the laboratory?

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(e) Name the an�microbial given empirically for this condi�on

(f) Give details of vaccines available for these microbial agents
(g) Name two other drugs which can be used for trea�ng this condi�on
Ans:

(a) What is the clinical diagnosis?

 Acute bacterial meningi�s
CNS

(b) Name SIX common probable causes of this clinical condi�on.

 Streptococcus pneumoniae
 Neisseria meningi�dis
 Streptococcus agalac�ae
 Haemophilus influenzae
 Listeria monocytogenes
 Escherichia coli
 Klebsiella
 Pseudomonas
 Acinetobacter

(c) Name two rapid tests to detect these causes.

 Direct An�gen Detec�on
 Molecular methods

(d) What are the confirmatory tests that can be done in the laboratory?

Laboratory diagnosis
 CSF collec�on:
CSF is obtained by lumbar puncture under strict asep�c precau�ons.
Divided into 3 sterile containers :  Cell count
 Biochemical analysis
 Bacteriological examina�on
 Transport : for culture, the sample should never be refrigerated.
 CSF analysis

Characteris�cs Normal Individual Pyogenic Tuberculous Viral meningi�s

meningi�s/bacterial meningi�s
meningi�s
CSF pressure Normal (50 - 150) Highly elevated Moderately Slightly
elevated elevated/Normal
Total WBC count 0-5 100-1000 10-500 25-500
(/mm3)
Predominant Lymphocytes Neutrophils Lymphocytes Lymphocytes
cell type
Glucose (%mg) 40-70 < 40 20-40 Normal
Protein 15-45 >45 100-500 20-80

*In suspected acute pyogenic meningi�s, CSF shows leukocytosis (except in listeria, where
lymphocytes increase predominantly), total protein content is elevated pressure is highly elevated.

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 CSF microscopy
 Gram staining of heaped smear is done to appreciate the morphology of bacteria causing
meningi�s.
 Streptococcus pneumoniae – gram posi�ve, flame shaped diplococci.
 Neisseria menigni�dis – gram nega�ve diplococci, capsulated with adjacent sides fla�ened.
 Haemophilus influenzae - Pleomorphic gram-nega�ve capsulated coccobacilli
 Escherichia Coli- gram nega�ve bacilli arranged singly.
 Listeria monocytogenes – Gram posi�ve short bacilli, o�en confused with diptheroids.
CNS

 Direct an�gen detec�on

 From CSF – a�er centrifuga�on of CSF, supernatant can be used for an�gen detec�on. Latex
agglu�na�on test is performed using latex beads coated with an�-capsular an�bodies.
 From urine – an�gen detec�on in urine is useful for pneumococcal an�gens.
 Culture
 Blood culture - blood agar, chocolate agar, MacConkey agar,
 Use BHI broth or automated blood culture bo�les
 Iden�fica�on
 Biochemical reac�ons, MALDI-TOF,VITEK
 An�microbial suscep�bility test
 Disk diffusion method / MIC based methods – VITEK

(e) Name the an�microbial given empirically for this condi�on

 IV cefotaxime / ce�riaxone + vancomycin
 If Listeria is suspected - IV ampicillin
+ IV dexamethasone

(f) Give details of vaccines available for these microbial agents

Polysaccharide Quadrivalent conjugate MenB Vaccine

0.5 mL
subcutaneous or IM
Anterolateral thigh or upper
arm
IAP schedule :-
High-risk categories; >2-year-
old (>3 months old in
outbreaks): One dose; repeat
a�er 3-5 years,
if required
A/E:-
Fever, local pain or redness
C/I :-
Anaphylaxis a�er previous
dose
Usage :- 2-8°C - protect from
light
Use within 30 minutes of
recons�tu�on
NIS :- Not included
0.5 mL Recombinant vaccine
IM Anterolateral thigh or Group B meningococcus
upper arm Adhesin A, heparin binding
IAP schedule :- an�gen, factor H binding
High-risk categories; >2 years protein and outer membrane
old: One dose 9-23 months old vesicles (OMV)
(in USA, not licensed in India: Two doses, given IM route 1
Two doses 3 months apart) month apart
A/E:- 16–25 years age.
Local pain, swelling or redness;
Guillain-Barre syndrome (rare)
C/I :-
May interfere with
pneumococcal vaccine;
separate administra�on by 4
weeks
Usage :-2 - 8° C - not freeze
NIS :- Not included

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(g) Name two other drugs which can be used for trea�ng this condi�on

 Rifampicin , Ciprofloxacin
 Penicillin , Ampicillin , Amoxicillin
CNS

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SHORT ESSAYS
SHORT ESSAYS
(May 2021)
1. Laboratory diagnosis of bacterial meningi�s
Ans:
Laboratory diagnosis
 CSF collec�on:
CSF is obtained by lumbar puncture under strict asep�c precau�ons.
Divided into 3 sterile containers:  Cell count.
CNS

 Biochemical analysis
 Bacteriological examina�on
 Transport: for culture, the sample should never be refrigerated.
 CSF analysis

Characteris�cs Normal Individual Pyogenic Tuberculous Viral meningi�s

meningi�s/bacterial meningi�s
meningi�s
CSF pressure Normal (50 - 150) Highly elevated Moderately Slightly
elevated elevated/Normal
Total WBC 0-5 100-1000 10-500 25-500
count (/mm3)
Predominant Lymphocytes Neutrophils Lymphocytes Lymphocytes
cell type
Glucose (%mg) 40-70 < 40 20-40 Normal
Protein 15-45 >45 100-500 20-80

*In suspected acute pyogenic meningi�s, CSF shows leukocytosis (except in listeria, where
lymphocytes increase predominantly), total protein content is elevated pressure is highly elevated.
 CSF Microscopy
 Gram staining of heaped smear is done to appreciate the morphology of bacteria causing
meningi�s.
 Streptococcus pneumoniae – gram posi�ve, flame shaped diplococci.
 Neisseria menigni�dis – gram nega�ve diplococci, capsulated with adjacent sides fla�ened.
 Haemophilus influenzae - Pleomorphic gram-nega�ve capsulated coccobacilli
 Escherichia Coli- gram nega�ve bacilli arranged singly.
 Listeria monocytogenes – Gram posi�ve short bacilli, o�en confused with diptheroids.
 Direct an�gen detec�on
 From CSF – a�er centrifuga�on of CSF, supernatant can be used for an�gen detec�on. Latex
agglu�na�on test is performed using latex beads coated with an�-capsular an�bodies.
 From urine – an�gen detec�on in urine is useful for pneumococcal an�gens.
 Culture
 Blood culture - blood agar, chocolate agar, MacConkey agar,
 Use BHI broth or automated blood culture bo�les
 Iden�fica�on
 Biochemical reac�ons, MALDI-TOF,VITEK
 An�microbial suscep�bility test
 Disk diffusion method / MIC based methods – VITEK

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SHORTANSWERS
SHORT ANSWERS

(September 2013)
1. Listeria monocytogenes

 Food borne pathogen.

 Serious infec�ons par�cularly in neonates, pregnant women, and elderly people
 Due to its ability to survive refrigera�on, it is commonly found in stored foods.
CNS

 Macrophage phagocytosis causing host cell polymeriza�on and further migrates to the adjacent
epithelial cells by direct cell to cell spread.
 It mainly causes meningi�s in extremes of ages, febrile gastroenteri�s, Immunosuppression.
 Neonates, Elderly, and pregnant women are prone to develop listeriosis.
 Mo�lity: tumbling mo�lity - 25°C nonmo�le - 37°C  differen�al mo�lity - temperature
dependent flagella expression
 Culture: It grows on blood agar (β-haemoly�c colonies), and chocolate agar.
 Selec�ve media such as PALCAM agar (containing mixture of an�bio�cs) - for isola�on

(May 2022)
2. Name four causa�ve agents of neonatal meningi�s
 Escherichia Coli
 Streptococcus agalac�ae
 Klebsiella
 Listeria monocytogenes

OBJECTIVE TYPE QUESTIONS

(July 2022)
1. Enumerate two bacteria causing neonatal meningi�s
 Streptococcus agalac�ae
 Escherichia coli
 Klebsiella
 Listeria monocytogenes

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TETANUS
TETANUS
ESSAY
ESSAY
(Nil)
SHORT
SHORTESSAYS
ESSAYS
(Nil)
SHORT
SHORTANSWERS
ANSWERS
(April 2013)
1. Prophylaxis of tetanus
CNS

 Most effec�ve method is Ac�ve immuniza�on/Tetanus Vaccina�on

 Tetanus Toxoid: prepared by incuba�ng toxin with formalin to become toxoid and then
adsorbed onto alum.
 DPT vaccine consists of diphtheria toxoid, pertussis whole cell killed prepara�on and tetanus
toxoid.
 Td vaccine: tetanus toxoid and adult diphtheria toxoid
 Pentavalent vaccine: DPT, Hepa��s B and Hib
 NIS of India - Total 7 doses are given.3 doses of pentavalent vaccine at 6,10,14 weeks
following birth.2 booster doses of DPT at 16-24 months and 5 years then 2 addi�onal doses
of Td at 10 years and 16 years.

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VIRAL MENINGITIS AND MYELITIS

VIRAL MENINGITIS AND MYELITIS

ESSAY
ESSAY
(March 2014)
1. A one year old child presented with history of inability to move limbs associated with neck
s�ffness following a bout of fever Immuniza�on history was not available. O/E the child has flaccid
paralysis.
a) What is the probable clinical diagnosis and name the ae�ological agent?
CNS

b) Describe the pathogenesis of the disease?

c) How is it diagnosed in the lab and men�on the prophylaxis available?

Ans:
a) What is the probable clinical diagnosis and name the ae�ological agent?
 Poliomyeli�s ; Ae�ological agent: Poliovirus

b) Describe the pathogenesis of the disease?

 Pathogenesis:
Virus enters body via Faeco-oral route, respiratory droplets, conjunc�val contact

Virus enters the host cells by binding to CD155 receptors present on the host cell

Mul�plies locally in the intes�nal epithelial cells, submucosal lymphoid �ssue, tonsils, and other
lymphoid �ssue

Virus then spreads to CNS/Spinal cord through hematogenous or neural routes

Final target site for poliovirus – anterior horn cells of spinal cord

This leads to muscle weakening and paralysis

Virus infected neurons undergo degenera�on

c) How is it diagnosed in the lab and men�on the prophylaxis available?

1. Virus isola�on
 Specimen:
 Poliovirus may be recovered from throat swabs ( up to 3 weeks of illness )
 From rectal swabs or stool samples ( up to 12 weeks of illness )
 Transport :
 Specimens should be kept frozen during transport to laboratory
 Cell line:
 Primary monkey kidney cell lines: most recommended cell lines
 Iden�fica�on of growth of polio virus
 Cytopathological effects – Crena�on and degenera�on of en�re cell sheet
 An�gen detec�on – Neutraliza�on with the specific an�serum / by immunofluorescence test
2. An�body detec�on - Neutraliza�on test
3. Molecular method – Real-�me mul�plex reverse-transcriptase PCR

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Prophylaxis:
CNS

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SHORT ESSAYS
SHORT ESSAYS

(September 2015, February 2016)

1. Prophylaxis of poliomyeli�s
 Oral Polio Vaccine (OPV) : The primary method for prophylaxis against poliomyeli�s is the
administra�on of the oral polio vaccine. This vaccine contains weakened (a�enuated) forms of
the three types of polioviruses (type 1, type 2, and type 3). It is typically given to children in
mul�ple doses, star�ng at an early age, to provide immunity. The OPV is easy to administer,
CNS

cost-effec�ve, and highly effec�ve in preven�ng polio.

 Rou�ne Immuniza�on : Rou�ne immuniza�on schedules in many countries include several
doses of the oral polio vaccine, o�en given at 2, 4, and 6 months of age, with booster doses at
later ages. This ensures that children develop strong immunity to polio.
 Inac�vated Polio Vaccine (IPV) : In some regions, the inac�vated polio vaccine is used in
addi�on to or in place of OPV. IPV contains inac�vated (killed) poliovirus and is administered
via injec�on. It is commonly used in countries where there is a low risk of wild poliovirus
transmission or in post-eradica�on phases.
 Na�onal and Global Immuniza�on Campaigns : Governments and interna�onal organiza�ons
conduct mass vaccina�on campaigns, known as Na�onal Immuniza�on Days (NIDs) or
Supplementary Immuniza�on Ac�vi�es (SIAs), to reach children who may have missed rou�ne
vaccina�ons. These campaigns are especially important in areas where polio is s�ll endemic or
where there is a risk of outbreaks.
 Travel Vaccina�on : Individuals traveling to or from regions where polio is s�ll present should
ensure they are adequately vaccinated before travel.
 Surveillance and Response : In addi�on to vaccina�on, an essen�al aspect of polio
prophylaxis is surveillance for poten�al cases. Rapid detec�on and response to any suspected
cases-ACUTE FLACCID PARALYSIS, are cri�cal for preven�ng the spread of the virus and
facilita�ng a coordinated public health response.(Acute flaccid paralysis)
 Global Polio Eradica�on Ini�a�ve : The Global Polio Eradica�on Ini�a�ve (GPEI) is a
comprehensive effort led by organiza�ons like the World Health Organiza�on (WHO), UNICEF,
and Rotary Interna�onal to eradicate polio worldwide. This ini�a�ve involves mass vaccina�on
campaigns, surveillance, and research to ensure that the poliovirus is eliminated from every
corner of the globe.

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CNS

(July 2022)
2. Pathogenesis and laboratory diagnosis of polio
 Pathogenesis:
Virus enters body via Faeco-oral route, respiratory droplets, conjunc�val contact

Virus enters the host cells by binding to CD155 receptors present on the host cell

Mul�plies locally in the intes�nal epithelial cells, submucosal lymphoid �ssue, tonsils, and other
lymphoid �ssue

Virus then spreads to CNS/Spinal cord through hematogenous or neural routes

Final target site for poliovirus – anterior horn cells of spinal cord

This leads to muscle weakening and paralysis

Virus infected neurons undergo degenera�on

 Laboratory diagnosis:
1. Virus isola�on
 Specimen:
 Poliovirus may be recovered from throat swabs ( up to 3 weeks of illness )
 From rectal swabs or stool samples ( up to 12 weeks of illness )
 Transport :
 Specimens should be kept frozen during transport to laboratory
 Cell line:
 Primary monkey kidney cell lines: most recommended cell lines

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 Iden�fica�on of growth of polio virus

 Cytopathological effects – Crena�on and degenera�on of en�re cell sheet
 An�gen detec�on – Neutraliza�on with the specific an�serum / by immunofluorescence test
2. An�body detec�on - Neutraliza�on test
3. Molecular method – Real-�me mul�plex reverse-transcriptase PCR

(July 2023)
3. Describe the pathogenesis, laboratory diagnosis and prophylaxis of Polio myeli�s
CNS

Ans:

Pathogenesis
Virus enters body via Faeco-oral route, respiratory droplets, conjunc�val contact

Virus enters the host cells by binding to CD155 receptors present on the host cell

Mul�plies locally in the intes�nal epithelial cells, submucosal lymphoid �ssue, tonsils, and other
lymphoid �ssue

Virus then spreads to CNS/Spinal cord through hematogenous or neural routes

Final target site for poliovirus – anterior horn cells of spinal cord

This leads to muscle weakening and paralysis

Virus infected neurons undergo degenera�on

Laboratory diagnosis
1. Virus isola�on
 Specimen:
 Poliovirus may be recovered from throat swabs ( up to 3 weeks of illness )
 From rectal swabs or stool samples ( up to 12 weeks of illness )
 Transport :
 Specimens should be kept frozen during transport to laboratory
 Cell line:
 Primary monkey kidney cell lines: most recommended cell lines
 Iden�fica�on of growth of polio virus
 Cytopathological effects – Crena�on and degenera�on of en�re cell sheet
 An�gen detec�on – Neutraliza�on with the specific an�serum / by immunofluorescence test
2. An�body detec�on - Neutraliza�on test
3. Molecular method – Real-�me mul�plex reverse-transcriptase PCR

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Prophylaxis of Poliomyeli�s
CNS

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SHORT ANSWERS
SHORT ANSWERS
(February 2017)
1. Asep�c meningi�s
 Viral meningi�s
 Inflamma�on of the meninges
 Generally, less severe

E�ology
CNS

 Enteroviruses – Coxsackieviruses, echoviruses, parechoviruses and Enterovirus 71.

 Herpesviruses - HSV , VZV , EBV
 Arboviruses - West Nile virus, Saint Louis encephali�s virus, Powassan virus, California
encephali�s virus , Colorado �ck fever virus
 LCM virus - Lymphocy�c choriomeningi�s virus
 Mumps virus
 Measles virus
 Influenza virus
 Human immunodeficiency virus

Clinical Features
 Fever
 Headache
 S�ff neck
 Photophobia,
 Sleepiness or
 Trouble in waking up from sleep,
 Nausea
 Irritability,
 Vomi�ng,
 Lack of appe�te
 Lethargy

Laboratory Diagnosis
 CSF Analysis (Cytological and Biochemical)
 Molecular Methods - Mul�plex PCR , mul�plex real-�me PCR , BioFire Film Array
 Viral Culture
 An�body Detec�on
 Oligoclonal Gamma Globulin Bands

Treatment
 Primarily symptoma�c - analgesics, an�pyre�cs, an�eme�cs and fluid and electrolyte
replacement
 Oral or intravenous acyclovir
highly ac�ve an�retroviral therapy – if HIV

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(February 2019)
2. List 2 important differences between live and killed polio virus vaccines

LIVE POLIO VIRUS VACCINE KILLED POLIO VIRUS VACCINE

Oral Sabin
Total 5 doses, zero dose at birth,1st, 2nd, and 3rd
dose given at 6th,10th and 14th weeks of age,
booster given at 16-24 months
CNS
Injectable Salk (intradermal route)
Total 2 frac�onal doses
Given at 6th and 14th weeks

Economical Expensive
Paralysis and intes�nal re infec�on, more chance Zero chance of VAPP
of VAPP and VDPV

(July 2019)
3. Vaccines used to prevent poliomyeli�s with immuniza�on schedule
Ans:
Vaccine When to give Maximum age Dose Dilu�on Route Site
OPV – 0 At birth or as Within first 15 2 drops No Oral Oral
(Sabin) early as days
possible
OPV 1,2,3 At 6 weeks, 10 5 years of age 2 drops No Oral Oral
(Sabin) weeks, and 14
weeks
IPV Two frac�onal 1 year of age 0.1 mL No Intradermal Right
(Salk) doses at 6 and upper arm
14 weeks of age

(February 2020)
4. Pulse polio programme
Ans:
The Pulse Polio Programme is a vital public health campaign in the fight against polio, as it helps
maintain immunity levels in the popula�on and contributes to the eventual eradica�on of the
disease.
 Immuniza�on Drive: A na�onwide or region-specific immuniza�on campaign aimed at
vaccina�ng children under the age of five against polio virus.
 Intensive Vaccina�on Rounds: The program conducts periodic vaccina�on rounds, o�en
referred to as "pulse" rounds, during which health workers visit communi�es, schools, and
public spaces to administer the oral polio vaccine (OPV).
 Polio Eradica�on Goal: The primary objec�ve of the Pulse Polio Programme is to achieve the
complete eradica�on of wild poliovirus, which has been largely successful in India.
 Public Awareness: The ini�a�ve involves extensive public awareness and mobiliza�on efforts to
ensure that all eligible children receive the polio vaccine, thereby contribu�ng to the global
effort to eradicate polio.

OBJECTIVE TYPE QUESTIONS

(Nil)

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VIRAL ENCEPHALITIS & ENCEPHALOPATHY

VIRAL ENCEPHALITIS & ENCEPHALOPATHY
ESSAY
ESSAY
(February 2016)
1. A 27 year old male was admi�ed in the intensive medical care unit with drooling of saliva and
fear of intake of liquids since morning. There was history of dog bite on his right leg for 10 days
back.
a) What is the provisional diagnosis?
b) Discuss briefly about the pathogenesis of the above clinical condi�on?
CNS

c) Describe the laboratory inves�ga�ons to confirm the diagnosis.

d) Explain the prophylaxis of the condi�on
Ans:

a) What is the provisional diagnosis?

 Rabies

b) Discuss briefly about the pathogenesis of the above clinical condi�on?

Mul�ply locally at the site of inocula�on  Enters into peripheral neurons  Spreads centripetally
and reaches up to CNS  Infects the CNS (most common sites are hippocampus and cerebellum) 
From CNS, virus spreads along sensory and autonomic nerves to various �ssues  Shed in saliva
Average incuba�on period – 20-90 days
Clinical spectrum consists of 3 phases:
 Prodromal phase, Acute neurologic phase and Coma and death.

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c) Describe the laboratory inves�ga�ons to confirm the diagnosis.

Specimen – saliva, serum, CSF, skin biopsies from hair follicles at nape of neck
Rabies an�gen detec�on Direct immunofluorescence test/Direct
florescent an�body test
Viral isola�on Mouse inocula�on, Cell lines like mouse
neuroblastoma cell line, baby hamster kidney
cell lines
An�body detec�on Mouse neutraliza�on test, Rapid fluorescent
CNS

focus inhibi�on test, fluorescent an�body virus

neutraliza�on test, Indirect fluorescence assay

Viral RNA detec�on RTPCR

Negri body detec�on – brain biopsy Postmortem diagnosis

d) Explain the prophylaxis of the condi�on

Local treatment of wound – Cleansing by soap and water, Chemical treatment,
Suturing only if necessary and an�bio�c and an� – tetanus measure.

IMMUNIZATION
1. Intramuscular
 Essen regimen: The 5-dose regimen prescribes 1 dose on each of days 0,3,7,14 and 28.
Zareb regimen: 4 dose abbreviated mul�site regimen – 2 doses on day 0,1 dose on each day 7
and 21.
2. Intradermal
 2 site intradermal regimen prescribes injec�on of 0.1 ml at 2 sites (deltoid or thigh) on days
0,3,7 and 28.

(February 2021)
2. A 20-year-old male pa�ent was admi�ed in hospital with the complaints of difficulty in
swallowing liquids, loss of appe�te and restlessness. He gave history of dog bite by a street dog
one month back
a) What is the diagnosis of this condi�on?
b) Discuss the pathogenesis?
c) Describe the laboratory diagnosis of the condi�on?
d) What is the post exposure prophylac�c measures of his condi�on?
Ans:
Refer previous ques�ons

(January 2023)
3. A four-year-old child was brought to paediatric casualty with fever, altered behaviour and
difficulty to swallow liquids. Mother gives a history of dog bite two months back and not
taking vaccine as per schedule.
(a) What is your clinical diagnosis?
(b) Name the causa�ve agent.
(c) Describe the pathogenesis of this condi�on.
(d) List the samples collected and the methods of antemortem diagnosis of this condi�on.
(e) Name cell culture vaccines for this disease.
(f) What is IDRV. Discuss the post exposure vaccina�on schedule

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Ans:
(a) What is your clinical diagnosis?
 Rabies

(b) Name the causa�ve agent.

 Rabies virus belongs to Rhabdoviridae family

(c) Describe the pathogenesis of this condi�on.

CNS

(d) List the samples collected and the methods of antemortem diagnosis of this condi�on.
Specimen – saliva, serum, CSF, skin biopsies from hair follicles at nape of neck
Rabies an�gen detec�on Direct immunofluorescence test/Direct
florescent an�body test
Viral isola�on Mouse inocula�on, Cell lines like mouse
neuroblastoma cell line, baby hamster kidney
cell lines
An�body detec�on Mouse neutraliza�on test, Rapid fluorescent
focus inhibi�on test, fluorescent an�body virus
neutraliza�on test, Indirect fluorescence assay

Viral RNA detec�on RTPCR

Negri body detec�on – brain biopsy Postmortem diagnosis

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(e) Name cell culture vaccines for this disease.

Cell culture vaccines
 Purified chick embryo cell (PCEC) vaccine - chicken fibroblast cell line
 Purified Vero cell (PVC) vaccine - Vero cell line
 Human diploid cell (HDC) vaccine - WI-38 (human embryonic lung fibroblast cell line)
CNS

(f) What is IDRV? Discuss the post exposure vaccina�on schedule

IDRV – Intra Dermal Rabies Vaccine
Local treatment of wound – Cleansing by soap and water, Chemical treatment, Suturing only if
necessary and an�bio�c and an� – tetanus measure

Risk categoriza�on and recommended an�-rabies prophylaxis

Category of risk Type of exposure Recommended prophylaxis

Category I (No risk)
Category II (Minor risk)
Category III (Major risk)
• Touching, or feeding of
animal
• Licks on intact skin
Minor scratches or abrasions
without bleeding or nibbling of
uncovered skin
• Single or mul�ple
transdermal bites with oozing
of blood
• Licks on broken skin (fresh
wounds) or mucous
membrane
• Direct contact with bats or
wild animals
(WHO)
• No treatment needed if
history is reliable
• Wound management
• Rabies vaccine
• Observe the dog for 10 days
• Wound management
• Rabies immunoglobulin
• Rabies vaccine
• Observe the dog for 10 days

1. Post exposure prophylaxis [PEP]

a. Previously not received PEP/PrEp
 ID PEP regimen (2-2-2): 2-site ID vaccine is given on days 0, 3 and 7
 1-site IM vaccine given on days 0, 3, 7 and the fourth dose between days 14 to 28
 2-site IM vaccine given on day 0 and 1-site IM on days 7 and 21.
b. Previously received PEP/PrEp
 1-site ID vaccine given on days 0 and 3 or
 1-site IM vaccine given on days 0 and 3 or
 4-site ID vaccine given on day 0 only

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SHORT ESSAYS
SHORT ESSAYS
(October 2016)
1. Japanese encephali�s
 Most common cause of epidemic encephali�s.
 Enveloped ssRNA virus.
 Transmi�ed - bite of Culex mosquito.
 Ardeid birds - natural reservoirs
 Pigs - amplifier hosts
CNS

 Ca�les and buffaloes act as mosquito a�ractants

 Man is the dead-end host
 Ardeid birds  Culex  Ardeid birds
 Pigs  Culex  Pigs (amplifier)

Clinical Features
 Incuba�on period: 5-15 days
 Clinical course: - consists of 3 stages-prodromal, acute encephali�c, late stage and sequelae

PRODROMAL ACUTE ENCEPHALITIC STAGE LATE STAGE AND SEQUELAE

Febrile illness, onset of which
may be abrupt, acute, or
subacute
Acute onset of fever, mental
confusion, disorienta�on,
delirium, seizures
Convalescent stage in which
the pa�ent may recover
completely or retain certain
permanent neurological
deficit.

Lab Diagnosis
 IgM capture - MAC ELISA
 Molecular methods - RT-PCR

Prophylaxis

Live a�enuated cell Inac�vated cell Inac�vated Vero cell

culture derived SA-14- culture derived SA-14- culture derived Kolar
14-2 14-2 (Jeev) (Jenvac)

Dose , route 0.5 mL; 1 – 3 yr : 0.25 0.5 mL ; intramuscular

subcutaneous mL; > 3 yr :0.5 mL ;
intramuscular

site Anterolateral thigh , Anterolateral Anterolateral thigh ,

upper arm thigh , upper arm upper arm

Schedule Only endemic areas ; Not used Not used

na�onal programme two doses at 9 and 16-
18 months

IAP 2016 Recommended in Recommended in Recommended in

endemic areas endemic areas endemic areas
Not available in ≥ 1 yr old ;two doses 4 ≥ 1 yr old ;two doses 4
private sector weeks apart weeks apart

Catch up Up to 18 years ; one Up to 18 years Up to 18 years

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dose to non-immune
adults

Adverse reac�ons Fever , malaise , Less common : fever , Uncommon

hypersensi�vity is rare pain , malaise

Chimeric Vaccine
 Live a�enuated YFV-17D/JEV vaccine
CNS

 Under development
 Phase 3 studies is ongoing
 Premembrane and envelop (prME) gene of SA-14-14-2 strain is inserted between core and
non-structural genes of YFV-17D strain.

(July 2022)
2. What are prions? Name human prion diseases. Discuss in detail any one of them.
Ans :
 Prions are infec�ous protein par�cles that lack any nucleic acid
 They are filterable like viruses
 But are resistant to wide range of chemical and physical agents of steriliza�on.
 There are several prion diseases of humans and animals

Human prion diseases

 Kuru
 Gerstmann- Sträussler - Scheinker syndrome
 Fatal familial insomnia
 Creutzfeldt-Jakob disease (CJD)

Creutzfeldt-Jakob Disease (CJD)

 Most common prion disease
 Rare disorder
 Rapidly progressive demen�a
 Sporadic form of CJD is about 85% of cases
 Familial forms are caused by muta�ons in PRNP.
 Peak incidence in the seventh decade

Types

Classical or sporadic (sCJD) Familial (fCJD) Iatrogenic (iCJD): Variant (vCJD)

 Spontaneous misfolding
of prion-protein in an
individual
 85% of cases
 fCJD and its variants  Blood transfusion  Consump�on of
Gerstmann Sträussler-  Use of human-derived contaminated
Scheinker syndrome and pituitary growth beef with BSE
fatal familial insomnia hormones, prions
are hereditary gonadotropin hormone
 Majority of the other therapy
15% of cases of CJD  Corneal and
meningeal transplants

Risk factors
 Corneal transplanta�on,
 Deep implanta�on of electrodes in the brain

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 Contaminated prepara�ons of naturally derived human growth hormone

Clinical Features
 Subtle changes in memory and behaviour
 Rapidly progressive demen�a
 Startle myoclonus
 Ataxia
 Uniformly fatal
CNS

 The average survival -7 months a�er the onset of symptoms

Pathogenesis
Prions enters in the body

Infec�ous protein par�cles are carried to brain

Induce misfolding of normal cellular prion proteins (PrPc)

Disease-causing isoform (PrPsc)

PrPsc are aggregated as amyloid-like plaques

internalized by neurons

get accumulated inside the cytoplasmic vacuoles

spongiform appearance
Laboratory Diagnosis
 Measurement of PrPsc by conforma�on dependent immunoassay
 Brain biopsies: spongiform degenera�on with lack of inflammatory response
 Sequencing the PRNP gene - familial forms of prion diseases
 Abnormal EEG - high-voltage, triphasic sharp discharges are observed
Treatment
 No known effec�ve therapy for preven�ng or trea�ng prion diseases

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(July 2023)
3. Discuss the pathogenesis, antemortem lab diagnosis and post exposure prophylaxis of
Rabies.
Ans:
CNS

Antemortem diagnosis
 An�gen detec�on from hair follicles at nape and from corneal smear—by direct IF test
 Viral Isola�on by: Mouse inocula�on Cell lines inocula�on—Mouse neuroblastoma and BHK
cell lines.
 An�body detec�on from serum and CSF—by MNT, RFFIT, FAVN, and IFA
 Viral RNA detec�on—by RT-PCR

Post exposure prophylaxis

Local treatment of wound – Cleansing by soap and water, Chemical treatment, Suturing only if
necessary and an�bio�c and an� – tetanus measure

Risk categoriza�on and recommended an�-rabies prophylaxis

Category of risk Type of exposure Recommended prophylaxis

Category I (No risk)
Category II (Minor risk)
• Touching, or feeding of
animal
• Licks on intact skin
Minor scratches or abrasions
(WHO)
• No treatment needed if
history is reliable
• Wound management

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without bleeding or nibbling of • Rabies vaccine

uncovered skin
Category III (Major risk) • Single or mul�ple
transdermal bites with oozing
of blood
• Licks on broken skin (fresh
wounds) or mucous
membrane
CNS
• Observe the dog for 10 days
• Wound management
• Rabies immunoglobulin
• Rabies vaccine
• Observe the dog for 10 days

• Direct contact with bats or

wild animals

Post exposure prophylaxis [PEP]

a. Previously not received PEP/PrEp
 ID PEP regimen (2-2-2): 2-site ID vaccine is given on days 0, 3 and 7
 1-site IM vaccine given on days 0, 3, 7 and the fourth dose between days 14 to 28
 2-site IM vaccine given on day 0 and 1-site IM on days 7 and 21.
b. Previously received PEP/PrEp
 1-site ID vaccine given on days 0 and 3 or
 1-site IM vaccine given on days 0 and 3 or
 4-site ID vaccine given on day 0 only

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SHORTANSWERS
SHORT ANSWERS
(April 2013, October 2016)
1. Prophylaxis of rabies
Local treatment of wound – Cleansing by soap and water, Chemical treatment, Suturing only if
necessary and an�bio�c and an� – tetanus measure

Risk categoriza�on and recommended an�-rabies prophylaxis

Category of risk Type of exposure Recommended prophylaxis

CNS

Category I (No risk)
Category II (Minor risk)
Category III (Major risk)
• Touching, or feeding of
animal
• Licks on intact skin
Minor scratches or abrasions
without bleeding or nibbling of
uncovered skin
• Single or mul�ple
transdermal bites with oozing
of blood
• Licks on broken skin (fresh
wounds) or mucous
membrane
• Direct contact with bats or
wild animals
(WHO)
• No treatment needed if
history is reliable
• Wound management
• Rabies vaccine
• Observe the dog for 10 days
• Wound management
• Rabies immunoglobulin
• Rabies vaccine
• Observe the dog for 10 days

1. Post exposure prophylaxis [PEP]

a. Previously not received PEP/PrEp
 ID PEP regimen (2-2-2): 2-site ID vaccine is given on days 0, 3 and 7
 1-site IM vaccine given on days 0, 3, 7 and the fourth dose between days 14 to 28
 2-site IM vaccine given on day 0 and 1-site IM on days 7 and 21.
b. Previously received PEP/PrEp
 1-site ID vaccine given on days 0 and 3 or
 1-site IM vaccine given on days 0 and 3 or
 4-site ID vaccine given on day 0 only
2. Pre exposure prophylaxis [PrEP]
 For individuals at higher occupa�onal risk
 For sub-popula�ons in remote endemic areas
 provide life�me protec�on
 no need to take PrEP booster periodically
 Regimen- 2-site ID vaccine given on days 0 and 7
1-site IM vaccine given on days 0 and 7

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Summarised

Type of Route of Dose of Day of No of Total No. Site of

Prophylaxis Administra�on Vaccine Dose Injec�ons Per Visit Injec�on

Pre Intra Dermal 0.1ml per Day 0,3, 7 2 4 Adults:

Exposure dose and 28 Deltoid
CNS

Prophylaxis Muscle
Intramuscular 1 en�re Day 0,3, 1 5
vaccine vial 7,14 and Infants and
28 Small
Children:
Pre Intra Dermal 0.1ml per Day 0,7, 1 3 Anterolateral
Exposure dose and Thigh
prophylaxis booster on
either day
21 or 28

Intramuscular 1 en�re Day 0,7, 1 3

vaccine vial and
booster on
either day
21 or 28

Re- Intra Dermal 0.1ml per Day 0&3 1 2

exposure dose

Intramuscular 1 en�re Day 0&3 1 2

vaccine vial

(September 2013, July 2023)

2. Prions
Ans:
 Prions are infec�ous protein par�cles that lack any nucleic acid
 They are filterable like viruses
 But are resistant to wide range of chemical and physical agents of steriliza�on.
 There are several prion diseases of humans and animals
Human prion diseases:
 Kuru
 Gerstmann-Straussler- Scheinker syndrome
 Fatal familial insomnia
 Creutzfeldt-Jakob disease (CJD)

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Pathogenesis
Prions enters in the body

Infec�ous protein par�cles are carried to brain

Induce misfolding of normal cellular prion proteins (PrPc)

Disease-causing isoform (PrPsc)
CNS


PrPsc are aggregated as amyloid-like plaques

Internalized by neurons

Get accumulated inside the cytoplasmic vacuoles

Spongiform appearance

Laboratory Diagnosis
 Measurement of PrPsc by conforma�on dependent immunoassay
 Brain biopsies: spongiform degenera�on with lack of inflammatory response
 Sequencing the PRNP gene - familial forms of prion diseases
 Abnormal EEG - high-voltage, triphasic sharp discharges are observed

Treatment
 No known effec�ve therapy for preven�ng or trea�ng prion diseases

(September 2013, July 2019)

3. Negri bodies
 Intracytoplasmic inclusion bodies - inner basophilic granules
 Composed of viral RNA and proteins.
 Stains used - H and E , Sellers stains
 IHC - Peroxidase labelled & formalin-fixed �ssues
 They are most observed in Purkinje cells of cerebellum and in pyramidal neurons of
hippocampus.
 Confirm the postmortem diagnosis of rabies.
 Absence of Negri bodies does not rule out the diagnosis of rabies - may not be detected in
20%

H and E staining of brain biopsy

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(February 2017)
4. Slow virus disease
Neurodegenera�ve condi�ons affec�ng both humans and animals.
It is characterized by :
 Long incuba�on period.
 Predilec�on for CNS
 High fatality
 Strong gene�c predisposi�on
CNS

 Absence of an�genicity
 Resistant to normal steriliza�on methods
Examples:
Progressive mul�focal leukoencephalopathy – JC virus
Polyoma virus / John Cunningham Virus
Subacute sclerosing panencephali�s – Measles
Progressive rubella encephali�s
Visna and Maedi
Maedi virus encephali�s

(February 2015, February 2018)

5. Name the non-neural vaccines for preven�ng rabies?
Ans:
 Purified chick embryo cell vaccine
 Purified Vero cell vaccine
 Human diploid cell vaccine

(July 2018)
6. Rabies vaccine and latest schedule for immuniza�on
1. Intramuscular
 Essen regimen: The 5-dose regimen prescribes 1 dose on each of days 0,3,7,14 and 28.
 Zareb regimen: 4 dose abbreviated mul�site regimen – 2 doses on day 0,1 dose on each day 7
and 21.
2. Intradermal
 2 site intradermal regimen prescribes injec�on of 0.1 ml at 2 sites (deltoid or thigh) on days
0,3,7 and 28.

OBJECTIVE TYPE QUESTIONS

(July 2023)
1. Write the mode of transmission of Japanese encephali�s
Ans:-Vector borne disease transmi�ed by culex tritaeniorhynchus and culex vishnuii

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Parasitic and Fungal Infections

Parasi�c and Fungal Infec�ons
ESSAY
ESSAY
(February 2022)
1. A 21-year-old female presented with recurrent episodes of seizures, headache and
vomi�ng and ver�go. MRI of the brain showed mul�ple ring-enhancing lesions in the
brain parenchyma. The causa�ve agent was thought to be a cestode.
(a) What is the probable causa�ve agent?
(b) Which is the infec�ve stage of the parasite responsible for the above-men�oned
CNS

condi�on?
(c) What is the mode of transmission?
(d) Name other four cestodes with their defini�ve hosts.
(e) Name two stool concentra�on methods.
(f) How do you treat the pa�ent?
(g) How to prevent this infec�on?
Ans:

(a) What is the probable causa�ve agent?

 Taenia solium

(b) Which is the infec�ve stage of the parasite responsible for the above-men�oned
condi�on?
 Eggs of T. solium

(c) What is the mode of transmission?

Inges�on of contaminated food or water containing eggs of T. solium
Autoinfec�on  External/Internal

(d) Name other four cestodes with their defini�ve hosts.

Cestodes Defini�ve host

Taenia saginata Man
Taenia solium Man
Echinococcus granulosus Dog
Hymenolepis nana Man
Diphyllobothrium latum Man

(e) Name two stool concentra�on methods.

Indica�ons
Parasite output is low in feces
Direct examina�on may not be able to detect the parasites
Methods
Sedimenta�on techniques - formalin-ether
Flota�on techniques - Zinc sulphate flota�on concentra�on technique
Sheather’s sugar flota�on technique

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(f) How do you treat the pa�ent?

Treatment

An�parasi�c agents Symptoma�c treatment Surgery

Albendazole (15 mg/kg per Seizures - an�epilep�c drugs Open craniotomy is rare
day for 8–28 days) High-dose glucocor�coids Surgery is indicated for
Praziquantel (50–100 mg/kg should be used to reduce the ocular
CNS

daily in three divided doses for inflamma�on spinal

15–30 days) Hydrocephalus: A�empts ventricular lesions because
should be made to reduce an�parasi�c drugs can provoke
intracranial pressure irreversible inflammatory
obstruc�ve hydrocephalus - damage
cys�cerci can be removed by
endoscopic surgery or
ventriculoperitoneal shun�ng.

(g) How to prevent this infec�on?

 Good personal hygiene to prevent autoinfec�on with eggs

 Effec�ve fecal disposal to prevent contamina�on of food and water with eggs
 Treatment and preven�on of human intes�nal taeniasis
 Vaccines to prevent porcine cys�cercosis

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SHORT
SHORTESSAYS
ESSAYS
(July 2018, February 2020, May 2021)
1. Cryptococcosis
 Caused by Cryptococcus neoformans
 Capsulated yeast
 Cryptococcal meningi�s mainly immunocompromised individuals.

Pathogenesis
CNS

By inhala�on of aerosolized forms


Pulmonary cryptococcosis
 Cutaneous
Pulmonary vasculature  manifesta�ons &
 osteoly�c bone disease
Disseminates into the CNS

Cryptococcus neoformans

Clinical features
 Chronic meningi�s
 C/O – headache
 Neck s�ffness,

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 And disorienta�on
 Lesions in skin, lungs, or other organs

Diagnosis
Specimens - cerebrospinal fluid (CSF), �ssue, exudates, sputum, blood, cutaneous scrapings, and
urine
 Detected by nega�ve staining microscopy – staining by Modified India ink or nigrosine stains.
 Gram staining – gram posi�ve round budding yeast cells
CNS

 Culture in SDA – mucoid creamy white and yeast like colonies

 Niger seed agar and bird seed agar :- brown coloured colonies
 Tests for GXM, capsular an�gen
 Latex slide agglu�na�on test or enzyme immunoassay (EIA)- Cryptococcal an�gen
 Lateral flow assay – GXM detec�on
 CSF analysis:
 CSF pressure and protein may be increased
 Cell counts elevated
 Glucose is normal or low

2. Cryptococcal meningi�s – risk factors, pathogenesis, and laboratory diagnosis

Ans:

Risk factors
 Pa�ents with advanced HIV infec�on
 Pa�ents with hematologic malignancies
 Transplant recipients
 Pa�ents on immunosuppressive or steroid therapy

Pathogenesis & Lab diagnosis: Refer previous questions.

(July 2022)
3. Primary amoebic meningoencephali�s – e�ology, mode of transmission, laboratory
diagnosis
Ans:
 Caused by naegleria fowleri - a free living amoeba found in warm fresh water.

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Pathogenesis
CNS

Tissue destruc�on:
 Amoebostome into which the cytopathic enzymes are liberated
 Contact dependent cytolysis mediated by hemoly�c proteins, cytolysins and phospholipase
enzymes.

Mode of transmission
 Nasal contamina�on during swimming in fresh hot water
 Rarely, if the flagellated or cyst form enters, soon it reverts into amoeboid form

Diagnosis
 CSF analysis – mimic bacterial meningi�s
 CSF microscopy: 1. Wet mount
2. Phase contrast microscope
3. Direct fluorescent an�body staining
 Histopathology - Brain biopsy – H&E/Giemsa - trophozoites having sky blue cytoplasm with a
pink nucleus
 Culture - non-nutrient agar (Page’s saline and 1.5% agar) with bacterial supplement like E. coli
– Trail sign
 Enflagella�on test
 Isoenzyme analysis
 Molecular methods - Mul�plex real-�me PCR of 18S rRNA
 Imaging methods- CT scan and MRI

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SHORT ANSWERS
SHORT ANSWERS
(September 2014)
1. Naegleria fowleri
Ans:
 Free living amoeba
 Seen in warm fresh water
 Cyst and trophozoite forms
 Acute suppura�ve fulminant infec�on of CNS
CNS

Pathogenesis

Tissue destruc�on:
 Amoebostome into which the cytopathic enzymes are liberated
 Contact dependent cytolysis mediated by hemoly�c proteins, cytolysins and phospholipase
enzymes.

Mode of transmission
 Nasal contamina�on during swimming in fresh hot water
 Rarely, if the flagellated or cyst form enters, soon it reverts into amoeboid form

Clinical Features
 Incuba�on period: 1–2 days to 2 weeks
 Changes in the taste and smell
 Headache
 Anorexia
 Nausea
 Vomi�ng

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 High fever
 Signs of meningeal involvement - s�ff neck and a posi�ve Kernig’s sign
 Confusion
 Hallucina�ons
 Lack of a�en�on
 Ataxia
 Seizures
CNS

Diagnosis
 CSF analysis – mimic bacterial meningi�s
 CSF microscopy: 1. Wet mount
2. Phase contrast microscope
3. Direct fluorescent an�body staining
 Histopathology - Brain biopsy – H&E/Giemsa - trophozoites having sky blue cytoplasm with a
pink nucleus
 Culture - non-nutrient agar (Page’s saline and 1.5% agar) with bacterial supplement like E. coli
– Trail sign
 Enflagella�on test
 Isoenzyme analysis
 Molecular methods - Mul�plex real-�me PCR of 18S rRNA
 Imaging methods- CT scan and MRI

Treatment
No effec�ve treatment is available for PAM
Amphotericin B
Rifampicin
Sulfisoxazole Found to be useful
Miconazole
Fluconazole
Miltefosine

(February 2016, October 2016, July 2022)

2. Cryptococcosis
Refer Short Essays

(February 2017)
3. Free living amoebae
 Small
 Freely living,
 Widely distributed in soil and water and
 Can cause opportunis�c infec�ons in humans.

The main 4 parasites belonging to this group

Free living amoebae Infec�on by it
Acanthamoeba species Primary amoebic meningoencephali�s (PAM)
Balamuthia mandrillaris Granulomatous amoebic encephali�s (GAE)
amoebic kera��s in contact lens wearers
Sappinia species Granulomatous amoebic encephali�s (GAE)
Encephali�s

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(August 2017)
4. Lab diagnosis of cryptococcosis
 Detected by nega�ve staining microscopy – staining by Modified India ink or nigrosine stains.
 Gram staining of culture isolate – gram posi�ve round budding yeast cells
 Culture in SDA – mucoid creamy white and yeast like colonies
 Niger seed agar and bird seed agar: - brown coloured colonies

(February 2018)
CNS

5. Name the causa�ve agent, infec�ve form, and complica�ons of neurocys�cercosis

Ans:
 Causa�ve agent: Tenia solium
 Infec�ve form- Cyst ,Cys�cercus cellulosae
 Complica�ons : -seizure, hydrocephalus, chronic meningi�s, cerebral arteri�s, demen�a, focal
neurological deficits

(May 2022)
6. Primary amoebic meningoencephali�s
Ans:
 Acute suppura�ve fulminant infec�on of CNS
 Caused by naegleria fowleri ; a free living amoeba found in warm fresh water.

Pathogenesis

Tissue destruc�on
 Amoebostome into which the cytopathic enzymes are liberated
 Contact dependent cytolysis mediated by hemoly�c proteins, cytolysins and phospholipase
enzymes.

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Clinical features
 Incuba�on period: 1–2 days to 2 weeks
 Changes in the taste and smell
 Headache
 Anorexia
 Nausea
 Vomi�ng
 High fever
CNS

 Signs of meningeal involvement - s�ff neck and a posi�ve Kernig’s sign

 Confusion
 Hallucina�ons
 Lack of a�en�on
 Ataxia
 Seizures

Diagnosis
 CSF analysis – mimic bacterial meningi�s
 CSF microscopy-
1. Wet mount
2. Phase contrast microscope
3. Direct fluorescent an�body staining
 Histopathology - Brain biopsy – H&E/Giemsa - trophozoites having sky blue cytoplasm with a
pink nucleus
 Culture - non-nutrient agar (Page’s saline and 1.5% agar) with bacterial supplement like E. coli -
Trail sign
 Enflagella�on test
 Isoenzyme analysis
 Molecular methods - Mul�plex real-�me PCR of 18S rRNA
 Imaging methods- CT scan and MRI

Treatment
No effec�ve treatment is available for PAM
Amphotericin B
rifampicin
sulfisoxazole found to be useful
miconazole
fluconazole
miltefosine

(May 2022)
7. Neurocys�cercosis
Ans:
 Parasi�c infec�on of the CNS
 By larvae of the pork tapeworm, Taenia solium
 Defini�ve and intermediate host – Man
 Infec�ve stage: Eggs of T. solium
 Mode of transmission: inges�on of contaminated food or water containing eggs of T. solium
autoinfec�on  External/Internal

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Pathogenesis
Embryo or oncosphere is released from the eggs

penetrates the intes�ne

Portal circula�on or mesenteric lympha�cs
CNS


Reaches to various organs like subcutaneous �ssue, muscle, eye and brain

Larval stage

Cys�cercus cellulosae in 7–9 weeks and deposited as cyst

Full development to mature cysts takes 2–3 months of �me

Clinical features
 Asymptoma�c NCC
 Seizure
 Hydrocephalus
 Increased intracranial pressure - headache, vomi�ng and ver�go
 Chronic meningi�s
 Focal neurological deficits
 Psychological disorders and demen�a
 Cerebral arteri�s
 Basal and ventricular involvement

Based on involvement :- 1. Parenchymal - brain parenchyma

2. Extra parenchymal - meninges, ventricles, spinal cord, and subarachnoid
space
Morphological stages
Vesicular

Necro�c

Nodular

Calcified stage

Laboratory diagnosis
 Radiodiagnosis—CT scan and MRI
 An�body detec�on in serum or CSF— ELISA &Western blot
 An�gen detec�on in serum or CSF—ELISA
 Lymphocyte transforma�on test
 Histopathology of muscles, eyes, subcutaneous �ssues, or brain biopsies—can detect cys�cerci
 FNAC of the cyst and then staining with Giemsa
 Fundoscopy of eye—detects larvae
 Modified Del Bru�o diagnos�c criteria

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CNS

Cys�cercus cellulosae Ring enhanced lesions in CT brain

(March 2014)
8. Intermediate and defini�ve host for toxoplasma gondii
Ans: Intermediate host - cats and other felines (sexual cycle)
defini�ve host - other mammals like rodents (asexual cycle)

(March 2014)
9. Acanthamoeba
 Free-living amoebae
 Infect CNS, skin, and eye
 They are ubiquitous and present worldwide
 Acanthamoeba astronyxis, A. castellanii, A. culbertsoni and A. polyphaga - cause human
infec�on
 Reservoir for bacteria: Legionella and may serve as a poten�al reservoir
 Trojan horse of the microbial world

Granulomatous Amoebic Encephali�s (GAE)

 Insidious onset
 Incuba�on period varies from several weeks to months.
 Subacute to chronic course: Lasts for months to years
 Pathology: It produces focal granulomatous lesions in brain
 Lymphocytosis of CSF can be seen
 In pa�ents with AIDS, no cells are seen in CSF

Symptoms
 Confusion
 Dizziness
 Nausea
 Headache
 S�ff neck
 Seizure
 Hemiplegia
 In HIV pa�ents: nasal ulcers, cutaneous ulcers and musculoskeletal abscesses also

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CNS

30 μm (25–40 µm) 10–25 μm

thorn or spine like pseudopodia double walled
acanthopodia outer wrinkled cyst wall
Nucleus is single with central karyosome
no peripheral chroma�n

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OBJECTIVE TYPEQUESTIONS
OBJECTIVE TYPE QUESTIONS
(July 2023)
1. Write two iden�fying features of Cryptococcus neoformans
Ans:
 Nega�ve staining - refrac�le delineated clear space surrounding the budding round yeast cells
against black background
 Gram staining - gram-posi�ve round budding yeast cells
 Mucicarmine stain - stains the carminophilic cell wall of C. neoformans „
CNS

 Masson-Fontana stain - produc�on of melanin

 Alcian blue stain - demonstrate the capsule.
 Niger seed agar and bird seed agar - demonstrate melanin produc�on (brown colored colonies)
Growth at 37°C
 Urease test is posi�ve
 Assimila�on of inositol and nitrate
 Mouse pathogenicity test
 Automated iden�fica�on system such as MALDI-TOF

(July 2023)
2. Name one free living amoebae and the infec�on caused by it
Ans:
Free living amoebae Infec�on by it
Naegleria fowleri primary amoebic meningoencephali�s (PAM)
Acanthamoeba species granulomatous amoebic encephali�s (GAE)
amoebic kera��s in contact lens wearers
Balamuthia mandrillaris granulomatous amoebic encephali�s (GAE)
Sappinia species encephali�s

44 Kerala University of Health Sciences