CNS

microbiology
SYLLABUS
Introduction to CNS infections:
Definitions, etiological agents, principles of laboratory diagnosis
Meningitis: (P. 899)
Pyogenic, Aseptic, and Chronic: agents, pathogenesis, clinical presentation, laboratory diagnosis, complications
Tetanus: (P. 905)
Agent, growth characters, pathogenesis, laboratory diagnosis, prophylaxis.
Botulism: (P. 907)
Agent, nature, pathogenicity, laboratory diagnosis
Encephalitis: (P. 908)
Rabies, (P. 910) Arbovirus, Poliomyelitis (P. 913)
Agent, pathogenicity, clinical features, laboratory diagnosis, prophylaxis, complications
Trachoma: (P. 915)
Agent, pathogenicity, clinical features, laboratory diagnosis, complications
Conjunctivitis: (P. 918) VIII
Agent, pathogenicity, clinical features, laboratory diagnosis, complications
Acute/Chronic Suppurative Otitis Media: (P. 919)
Agent, pathogenicity, clinical features, laboratory diagnosis, complications
Slow virus, Prion diseases, etc (introductory): (P. 920)

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VIII

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 CNS

MICROBIOLOGY

MENINGITIS 6. Explain the types of meningitis. Describe the lab

diagnosis of bacterial meningitis.
Past Questions:
(3+7=10) [05 June]
1. Explain the types of meningitis. Describe the
laboratory diagnosis of fungal meningitis. 7. Write about the pathogenesis and lab diagnosis
of pyogenic meningitis. (5+5=10) [04 Dec]
(3+7=10) [10 Jan]
8. Name the agents, mode of infection and lab
2. Define bacterial meningitis. Describe the lab
diagnosis of pyogenic meningitis.
diagnosis of bacterial meningitis. (2+8=10) [09 Jan]
(3+2+5=10) [02 Dec]
3. List the etiology of bacterial meningitis in
9. Short notes on Fungal meningitis [04 Dec]
children. Write in detail laboratory diagnosis of
pyogenic meningitis. (3+7=10) [10 July] 10.Short notes on viral meningitis [01, 02]
4. List the agents causing meningitis. Discuss the  Meningitis refers to an inflammatory process of
pathogenesis and lab diagnosis of bacterial the leptomeninges and CSF within the
meningitis. (2+3+5=10) [07 Dec] subarachnoid space.
5. Define meningitis. List the agents causing Types
pyogenic meningitis. Discuss the lab diagnosis in a. Acute pyogenic (Bacterial) meningitis
case of acute bacterial meningitis. b. Acute aseptic (Viral) meningitis
(2+2+6=10) [07 July] c. Chronic meningitis
CSF Findings in various Meningitis
S.N. Features Normal CSF Pyogenic Tuberculosis Viral Meningitis
VIII
1. Naked eye Clear and Cloudy or frankly Clear or slightly turbid; Clear or slightly turbid
appearance colourless purulent forms fibrin coagulum
on standing
2. Pressure 60-150 mm Elevated (above 180 Elevated (above 300 Elevated (above 250
H2O mmH2O) mmH2O) mmH2O)
3. Chemical
Protein 15-45 mg/dl Highly increased (100- Slightly increased (80- Slightly increased (60-80
600 mg/dl) 120 mg/dl) mg/dl)
Sugar 40-80 mg/dl Highly decreased (10- Decreased 30-50 mg/dl Normal
20 mg/dl
4. Cell count (total 1-3 50 - 10,000 50 - 500 4-10
cell per cu.mm.) Lymphocytes Neutrophils: 95% Lymphocytes: 90% Lymphocytes
Lymphocytes : 5% Neutrophils: 10%
5. Bacteriological (smear made from centrifuged deposit)
Gram film Nil Gm -Ve or Gm +Ve, Nil Nil
cocci or bacilli
Acid fast film Nil Nil Acid fast bacilli Nil

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A. Acute Pyogenic (Bacterial) Meningitis Clinical manifestations

[02, 04, 05, 07, 10] - Nuchal rigidity
- Photophobia
Aetiologic agents
- Morning Headache
- Neonates: Escherichia coli, Streptococci
- Projectile vomiting
(group B)
- Irritability
- Infant and Children: Streptococcus
pneumoniae, Haemophilus influenzae, - Kernig’s sign and Brudzinski sign
Neisseria meningitidis [KU 2013 MCQs] Lab-diagnosis
- Adolescents: Streptococcus pneumoniae, i. Sample collection
Neisseria meningitidis - CSF collected by lumbar puncture about (5-10
- Elderly: Listeria monocytogenes, Streptococcus ml)
pneumoniae - Ventricular puncture in neonates
Pathogenesis - It is divided into three portions for further
investigation
Bacteria
1st portion: Microscopy examination
2nd portion: Biochemical test
Inhalation of contaminated Direct spread 3rd portion: Culture
droplets ii. Microscopy
- Sample is centrifuged
Attaches to mucosal cell of nasopharynx
- Deposit is gram stained
Capsule resist phagocytosis by neutrophils,  Neisseria meningitidis: gram negative,
VIII RES cells, complement pathway diplococci
 Haemophilus influenzae: gram negative,
Bacteremia pleomorphic bacilli
 Streptococcus pneumoniae: gram positive,
Receptor for adhesion diplococci
factor in choroid plexus - Supernatant is used for Antigen detection.
iii. Examination of CSF
CNS penetration  For examination of CSF refer table
iv. Culture
Bacteria multiply rapidly and produce toxins
- Concentration of sample is done by
centrifugation at 1500 rpm for 5-10 min or
Inflammation of pia and arachnoid mater membrane filtration
- Centrifuged deposit inoculated into
Excessive production of CSF and decreased
absorption of CSF, obliteration of CSF pathway  Mac-Conkey Agar: For E. coli
 5% sheep blood agar: For Streptococcus
pneumoniae, Streptococci (group B)
Increased ICP
 Chocolate agar: Haemophilus influenzae,
Clinical manifestations Neisseria meningitidis
v. Rapid Diagnostic Test
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 CNS

- To detect bacterial antigen or antibodies C. Chronic Meningitis

 Countercurrentimmunoelectrophoresis  Tuberculous meningitis
(CIEP)  Fungal meningitis
 Latex agglutination  Spirochetal meningitis
 ELISA Tuberculous Meningitis
- To detect endotoxin Etiological agent
 Litmus Lysate test - Mycobacterium tuberculosis
Complications Pathogenesis
- Hydrocephalus - Tubercular meningitis occurs most commonly
- Damage cranial nerves shortly after a primary infection in childhood or
- Secondary cerebral infarction as part of miliary tuberculosis.
- Encephalitis - Source of infection: Caseous focus in meninges
or brain substance adjacent to CSF pathway
B. Acute Aseptic (Viral) Meningitis
Route of entry:
[01, 02]  Hematogenous
Etiologic agent  Lymphatic
Enterovirus, Epstein-Barr virus, Arbo virus, Herpes  Direct spread
simplex virus, Varicella-zoster virus, Mumps
Tubercle bacilli Direct Lymphatic
Clinical Manifestations in blood spread Spread
- Acute Headache
- Irritability Submeningeal tubercular foci VIII
- High pyrexia
Proliferation to cause perivascular exudation
Lab Diagnosis followed by cessation, gliosis, giant cell
i. Sample collection formation
- CSF collected by lumbar puncture (about 5-10 Endarteritis infarction of brain
ml)
Clinical Manifestations
1st portion: Microscopic observation
- Headache
2nd portion: Biochemical test
- Vomiting
3rd portion: Culture
- Low-grade fever
ii. Microscopic observation - Lassitude
- Only lymphocytes observed - Depression
- Virus not visible - Confusion
iii. CSF examination - Behavioral changes
- Papilloedema
 For examination of CSF refer table
- Oculomotor palsies
iv. Culture
- Focal hemisphere signs
- It grows in primary monkey kidney, HEP-2 cells
- Depression of conscious level
- Growth is indicated by cytopathic effects
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Lab Diagnosis Clinical Manifestations

i. Sample Collection - Headache
- CSF collected by lumbar puncture (about 5-10 ml) - Vomiting
- Sample is divided into three portions for - Irritability
further investigation
Lab Diagnosis
1st portion: Microscopic examination
i. Sample collection
2nd portion: Biochemical test
- CSF collected by lumbar puncture (about 5-10 ml)
3rd portion: Culture
- It is divided into three portions
ii. Microscopic Examination
- Sample is centrifuged 1st portion: Microscopic examination
- Centrifuged deposit is Ziehl-Nelsen stained 2nd portion: Biochemical test
 Mycobacterium tuberculosis: Acid fast, pink, 3rd portion: Culture
slightly curved ii. Microscopic Examination
iii. Examination of CSF - Smear from centrifuged deposit stained with
 For examination of CSF refer table  India ink (negative staining)
iv. Culture Cryptococcus neoformans: Reveals capsule
- Centrifuged sample is cultured in selected
 Giesma stain
medium i.e. Lowenstein Jensen media.
v. CT scan Histoplasma capsulatum: Round to oval
To detect several pathological conditions like yeast cells within macrophages
- Basal exudates  KOH mount
- Inflammatory granulomas Candida albicans: Budding yeast cell with
- Hydrocephalus pseudohyphae
VIII D. Fungal Meningitis [04, 10] iii. Examination of CSF
a. Macroscopic examination
Etiological agent
CSF: Clear or slightly turbid
- Candida albicans
b. Biochemical examination
- Cryptococcus neoformans
Sugar: Normal or decreased
- Histoplasma capsulatum
Protein: Usually increased
- Blastomyces dermatitidis
c. Cell count
- Coccidioides immitis
Total cell per cu. mm = 50-500
Pathogenesis
Route of entry: Inhalational Type of cell:
Source of infection: Contaminated air  Lymphocytes - 90%
Transmission of infectious particles (fungus)  Neutrophil - 10%
 iv. Culture
Immuno-compromised patient Centrifused deposit is cultured on Sabouraud’s
 Dextrose Agar (SDA)
Fungus multiplies and disseminate
hematogenously a. Cryptococcus neoformans: Creamy, white,
 mucoid colonies
Reaches to CNS b. Histoplasma capsulatum: White cottony mycelium
 c. Candida albicans: Smooth creamy white with
Meningitis yeasty odour

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v. Serology/Ab detection
- Agglutination test
- Immunoflorescence test
- Complement fixation test
- Precipitation test
vi. Ag detection
- Latex agglutination test
- ELISA
NEISSERIA MENINGITIDIS
Morphology
- Capsule present (Fresh)
- Motility absent
- Spore absent
- Gram stain: Gram negative
- Aerobic
- Oval, diplococcic, 0.6-8
N.gonorrhoae adjacent sides are flattened.
Classification
a. Serotypes: Based on specificity of capsular
polysaccharide antigens
- 13 serogroups
- A,B,C,D,X,Y,Z, W135, 29E, H, I, K, L
- A,B,C,X,Y and W135
meningococcal disease
CNS
b. Serotypes:
- Group A: Single serotype
- Group B and C: Multiple serotypes
Virulence factors
i. Adhesion factor: Pilli
ii. Capsule: Anti-phagocytic
iii. Lipopolysaccharide (LPS): Endotoxin
iv. IgA protease: cleaves IgA molecule
Pathogenesis
- Source of infection: Contaminated droplets
- Mode of transmission: Air borne
- Incubation period: 3 days
- Organism may enter the subarachnoid space
by following routes:
i. Haematogenous route: Organisms reach
the subarachnoid space through the blood,
µm, unlike vessels of brain (most common)
ii. Direct spread from an infected site such as
otitis media, sinusitis and conjunctivitis.
iii. Anatomic defects in the CNS structures or
congenital abnormalities can allow
organisms easily enter the CNS.
VIII
iv. Travel along nerve (Perineural sheath of
olfactory nerve) leading to the brain
Inhalation of contaminated droplets

N. meningitidis attach to mucosal cells of
nasopharynx through Pilli

In a non-immune, susceptible host, organism
invade locally

Spread from nasopharynx to meninges through
blood stream

Internalised by phagocytic cell

Able to avoid intracellular death, replicated

Migrate to sub-epithelial space
associated with 
Meningitis
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- Absence of bacterial antibody in blood is an V. Immunological methods

important factor to susceptibility to clinical - Supernatant is tested for detection of soluble
infection. polysaccharide antigen of N. meningitidis by
Clinical Manifestations Counterimmuno electrophoresis (CIEP) or by
i. Meningitis agglutination of the latex particles coated with
ii. Afebrile illness specific antibodies.
iii. Meningococcal septicaemia - Useful at later stage of the disease

Lab-diagnosis CRYPTOCOCCUS NEOFORMANS

I. Sample collection: Depending on the type of  Capsulated yeast
infection, the specimen could be:
 Cause sub-acute or chronic infection called
- CSF
cryptococcosis
- Blood
 Reservoir: Ubiquitous saprophyte found in bird
- Synovial fluid droppings.
- Nasopharyngeal swab
Morphology
Examination of CSF:
- Spherical budding cell (5 -10 µm diameter)
- Collected by lumbar puncture:
- Prominent polysaccharide capsule
Divided into three portions
- Does not produce pseudomycelium
1st portion: Microscopy
- Gram positive
2nd portion: Biochemical test
Antigencity
3rd portion: Culture
- Antigenically C. neoformans are of four types:
II. Microscopy
A, B, C, D
VIII - CSF is centrifuged
 A & D: Found in Birds (Birds are not affected
- Centrifuged deposit is Gram stained
due to high body temperature)
- Neisseria meningitidis: Gram negative,
 B & C: Found in flower of Eucalyptus
intracellular, diplococci
camaldulensis
- Lymphocytes: 90-99%
Determinants of Pathogenecity
- Supernatant is kept for detection of
- Anti-phagocytic polysaccharide capsule
meningococcal antigen.
- Melanin produced (gets deposited in the cell
III. Biochemical test
wall and thereby protects itself from oxidants
- Glucose markedly decreased or absent
released by phagocytic cells)
- Protein markedly increased
Pathogenesis
- Ferment glucose and maltose with production
of acid only Inhalation of Aerosolised infectious particle
- Catalase and oxidase positive 
- Indole negative Immunocompromised person
- Nitrate not reduced 
IV. Culture Fungus multiplies and disseminates hematogenously
- Fastidious organism 
- Inoculated into chocolate agar Reaches to CNS
- Incubated at 35-360C in 5-10% CO2 and high 
humidity Meningitis
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Clinical features TETANUS

i. Cryptococcal meningitis Past Questions:
ii. Skin and other infection 1. Describe the pathogenesis, lab diagnosis and
iii. Lungs infection prophylaxis of tetanus. (3+4+3=10) [06 Dec]
Lab-diagnosis 2. Describe the pathogenesis, laboratory diagnosis
i. Sample collection and prophylaxis of tetanus (10) [11 July]
- CSF collected by lumbar puncture 3. Descibe the lab diagnosis and pathogenesis of
- Divided into 3 portion tetanus. (5+5=10) [01 July]
1st portion: Microscopic examination 4. Descibe the lab diagnosis and prophylaxis of
nd
2 portion: Biochemical test tetanus. (6+4=10) [03 Dec]
3rd portion: Culture 5. Prophylaxis of tetanus [02 June, 02 Dec]
ii. Microscopic examination Clostridium tetani
 India ink preparation: It is a negative stain Morphology
(stain all except the organism) - Non capsulated
iii. Examination of CSF - Motile, peritrichous flagella
- Macroscopic examination: Clear or slightly - Terminal spore
turbid - Gram positive
- Biochemical examination: - Obligatory anaerobes
Protein: Increased level - 2-5 x 0.4-0.5 µm
Glucose: Decreased level - Drum-stick appearance
- Cell Count
Susceptibility
Total cell per cu.mm = 50 -500 VIII
- Boiling for 15 min: Majority of strains get killed.
Lymphocytes = 90%
- Autoclaving at 1210C for 15 min: Kills the
Neutrophil = 10%
spores of most strains readily
iv. Culture
- Iodine (1%) and Hydrogen peroxide (10
- Inoculated in Sabouraud’s dextrose agar. volumes): Kill the spores within few hours
- Colonies are creamy, white and mucoid and
Toxin
become visible in 24-28 hours.
i. Tetanolysin: Heat and oxygen labile, haemolysin
- C. neoformans identified by Urease production
and carbohydrate assimilation test ii. Tetanospasmin: Oxygen stable
- Confirmed by Direct immunoflorescence using - Heat labile (650C in 5 minutes)
a fluorescein labeled anti - C. neoformans - Neurotoxin
antibody
- Cause spastic paralysis
v. Detection of Antigen
Pathogenesis
- Latex agglutination test
- Mode of transmission: Injury, trauma
- Sandwich ELISA
vi. Serological test - Source of infection: Contaminated soil, rusted
- Agglutination iron
- Immunoflorescence - Incubation period: 5-15 days (depend on site
of injury and the dosage of organism)

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Clostridium tetani enters by injury, trauma Lab Diagnosis

 i. Sample collection
Growth of the organism - Wound swab, exudates or tissue from the
 wound
Produce toxin (tetanospasmin) ii. Microscopic examination
 - Gram positive bacilli having ‘drum stick’
Toxin binds to peripheral motor nerve endings appearance
 iii. Culture
Toxin is then internalized and travels along the - Anaerobe, optimum temperature 370C
motor neurons of peripheral nerve via - Can grow on ordinary nutrient media,
retrograde intra-axonal transport to the anterior enhanced when blood is added
horn cells of spinal cord or brain stem
- Blood agar and aminoglycoside blood agar

- Under anaerobic condition
Interferes with the activity of the inhibitory
interneuron - Produce -hemolysis due to production of
 tetanolysin
Muscle spasm (spastic paralysis) - Robertson’s cooked meat medium
Clinical Manifestations - Turbidity and some gas formation
i. Localized tetanus iv. Biochemical test
- Persistent spasm of the musculature at the site - Slightly proteolytic
of primary infection - Does not ferment any sugar
- Disease remain confined at the primary site - Indole: Positive
VIII ii. Cephalic tetanus - Methyl red and VP: Negative
- Primary site of infection is head particularly ear - H2S not produced
- Dysfunction of Cranial nerve VII - Nitrates not reduced
- Poor prognosis - Gelatin liquefaction occurs slowly
iii. Generalized tetanus v. Animal Inoculation
- Most common - Two mice taken as test and control animal.
- Trismus or lockjaw: Spasm of masseter muscle - 0.2 ml of 2 to 10 days old cooked meat broth
- Risus sardoricus: Characteristics sardonic smile culture filtrate is injected subcutaneously into
due to sustained spasm of facial muscle. the right side of the base of tail of one mouse
- Opisthotonos: Persistent back spasm (test animal)

- In severe disease, autonomous nervous system
involved leading to sweating, hyperthermia,
cardiac arrhythmia and fluctuation in blood
pressure.
iv. Neonatal tetanus
- Typically originates from the umbilical stump
which then progress to generalized disease
- Poor prognosis, mortality > 90%
- Developmental defects in survivors
- Same amount of toxin injected into other
mouse (control) which has received 1,000 units
of tetanus antitoxin one hour before test.
- Positive case: Stiffness and spasm of tail and
inoculated hind limb (12-24 hrs); death in (1-2) days
- In control animal: No change
Prophylaxis
i. Debridement: Wound is debrided
ii. Antibiotic: Penicillin, drug of choice

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iii. Immunization - Toxin A through F are neurotoxins that leads to

a. Active flaccid paralysis
- DPT vaccine: 3 doses given at 6, 10, 14 - Botulinum is heat sensitive.
week of age Pathogenesis
- Immunity for 7-10 years - Mode of transmission
- Booster of tetanus toxoid given after 5  Ingestion of preformed toxin in food
years.  Absorption of toxin produced by the
b. Passive organism at the site of wound infection

- Anti Tetanus Serum (ATS) 1500 IU or Human  Feeding of food (honey) contaminated by
spores
Anti-Tetanus Immunoglobulin (HTIG) 250 IU
Ingestion of preformed Ingestion of food
c. Combined immunization
toxin contaminated with
- Tetanus toxoid in one arm and HTIG (250
spores
IU) or ATS in another arm.

BOTULISM In anaerobic condition,

germination of spore
Past Question:
then multiplication of
1. Write short note on Botulism [04 Dec, 01 July] bacilli
Clostridium botulinum
Morphology Toxin production
- Non-capsulated
- Motile, peritrichous flagella Toxin absorption from intestine VIII
- Sub terminal, oval and bulging spore
- Gram positive Toxin produced by
- Anaerobes Blood circulation organism at the
- Large, 4-8 µm x 0.8-1.2 µm site of wound
Resistance infection is
absorbed
- Moist heat at 1000C for 4-5 hours: withstand by
spore. Reaches peripheral cholinergic synapses
0
- Autoclaving at 121 C within 15 min; all spores
destroyed Block release of acetylcholine at synapse and
Botulinum Neurotoxin (BONT) neuromuscular junction
- Exceedingly potent lethal poison
- Eight antigenic toxin types of C. botulinum (A, Flaccid paralysis
B, C1, C2, D, E, F and G) distinguished on the
basis of their antigenically distinct toxins. Clinical manifestations
- Type A toxin is most potent and toxic i. Infant botulism
- Possess an active (A) region and a binding (B) - Affects babies from 3 to 20 weeks
region - Antigenic variation types A/B

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- Due to feeding of honey contaminated by
spores
- Spores germinate and produce toxin
- Characterized by: Constipation, Weakness,
lethargy, Cranial palsies
ii. Food borne botulism
- By ingestion of preformed toxin in food
- Antigenic variation types A/E
- Incubation period: 12-36 hours
- Non-commercially canned food is at higher risk
for being contaminated
- Characterized by
 Constipation
 Vomiting , thirst
 Ocular paresis
 Difficulty in swallowing, speaking and
breathing
- Flaccid paralysis: Paralysis is descending and
symmetric
 First, affect cranial nerves (diplopia,
VIII
dysphasia, flaccid facial expression)
 Progress centripetally (weakness
peripheral muscle, urinary retention)
 Eventually respiratory paralysis
- Prognosis: Poor
iii. Wound Botulism
- By absorption of toxin in blood, produced by
the organism at the site of wounded infection
- Incubation period: 4-14 days.
Lab-diagnosis
- Diagnosis is primarily made by clinical
presentation, which may be confirmed by
demonstration of toxin or bacillus.
i. Sample Collection
- Residual food, patients serum, intestinal
contents, faeces or postmortem specimens of
blood or liver.
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ii. Demonstration of toxin
- Specimen is macerated in sterile isotonic saline
and filtered extract is divided into three parts.
One portion is heated at 1000C for 10 minutes.
 1st mice  Protected with polyvalent
botulinum antitoxin  Inject 2ml of
unheated filtrated  No change
 2nd mice  Injected 2ml of unheated filtrate
 dyspnoea, flaccid paralysis and dies
within 24 hrs.
 3rd mice  Injected 2ml of heated filtrate
 No change
iii. Demonstration of Organism
a. Microscopy: Gram staining show Gram positive
sporing bacilli
b. Culture
- Grow in Nutrient agar and blood agar in
anaerobic condition
- Also grow in Robertson’s cooked meat
medium in 24-48 hrs at an optimum
temperature of 350C.
Prophylaxis and treatment
of
i. Home processing of meat and vegetable for
preservation is not advisable
ii. Active immunization
- Done for cattle
- Administered to all during on outbreak who
has consumed suspected food.
ENCEPHALITIS
ARBOVIRUSES
Past Questions:
1. Classify arbovirus. Describe Japanese B
Encephalitis. (2+8=10) [03 June]
2. Japanese B Encephalitis virus [02 Dec]
 Arthropod – Borne viruses
 Transmitted by bloodsucking arthropods
 Humans are incidental host (dead-end)
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Major arboviruses [KU 03]

S.N. Family Genome+ envelope Genus Viruses
1. Togaviridae +RNA, enveloped Alpha viruses Eastern equine encephalitis virus
Western equine encephalitis virus
California equine encephalitis virus
Venezuelan equine encephalitis virus
2. Flaviviridae +RNA, enveloped Flavivirus Yellow fever virus
Japanese B encephalitis virus
Dengue Virus
St. Louis encephalitis virus
Central European encephalitis virus

3. Bunyaviridae – RNA, enveloped Bunyaviruses California encephalitis virus

Phleboviruses Sand fly fever virus
Nairoviruses Crimean-congo hemorrhagic fever virus
Hantavirus Hantaan virus
4. Reoviridae dsRNA naked Orbiviruses Colorado tick fever virus
Japanese B encephalitis Virus Pathogenesis
 Family: Flaviviridae Infected Culex tritaeniorhynchus bites incidental
 Genus: Flavivirus host (man) VIII
Morphology 
- Size: 40 -50 nm diameters Virus in capillary circulation [Primary Viremia]
- ssRNA virus (positive sense) 
- Enveloped Endothelial cells of capillaries monocytes,
- Icosahedral capsid macrophages cells by RES
Life cycle 
st
- Host: 1 replication in endothelial cells & RE cells
 Reservoir host: Birds 
 Amplifier host: Pig Secondary Viremia
 Incidental host: Horses, humans 
- Vector: Culex tritaeniorhynchus [2013 MCQ] Virus infect brain by infecting small blood vessels
- Incubation period: 5-15 days of brain or choroid plexus

Birds  mosquito  pig  mosquito  Birds 

 Inflammation of Brain
Human 

Encephalitis Encephalitis

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Clinical Manifestation Morphology

0
i. During 2 viremia: Abrupt onset with fever, - Bullet shaped
headache, rash and vomiting
ii. Encephalitic stage: High fever, nuchal rigidity,
convulsion, altered sensorium, coma
Lab-diagnosis
i. Sample collection: Blood / serum, CSF
ii. Culture: In Hamster kidney cells, chorioallantoic
membrane, Hela, or Vero cells
iii. Animal inoculation: Intracerebrally in suckling
mice.
iv. Serology: Diagnostic test
- Paired sample of serum shows rising titre (four-
fold or greater) of haemagglutinating and
neutralizing antibodies.
Control and prevention
i. Control:
- Mosquito abatement programmes
- Size: 76 x 175 nm
- Regular use of mosquito net
- Nucleocapsid: Helical symmetry
ii. Prevention:
- Contains:
VIII - Killed ‘mouse brain’ vaccine (2 doses, 1 ml each
 ssRNA genome
at an interval of 7-14 days booster does of 1ml
 Nucleoprotein
after few months)
 Plus large and nonstructural proteins
- Killed chick embryo vaccine (very effective)
- Outer lipoprotein envelope contain protruding
Complication hemagglutinating Peplomer Spikes
- Paralysis - Street virus: Freshly isolated viruses from
- Seizures natural human or animal infection
- Coma  Produce fatal encephalitis
- Death  Incubation period: 21-60 days
 Negri body present
RABIES VIRUS - Fixed virus: Strain adapted to laboratory
Past Questions: animals by several serial intra cerebral passage
in rabbits
1. Describe the lab diagnosis and prophylaxis of  Do not grow in extra neural tissue
rabies. (5+5=10) [04 June]  Incubation period: 4-6 days.
2. Prophylaxis of rabies [04 Dec, 01 Dec] Pathogenesis
Family: Rhabdoviridae - Source of infection: Dog infected by wild
animal or infected unvaccinated dogs.
Genus: Lyssavirus
- Mode of transmission: Animal bite

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- Incubation period: 1-3 months. Lab diagnosis

i. Diagnosis in man
a. Antemortem diagnosis
- Diagnosis based on clinical findings of
neurological symptoms and history of
animal bite.
- Specimen: Corneal impression smears or
skin biopsies
- Immunoflourescence test: To detect
presence of virus, viral nucleic acid or viral
antigen
- ELISA: To detect presence of antibodies in
serum in an unvaccinated individual
b. Postmortem diagnosis
- Specimen: Impression smears of cut section
of brain and salivary gland, CSF, Urine
- Isolation of virus: By mouse inoculation
- Demonstration of Negri bodies:
 Brain smear from hippocampus, brain
stem, cerebellum
Clinical Manifestation
 Demonstrated by Seller’s technique
i. Subclinical disease: Not known to occur in human
(basic Fuschin and Methylene blue in
ii. Clinical disease:
alcohol) VIII
- Prodromal (1-10 days)
 Intracytoplasmic, oval, purplish pink,
 Headache eosinophilic inclusion with basophilic
 Malasie granules
 Low grade fever
 Anxiety
 Sore throat
- Hydrophobia
 Person get thirsty but attempt at drinking
prevokes violent contraction of diaphragm
and inspiratory muscle.
 Therefore, mere site or sound of water
precipitate distressing muscular spasm.
- Further progression
 Patient develop focal and generalized
seizures, disorientation and delirium
 Intolerance to noise, bright light, cold air
Negri Bodies
 Increased perspiration, salivation, lacrimation
 Eventually, death due to neurological and - Immunoflorescence: Show presence of
pulmonary failure. virus particle.

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 Microbiology

ii. Diagnosis in Animal - 2 intra dermal injections of 0.1 ml Human

- Brain of rabid animal is removed Diploid Culture Vaccine (HDCV) are given at 4
weeks interval
 Some part: Preserved in 50% glycol saline
Isolation of virus - Yearly boosters are given.

 Another part: Preserved in Zenker’s fixative ii. Post-exposure prophylaxis

 Demonstration of Negri bodies - For wound:
- Biting animal should be kept in strict isolation  Thoroughly cleaned with water and soap
for 10 days. If it remains healthy for 10 days,  Disinfection with Quaternery ammonium
rabies may be excluded. detergent (cetavlon) or tincture iodine or
Prophylaxis alcohol
i. Pre-exposure prophylaxis - Vaccination:
- For people who handle potentially infected  1ml of cell culture vaccine should be given
animals. intramuscularly on day 0, 3, 7, 14, 30 with
booster dose on day 90.
Different Antirabic Vaccines
Nature Name

A. Neural

1. Sample vaccine: 5% suspension of infected brain, inactivated by 5%

phenol at 370c.
VIII Inactivated Fixed virus grown in 2. Betapropiolactone (BPL) vaccine
sheep brain, inactivated by Modified sample vaccine with BPL as inactivating agent instead of phenol
chemical and physical methods
3. Infant brain vaccine:
Vaccine prepared in brain of suckling mice, inactivated by ultraviolet
radiation, BPL or phenol

B. Non neural
a. Duck egg vaccine
i. Inactivated b. Tissue culture vaccine (HDCV): Fixed virus grown in WI-38 or MRC5
human diploid fibroblast cell line, inactivated by BPL
Chick embryo vaccine: 2 types, low egg passage of 40 - 50 (LEP) and High egg
ii. Live attenuated
passage of 180 (HEP)
Surface glycoprotein: Protective antigen cloned and recombinant vaccines
C. Subunit vaccine
produced.

Complications - Respiratory failure

- Brain infection - Death
- Cardiac failure - Coma

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 CNS

POLIO VIRUS 
Past Questions: In patient who fail to control initial viremia

1. Describe the important characteristics of Polio 

virus. Explain the pathogenesis of polio virus. Further multiplication of virus in Reticulo
Describe the advantages and disadvantages of Endothelial system (RES) and again enter
available polio vaccines. (3+3+4=10) [09 July] blood stream
2. Explain the pathogenesis and causative agents of 
Poliomyelitis. (5+5=10) [02 June] Second Viremia
3. Discuss the character, pathogenesis and lab 
diagnosis of poliomyelitis. (3+4+3=10) [01 Dec] Virus disseminated in spinal cord and brain
 Family: Picornaviridae (by passage across the blood-CNS-barrier and
 Genus: Enterovirus alternately via motor neurons at peripheral
neuromuscular junction)
Morphology

- Size: Small, 20-30 nm diameters.
Virus multiplies in neurons and destroys
- Single stranded RNA virus (positive sense)
anterior horn cells of spinal cord, as well as
- Virus replicates in cytoplasm: Cytolytic
nerve cell in medulla oblongata and in the
- Non-enveloped bulbar pons.
- 60 capsomeres in icosahedral symmetry
Clinical manifestation
Types i. In apparent infection: 90%
- Based on neutralization test ii. Abortive illness or minor illness
 Type 1  Most epidemics of paralytic - 4-8%
poliomyelitis - Associated with fever, headache, malaise and VIII
 Type 2  Inapparent infections sore throat
iii. Non paralytic poliomyelitis (Aseptic meningitis)
 Type 3  Epidemics
- 1%
Pathogenesis
- Associated with headache, neck stiffness, back
- Source of infection: Faeces of patient and pain
carrier - Illness last for 2-10 days.
- Mode of transmission: Feco-oral route vi. Paralytic poliomyelitis/major illness
- Incubation period: 9-12 days - 0.1 - 2%
Ingestion of virus contaminated food or water  Appear 3-4 days after minor illness has
subsided

 Flaccid paralysis occurs
Spread to adjacent lymphatic tissue of  Paralysis classified as: Spinal, bulbar and
oropharynx (tonsils) and intestine (Peyer’s bulbospinal
patches)  Maximal recovery takes place within 6
 months.
Enter the blood stream v. Encephalitis: Complication of poliomyelitis, grave
prognosis

vi. Post-polio syndrome: Complication of
Initial Viremia
poliomyelitis (20-30%), deterioration of originally
 affected muscle.

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 Microbiology

Lab Diagnosis  Cytopathic effect: Observed in 3-6 days.

i. Sample collection  Identification of virus: Neutralization test.
- Blood: At time of viremia iii. Direct demonstration of Virus
- Pharyngeal aspiration: First 3-5 days - Virus detection in stool
- Stool sample: Upto 5 weeks  By direct electron microscopy
- Specimen should be kept frozen during  By immune electron microscopy
transport to the laboratory. iv. Serology
ii. Isolation of Virus - Neutralization
- Samples are cultivated in human or simian cell - Complement fixation
lines - Immunofluorescence test.
Immune Prophylaxis
Sabin’s vaccine Salk’s vaccine
i. Immunizing agent - Live attenuated virus - Killed virus
ii. Route of - Oral - Parenteral
administration
iii. Induction of Herd - Yes - No
immunity
iv. Dose & time of - 4 doses, 1st at 2 month of age, 2nd & 3rd at - 3 doses at an interval of 4-5 weeks
administration interval of 2 month & 4th at 1½ yrs. - Booster dose 6 months after 3rd
- No booster dose required. dose
VIII - Immunity : Mucosal (IgA) & Humoral (IgM, - Reversion of virulence is not seen
IgG, IgA) - Does not require stringent
v. Advantages - Prevent paralysis and intestinal infection condition during storage and
- Long lasting immunity transport
- Easy to administer
- Easy to manufacture
vi. Disadvantages - Reversion of virulence is seen - Immunity : Only humoral
- Require stringent condition during storage - Do not prevent paralysis and
and transport intestinal infection
- Short lasting immunity
- Difficult to administer
- Difficult to manufacture

 Chicken pox follows primary contact of a non-

VARICELLA ZOSTER VIRUS immune individual with the virus.
Past Questions:  Zoster is reactivation of the latent virus.
1. Short notes on Varicella zoster [11 July] Varicella
 Varicella (Chickenpox) and herpes zoster (shingles)  Mode of transmission: Respiratory route
are caused by a single virus.  Incubation period: 10-21 days
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 CNS

Virus enters body TRACHOMA


Past Questions:
Multiplies locally
Short notes on:

Circulates in blood a. Chlamydia trachomatis [02 June]
b. Trachoma [11 July]

Localizes in skin, mucous membrane c. Neonatal conjunctivitis [06 June, 03, June]

Clinical Manifestation Chlamydia trachomatis

- Chickenpox is a mild but highly infectious
childhood viral disease
- Characterized by vesicular rash (mostly in
trunk)
- Rash progresses through: Macule, papule,
vesicle, postule and scab.
Complication
- Pneumonia
- Post viral encephalitis
- Hemorrhagic (Fulminating) varicella
Herpes zoster (Shingles)
 Disease of old age, several years after chickenpox
 Reactivation occurs in cancer patients and in
patients on immunosuppressive therapy and also
in trauma patients.
 Inflammatory reaction in nerve roots and ganglia
accompanied by eruption of painful vesicles in
area supplied by affected sensory nerves.
Clinical manifestation
- Vesicles are like those of varicella
- Eruption is unilateral
- Thoracic nerve are frequently involved with
sudden onset of pain and rash appear around
trunk.
Complication
- Ophthalmic zoster: When ophthalmic branch
of trigeminal nerve infected.
- Keratoconjunctivitis
- Disease may disseminate when patients is on
immunosuppressive drugs or has lymphoma
treated by radiotherapy.
 Almost exclusively human pathogen
Serotypes:
- 15 serotypes
i. Types a, B, Ba and C:
 Endemic trachoma
 Major cause of blindness
ii. Types D to K: Non-gonococcal urethritis and
mucopurulent cervicitis
iii. Types L1, L2 and L3: Lymphogranuloma venerum
Morphology
- Small, non-motile and Gram negative
- Obligate intracellular bacteria
- Possess both RNA and DNA
- Have no peptidoglycan in their cell wall (not VIII
true bacteria)
- Ribosomes present, protein synthesis occurs
but ATP cannot be synthesized
- Multiply in cytoplasm of host cell forming micro
colonies or inclusion bodies which encloses the
nucleus of the cell as a Helmet or Mangle.

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 Microbiology

- Two distinct morphological forms:  Divide by binary fission

i. Elementary body  800-1000 nm in size, containing inclusion
 Infectious bodies
 Extracellular form of the organism iii. Intermediate body
 Spherical particle (D = 20 – 300 nm)  Form after condensation of RB which
 Metabolically inert looks like Bulls Eye microscopically
 Responsible for spreading infection  Intermediate body condense into
elementary body
ii. Reticulate body
 Forms 5-6 hours after EB is
phagocytosed into the target cells
Life Cycle

VIII

Clinical disease: Inflammation of mucous membrane and

- The target cell of C. trachomatis is usually conjunctiva
mucosal cells 
i. Ocular disease (Trachoma)
Neo-vascularization of cornea
- Incubation period: 3 -10 days
- Transmission route: Close contact with an 
infected person Scar formation (pannus)
- Associated with poverty, overcrowding and 
poor hygiene
- Has abrupt onset Blindness

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- Early symptoms
 Lacrimation
 Muco-purulent discharge
 Conjunctival hyperemia
 Follicular hypertrophy
ii. Lympho granuloma Venerum
iii. Non-gonococcal urethritis
iv. Mucopurulent cervicitis
v. Neonatal infections
- Acquired during passage through the
infected birth canal
- Types D to K
- Remain asymptomatic with colonization of
the nasopharynx
a. Neonatal conjunctivitis [06,03]
 Incubation period: 5 – 14 days
 Transmission route: During passage
though birth canal
 Begin as mucopurulent conjunctivitis 7-
12 days after delivery
 Presentation range from mild hyperemia
with scant mucoid discharge to eyelid
swelling, chemosis and pseudo
membrane formation
 Good prognosis
 Other infection like gonococcal,
staphylococcal and herpetic infection
also cause neonatal conjunctivitis
Opthalmia neonatarum: If organism comes
from birth canal. e.g. N. gonorrhoea and C.
trachomatis
b. Pneumonia
 During first three months of life
 Complication of neonatal conjunctivitis
Lab diagnosis
i. Sample collection
- Ocular disease: Conjunctival scrapping
- Urethritis: Scrapping of urethra
- Cervicitis: Scrapping from columnar
surface of endocervical canal.
FAST TRACK
CNS
ii. Microscopic examination
- Smear stained with Gram stain
- Show inclusions (Miyagawa’s granulocorpuscles)
iii. Isolation
- Isolation of C. trachomatis in cell culture is the
most specific method of diagnosis.
- Cannot be cultured in bacteriologic media
- Can be grown in
 Yolk sac of embryonated egg
 Monkey kidney cell
 McCoy cells
- Incubation is done at 350C for 48-72 hours
- Identification is done by
 Fluorescent antibodies
 Iodine (specific for C. trachomatis)
 Demonstration of inclusion bodies
iv. Antigen detection
- Direct immune-flourescence staining (DFA)
- Enzyme linked immunoassay (ELA)
Antibodies against either the Chlamydial
MOMP or the cell wall LPS are used.
v. Nucleic acid probes
VIII
- Detection of species specific sequence of 16s
rRNA
- Polymarase Chain Reaction (PCR) and Ligase
Chain Reaction (LCR) (based on Nucleic Acid
Amplification test)
vi. Serological test
- Complement Fixation Test (CFT) becomes
positive (2 weeks after infection)
- An antibody titer of 64 or more is significant
Treatment
i. Trachoma: Sulphonamide and tetracyclines
ii. Non gonococcal urethritis: Doxycyline or
Erythromycin
Complication
- Scarring of inner eyelid
- Eyelid deformation
- Inward folding of eyelid
- Ingrown eyelashes
cell
- Corneal scarring or cloudiness
- Partial or complete vision loss
BASIC SCIENCE MBBS -917-
 Microbiology

CONJUNCTIVITIS  Dry eye

 Toxic
Past Questions:
 Idiopathic
Write short notes on:
Pathogenesis
a. Conjunctivitis [09 Jan]
- Mode of infection
b. Neonatal conjunctivitis [06 June,03 June]
a. Exogenous infection (Common)
Definition
 Close contact (e.g. air borne, water
Inflammation of the conjunctiva characterized by borne infection)
conjunctival hyperemia with discharges, which may
 Vector transmission (e.g. flies)
be watery, mucoid, muco-purulent or purulent.
 Infected clothing
Types
b. Local Spread
i. Based on onset
 From infected lacrimal sac, lids,
- Acute nasopharynx etc.
- Sub-acute c. Endogenous infections (rare)
- Chronic
 Through blood
ii. Based on types of exudates
Infectious agent invade from adjacent sites by
- Serous
blood borne pathway
- Catarrhal

- Purulent
Replicate within conjunctival mucosal cells
- Muco-purulent

- Membranous
Initiate leukocyte or lymphocytic inflammatory
VIII - Pseudo-membraneous cascade
iii. Based on conjunctival response
Clinical Manifestation
- Follicular
a. Bacterial conjunctivitis
- Papillary
- Fiery red (pink eye)
- Granulomatous
- Coloured halo
iv. Based on Etilogy
- Purulent or muco-purulent discharge
- Infectious:
- Edema, small ecchy moses and
 Bacterial (S. aureus, H. influenzae, H.
aegypticus, S. pneumonia) pseudomembrane (Pneumococcal conjunctivitis)
 Viral (Herpes virus – 1, Adeno viruses – 7, 8, - Moderate to severe pain and lid swelling
14, Coxsakie A, enterovirus, measles, (Nesseria gonorrhoeae)
mumps) b. Viral Conjunctivitis
 Fungal (Aspergillus, Candida, Nocardia, - Swelling , congestion, watering and pain in eye
Actinomyces) - Keratoconjunctivitis
 Parasitic - Acute hemorrhagic conjunctivitis
c. Allergic conjunctivitis
 Chlamydal (D-K)
- Caused due to dust, pollen grains, certain
- Non – infectious:
medicines, chemicals, etc.
 Allergic - Necrosis of conjunctiva
 Irritants - Complete white eye due to vascular closure
 Endogenous or auto-immune
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 CNS

Lab-diagnosis ACUTE/ CHRONIC SUPPURATIVE

i. Sample Collection: OTITIS MEDIA
- Tear, discharge, scrapping from conjunctiva Chronic Suppurative Otitis Media
ii. Microscopy (CSOM) [09, 08, 01]

a. Gram’s stain Past Questions:

- Gram smear shows Gram positive or Gram 1. Define chronic suppurative otitis media (CSOM).
negative bacteria Describe the lab diagnosis of CSOM.
b. Giemsa stain (2+8=10) [08 July]
- C. trachomatis shows intracytoplasmic 2. Write short notes on: Chronic suppurative otitis
media [09 July, 01 July]
inclusion
 Chronic: Duration > 3 months
c. KOH Mount
 Suppurative: Pus forming
- Candida albicans:
 Otitis media: Inflammation of middle ear
 Budding yeast cell with pseudohyphae
Causative Agent
iii. Culture a. Aerobes
a. Blood agar, MacConky Agar, Chocolate agar - Pseudomonas aeruginosa
- For bacterial agent - Streptococcus pneumoniae
b. Sabouraud’s Dextrose Agar (SDA) - Staphylococcus aureus
- For fungal agent - Hemophilus influenzae
- Proteus
c. McCoy, Hela – 229
b. Anaerobes VIII
- For C. trachomatis and Viruses
- Bacteroids
iv. Biochemical test - Fusobacterium
a. Staphylococus aureus - Peptostreptococcus
Catalase test: +ve, - Peptococcus
Coagulase test: +ve Pathogenesis
b. Streptococcus pneumoniae Episode of acute infection
Catalase test: -ve 
Irritation and subsequent inflammation of
Coagulase test: -ve middle ear mucosa
c. Hemophilus influenzae: 
 Sattlelitism phenomenons: When grown on Inflammatory response creates mucosal edema
blood agar with Staphylococcus aureus. 
Mucosal ulceration and consequent breakdown
Complication of the epithelial lining
- Chronic conjunctivitis 
- Abrasions of cornea Formation of granulation tissue after repeated
infection
- Superficial keratitis

Destruction of the surrounding bony margins

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 Microbiology

Clinical Presentation Eg: Rhino virus

- Ear pain, fever and irritability Measles virus
- Ottorrhea (purulent discharge) RSV (Respiratory syncytial virus)
- Perforation in ear drum Influenza virus
Lab Diagnosis Parainfluenza virus
i. Sample Collection Pathogenesis
- Pus swab from the discharge Viral upper respiratory tract infection
- Needle aspirate from middle ear 
ii. Microscopy Swelling of mucous membrane in Nasopharynx
a. Gram staining: Shows Gram +ve and Gram –ve 
organisms Blockage of Eustachian tube
 Gram +ve: 
Mild vacuum formed
i. Peptococcus

ii. Peptostreptococcus
Fluid accumulation
 Gram –ve:

i. Bacteroids Otitis media
ii. E. Coli 
iii. Klebsiella Bacteria reach
iv. Proteus 
v. Pseudomonas Suppurative infection
b. Acid fast staining: For Mycobacterium Clinical features
VIII tuberculosis - Ear pain
iii. Culture - Fever
- Blood agar, chocolate agar and Mac-Conky - Irritation
Agar: For aerobic bacteria
Complication
- Sabouraud’s dextrose (SD) Agar: For fungus
- Chronic otitis media
- Robertson’s cooked meat medium: For
anaerobic infections SLOW VIRUS
iv. Biochemical test  A virus or virus like agent, having a long incubation
- Oxidase +ve = Pseudomonas period (months to years) and then a gradual onset of
- Urease +ve = Proteus symptoms which progress slowly but irreversibly and
- Coagulase +ve = Staphylococcus aureus terminate in severe compromised state.
Complication Eg: Visna Maedi Virus
- Glue ear (persistent middle ear effusion)
PRION DISEASE
- Deafness
 Disease having long incubation period,
- Meningitis
characteristics spongiform changes with neuronal
- Facial nerve paralysis loss and a failure to induce inflammatory response.
Acute Otitis Media Eg: Creutzfeldt-Jakob disease
 Caused by upper respiratory tract infection Total familial insomnia
causing viruses (mostly)

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 CNS

SPECIAL POINTS FOR MCQs

1. Classic "Volcano” exudates in biopsy are seen C. difficile infection (Pseudo membranous colitis)
2. Clostridium tetani causes spastic paralysis whereas Clostridium botulinum causes flaccid paralysis.
3. Terminal spore with characteristic drum –stick appearance is seen in Clostridium tetani.
4. Toxin mainly responsible in causing tetanus is Tetanospasmin.
5. Characteristic smile resulted from sustained contraction of facial muscles in tetanus patients are
known as Risus sardonicus.
6. Tetanus causes spasm of jaw muscles (locked jaw, trismus) and facial muscle (risus sardonicus)
and arching of body (opisthotonous).
7. Tetanus toxin mainly inhibits inhibitory interneurons causing spastic paralysis. It acts
presynaptically, unlike strychnine, which acts postsynaptically.
8. Botulinum Toxin acts on parasympathetic system i.e. blocks calcium dependant release of
acetylcholine at synapse and neuromuscular junction.
9. Unlike C. tetani, spore of C. botulinum is oval and subterminal.
10. Minimum lethal dose of botulinum toxin for a mouse is 0.03ng and that for humans may be 1Ug.
11. Death in botulism is due to respiratory failure.
12. Floppy child syndrome is caused by C. botulinum.
13. Bacteria showing swarm on blood agar is C. tetani.
14. Antibiotic associated diarrhea is mainly due to C. difficile.
15. Stormy clot reaction is useful in dentification of C. perfringens.
16. Nagler's reaction is useful in identification of C. perfringens.
17. Clostridium perfringens is different from other species of clostridia in being non-motile and
capsulated. Most of other are motile and non capsulated. VIII
18. Reddening of meat in cooked meat broth is produced by C. perfringens.
19. Blackening of meat in cooked meat broth is produced by C. histolyticum.
20. C. botulinum food poisioning is due to preformed toxin.
21. C. perfringens is the most common of clostridial species isolated-from tissue infections and
bacteremias.
22. Of 30 or more species that normally colonize humans, Clostridium ramosum is most common.
23. Differentiation of N. gonorrhoeae and N. meningitidis is done by maltose fermentation test i.e N.
gonorrhoeae ferments glucose only while N. menigitidis ferments glucose and maltose.
24. N. gonorrhoae is arranged in pairs with adjacent side concave while N. meningitidis is arranged in
pairs with adjacent sides flat.
25. Causative agent of waterhouse-Friderichsen syndrome is N. meningitidis.
26. Unlike Pneumococcus, in Neisseria long axis of pair is parallel and not in line.
27. N. meningitidis has been divided in 13 serogroups (A, B, C, D, X, Y, Z, W-135, 29E, H, I, K and L)
on the basis of immunological specificity of capsular polysaccharide.
28. Rapid test used for growth of Neisseria is Thayer - Martin medium.
29. Capsule of N. meningitidis is polysaccharide and that of N. gonorrhoeae is polyphosphate.
30. People with defect in late complement pathway (C6-C9) are prone to Neisseria infection.
31. N. meningitidis is transmitted via respiratory droplets.
32. Skin lesion in meningococcal meningitis is due to endotoxin.
33. Rabies virus is Bullet –shaped.
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 Microbiology

34. Rabies virus isolated from natural human or animal infection is called street virus. By several
serial intracerebral passages in rabbits, the virus undergoes certain changes and is termed as fixed
virus.
35. For vaccine production, fixed rabies virus is utilized.
36. Negri bodies are intracytoplasmic inclusions particularly found in hippocampus.
37. Negri bodies can be demonstrated in infections with street rabies virus but not with fixed rabies
virus.
38. Rabies virus travels along the axon towards the central nervous system at a speed of 3mm per
hour.
39. Rabies is the only human disease that can be prevented by active immunization after infection.
40. For postexposure prophylaxis 1 ml of cell culture vaccine should be given intramuscularly on day
0, 3, 7, 14, 30 with booster dose on day 90.
41. Route of administration of purified chick embryo cell vaccine is intramuscular and is administered
in deltoid region.
42. Rabies viral antigens can be detected in corneal impression smears and facial skin biopsies or
saliva by direct immunoflorescense. It is very useful for antemortem diagnosis. Same method
may be used on brain for postmortem diagnosis.
43. Seller’s technique (basic fuchsin and methylene blue in alcohol) is used to demonstrate negri
bodies.
44. Fixative used for demonstration of Negri bodies is Zenker’s fixative. Zenker’s fluid contains
potassium dichromate, mercuric chloride and distilled water.
45. Polio virus belongs to picorna virus family and has icosahedral symmetry.
46. Most common type of polio virus is type 1 and it is most common cause of polio epidemics and is
most difficult to eradicate.
47. Most antigenic strain of polio is Type 2.
VIII 48. Most common manifestation of polio is subclinical infection (90%).
49. Descending asymmetrical paralysis is the predominant sign of polio.
50. Spread of polio is both by haematogenous and neural route.
51. Death in polio is mostly due to respiratory paralysis.
52. Most definitive method for lab diagnosis of poliomyelitis is serological diagnosis.
53. Polio virus is transmitted by feco-oral route.
54. Viral meningitis is most commonly due to enterovirus.
55. Viral encephalitis shows perivascular cuffs, microglial nodules and neuronophagia.
56. Japanese encephalitis is transmitted by Culex tritaeniorhynchus.
57. In Japanese encephalitis, Pigs act as amplifier.
58. ''Soap bubble'' lesions in brain are seen in Cryptococcal meningitis.
59. India Ink stain is used to demonstrate the capsule of Cryptococcus.
60. Capsule of Cryptococcus is polysaccharide in nature.
61. Fungus present abundantly in feces of pigeons is Cryptococcus neoformans.
62. Cryptococcus neoformans produce brown colonies on niger seed agar.
63. Cryptococcus neoformans can be differentiated from non-pathogenic Cryptococci by growth at 370c,
urea hydrolysis and production of brown colonies.
64. Cell wall of Chlamydia contains Lipopolysaccharide but does not have peptidoglycan layer.
65. Infective form of Chlamydia is Elementary body.
66. Reniform inclusion bodies can be demonstrated in Chalymidial infections.

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