BPC 2.

1 MICROBIOLOGY 1
COURSEWORK
BY DR. IMMACULATE AKASO
Presentation by
Group Five

S/NO. NAME REGISTRATION

NUMBER
1. SSENTONGO JOSEPH VU-BPC-2407-0817-
DAY
2. NASINGURA HELLEN VU-BPC-2407-2593-
DAY
3. MITTI TONNY VU-BPC-2407-1567-
DAY
4. TIBAKIMUWE SABRA VU-BPC-2407-0637-
DAY
5. AZIKU SAID VU-BPC-2407-0185-DAY

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Question 1
Describe the various methods of horizontal gene transfer
among bacteria and mention their significance.

Answers

Horizontal methods of gene transfer of DNA in bacteria cell.

Horizontal gene transfer (HGT): Is the process by which bacteria

acquire genetic material from other bacteria, or even other organisms,
without being the direct offspring of those organisms. This is a key
mechanism for bacterial evolution and adaptation. The three primary
methods of HGT are:
 Transformation

 Transduction

 Conjugation

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 Genetic overview of bacteria
• Characteristics of genetic material
• Storage of Information
• Expression of Information
• Replication
• Variation by mutation

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 The bacterial chromosome

• The bacterial chromosome is a double

stranded DNA molecule, haploid in nature and
surrounded by the nuclear membrane
• Process by which bacteria procreate is called
binary fission. Here Bacteria undergo gene
replication, forming an exact copy of their
genome, and then split in two, taking a copy
with each half

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 MOBILE GENETIC ELEMENTS(MGEs’)

• MGEs are segments of DNA in bacteria that have the ability to

move,
• or "jump," from one location to another within a cell's genome,
or
• even be transferred to a different cell or organism.
• They include;
• Insertion sequences (IS elements): these are simple transposons
that encode only the proteins needed for their own movement.
• Pathogenicity islands. These are clusters of genes, often including
virulence factors, that are found on the bacterial chromosome
and can be transferred between bacteria.
•
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 Cont’d
• Plasmids; are circular DNA molecules that
replicates independently of the bacterial
chromosomes. They often carry antibiotic
resistance genes.
• Bacteriophages; these are viruses with their
own DNA that infect bacteria with their own
DNA and carry genetic material from one
bacteria to another.

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 Cont’d

 Transformation

The process by which bacteria takes naked DNA from the

extracellular environment and incorporates it into its own DNA.

This may occur either in nature or in a laboratory.

• In nature, DNA is released from a bacterium by lysis, which may

be taken up by recipient bacterium that must be competent and
usually of the same species.

• In such instances the if the naked DNA belonged to a harmful

bacteria and its incorporated into a previously competent harmless
bacteria, then the genes of the harmful bacteria can transcribe the
RNA to translate nasty proteins such as toxins thus transforming a
previously harmless bacteria into a harmful bacteria
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 significance
• Streptococcus Pneamoniae
• Hormophillus Influenza type B
• Niesseria Meningitidis

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 Cont’n

• In laboratory conditions, DNA may be

extracted from one type of bacterium and
introduced into genetically different bacteria.
The cell walls of bacteria in vitro are made more
permeable for DNA uptake by using substances,
such as calcium chloride.

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 illustration
• For transformation to
be feasible
• The naked DNA must be
able to bind and enter
the competent bacteria
• Their must be enough
homology between the
strands for it to
incorporate itself into
the recipient’s genome
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 Transduction
• Bacteriophages encode diphtheria toxin,
botulinum toxin, cholera toxin, and erythrogenic
toxin and can be transferred from one bacterium
to another by transduction.
• Transduction is of two types:

(a) generalized transduction and

(b) specialized transduction.

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 Transduction

• Transduction is the transfer of DNA from one bacterium to another

mediated by a bacteriophage.
• The protein coat binds to the bacterial surface, then injects the phage
DNA into the bacteria
• The phage DNA the takes over the cell’s machinery here, it replicates
phage DNA, release enzymes that break down and disintergrates the
bacterial DNA, synthesizes cupsids.
• The process of lysogenic conversion confers a new property to the
bacterial cell; for example, by lysogenic conversion non-pathogenic
bacteria can become pathogenic.
• Performed by two types of phages the virulent phages and temperate
phages.

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 (a) Generalised transduction

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 illustration
• The bacteriophage
incorporated with
the bacteria DNA
then passes it DNA
to a new bacteria
forming a new trait
with new evolution
and adptations

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 Specialized transduction

• This is the case

for HVS

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 significance
bacteria toxins

Group A streptococcus pyogenes Group A Erythrogenic toxins

Clostridum Botulinum Botulinum toxins

Vibreo Cholera Cholera toxins

Cornea diphtheria bacteria Diptheria toxins

Shigella bacteria Shiga toxins

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 Cont’n

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 conjugation

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 Significance
• When a bacteria has a plasmid and which
transcribes for the synthesis of beta-
lactamase protein. The beta lactame ring will
be broken down in rendering this bacteria
resistant to penicillin

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 cont’n

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 significance
• For example if an enterococcus has a VAN A
gene, it can be passed on to another bacteria
• The VAN A gene has the ability to alter the
peptidoglycan layers in the bacterial cell wall
in such a way that it will become vancomycin
resistant. This bacteria will now be
vancomycin resistant Enterococcus

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 Cont’d
• Passing this VAN A gene from Enterococcus to
staphylococcus Aures by either transduction,
transformation, will result into Vancomycin
resistant staphylococcus Aureus

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Question 2
Distinguish between lytic and lysogenic
phage with the help of diagram.
Answers
Introduction
• A phage: It is a short for bacteriophage, and it is a
virus that cause infection to a bacterial cell.
• Viruses use the lytic and lysogenic cycles to make
more copies of themselves in a host cell.
• This happens when the virus takes over the cell’s
machinery. Bacteriophages, which infect bacteria,
are great models for studying these cycles.

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 Cont’n
• All viruses require host cells to reproduce because they
cannot do so independently. They use the cell’s
machinery to create new viral particles. Bacteriophages
replicate in bacterial cytoplasm, whereas most DNA
viruses replicate in animal nuclei.
• Bacteriophage research provides insight into how viruses
affect cells. Some viruses cause immediate cell death
(lytic), while others can remain inside the cell
(lysogenic).
• Understanding these cycles is similar to figuring out how
viruses behave in the cells they infect. This will explain
the difference between lytic and lysogenic phage.
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Cont’n

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 Cont’n

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 Cont’n
• The lytic and lysogenic cycles differ because the
former destroys the host cell, whereas the latter does
not. The lytic and lysogenic cycles are viral replication
processes that can occur simultaneously. During the
lytic cycle, viral DNA damages the host cell’s DNA,
causing the cell to cease to function normally.
• However, viral DNA may integrate with host DNA
during the lysogenic cycle.
• A virus is an infectious agent that consists of a nucleic
acid molecule enclosed in a protein coat.

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 Bacteriophage

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 Lytic cycle

• The lytic cycle begins with a virulent phage

invading the host cell, causing the production

of new phage particles that eventually lead to

the host cell’s destruction.

• The T-phage is a good example of how the lytic

cycle works.

• It infects the Escherichia coli and other

Enterobacteria spp.
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 Cont’n
First Stage: The phage attaches to the host’s bacterial

surface receptors via specific lipopolysaccharides and

the OmpC ( outer membrane protein C ) protein.

• Most phages have a limited host range, infecting only a

specific bacterial species or strain within a species.

• This recognition capability can be harnessed for

targeted treatment in bacterial infections, as seen in

phage therapy.

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 Cont’n

Second Stage: The second stage of the

lytic cycle is entry or penetration,
characterized by the contraction of the tail
sheath, which acts like a hypodermic
needle, injecting the viral genome through
the cell wall and membrane.
• The phage head and other components
remain external to the bacterial cell.

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 Cont’n
Third Stage: Proceeding to the third stage,
biosynthesis of viral components occurs after
the phage enters the virus particle, and viral
endonucleases degrade the bacterial
chromosome.
• The phage effectively takes control of the host,
orchestrating the replication, transcription,
and translation of all viral components
necessary to assemble new viruses.
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 Cont’n

Fourth Stage: The fourth stage involves

maturation, generating new virions. This is
followed by the final stage, in which the mature
viruses are released.
• The fully developed viruses initiate a process
known as lysis, causing the host cell to burst,
and the progeny viruses are then liberated
into the environment, poised to infect new
host cells.
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 Cont’n

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 Lysogenic cycle

• During the lysogenic cycle, attachment and

penetration processes enable the phage
genome to enter the host cell.
• An example of a phage with this life cycle is
the lambda phage. In contrast to the lytic
cycle, which results in host cell death, the
lysogenic cycle integrates the phage genome,
called a prophage, into the bacterial
chromosome.
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 Lysogenic cycle

• The bacterium carrying the prophage is known

as a lysogen.
• The overall process of a temperate phage
infecting a bacterium is referred to as
lysogeny.
• As the bacterium replicates its chromosome,
the phage’s DNA is replicated and transmitted
to new daughter cells during bacterial
reproduction lysogen.
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 Cont’n

• The presence of the phage may alter the

bacterium’s phenotype, as the phage can
introduce additional genes, such as toxin genes,
that enhance bacterial virulence.
• This change in the host phenotype is known as
lysogenic or phage conversion.
• Certain bacteria, like Vibrio cholerae and
Clostridium botulinum, exhibit reduced

virulence without the prophage.

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 Cont’n

• Throughout the lysogenic cycle, the

prophage remains in the host chromosome
until induction occurs, leading to the
excision of the viral genome from the host
chromosome.
• After induction, the temperate phage can
enter a lytic cycle and subsequently undergo
lysogeny again in a newly infected cell.

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 Cont’n

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 Cont’n

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 Cont’n

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Question 3
Identify the biological processes that occur
in the development of antibiotic resistance.
Answers
Overview
Biological processes: are the series of chemical,
physical and mechanical events that occur within
living organisms to maintain life, support growth,
enable reproduction and respond to environmental
changes. These processes are regulated by genetic
and biochemical mechanisms and are essential
for survival and adaptation.
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 Cont’n
Antimicrobial Resistance (AMR): According to the WHO

definition “Antimicrobial resistance occurs when

microorganisms such as bacteria, viruses, fungi and parasites

change in ways that render the medications used to cure the

infections they cause ineffective.

• Antimicrobial resistance is facilitated by the inappropriate

use of medicines, for example, when taking substandard

doses or not finishing a prescribed course of treatment.

• Low-quality medicines, wrong prescriptions and poor

infection prevention and control also encourage the

development and spread of drug resistance”.

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Some instances of AMR
 The resistance of malaria parasites has caused several
changes in antimalarial regimens in the last 15 years.
 MDR-TB (multi-drug resistant tuberculosis) is spreading
and requires long and complex treatments.
 HIV resistance is a serious concern, especially after long-
term treatment
 AMR is spreading and, in some cases, commonly used
antimicrobials are not as effective as before.
 Antimicrobial resistance among bacteria other than TB and
fungi that affect the immunocompromised is evolving,
spreading and responsible for death from sepsis in general
and high dependency units
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Biological processes that occur in the
development of antibiotic resistance.
1. Mutation: Spontaneous changes in a bacterium’s DNA can alter genes

involved in antibiotic targets, uptake, or efflux, conferring resistance.

These mutations occur naturally during DNA replication and are selected

under antibiotic pressure, as resistant mutants survive and reproduce.

Mechanism: The mutations modify antibiotic binding sites (e.g.,

penicillin-binding proteins [PBPs] in S. pneumoniae), increase efflux

pump activity, or reduce drug uptake. E.g., in S. pneumoniae, mutations in

PBP genes (e.g., pbp2x, pbp2b) reduce penicillin affinity, leading to

penicillin resistance, a common trait in multidrug-resistant strains.

• Mutations are a primary source of resistance, especially in bacteria with

high mutation rates, and are amplified by repeated antibiotic exposure.

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 Cont’n

2. Horizontal Gene Transfer (HGT): Bacteria acquire resistance genes from other

bacteria via three mechanisms: transformation, transduction, or conjugation. This allows

rapid dissemination of resistance across populations or species.

Mechanisms:

Transformation: Uptake of naked DNA from the environment. S. pneumoniae is

naturally competent, readily acquiring resistance genes from lysed cells.

Transduction: Phage-mediated transfer of resistance genes. Less common in S.

pneumoniae but relevant in other species.

Conjugation: Direct transfer of plasmids via cell-to-cell contact. While less frequent in S.

pneumoniae, it occurs in other gram-positive bacteria. E.g., S. pneumoniae acquires

mosaic PBP genes via transformation, leading to beta-lactam resistance, or ermB genes

for macrolide resistance, likely contributing to the patient’s MDR strain.

• HGT accelerates resistance spread, especially in settings with high antibiotic use

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 Cont’n

3. Overexpression of Efflux Pumps: Bacteria upregulate efflux

pumps, membrane proteins that actively expel antibiotics, reducing
intracellular drug concentrations.

Mechanism: Genetic changes (mutations or acquired genes) increase

pump expression or efficiency, removing antibiotics like tetracyclines
or macrolides before they act. E.g., In S. pneumoniae, the mefA gene
encodes an efflux pump conferring macrolide resistance, potentially
contributing to the patient’s strain resisting azithromycin.

• Efflux pumps broaden resistance to multiple antibiotic classes,

complicating treatment in MDR infections.

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 Cont’n

4. Enzymatic inactivation: Bacteria produce enzymes that

chemically modify or degrade antibiotics, rendering them
ineffective.
Mechanism: Enzymes like beta-lactamases cleave antibiotic
structures (e.g., beta-lactam ring in penicillin). While S.
pneumoniae typically resists beta-lactams via altered PBPs,
other bacteria use enzymes.
E.g., Although less common in S. pneumoniae, related
streptococci may produce beta-lactamases, and co-colonizing
bacteria in the patient’s respiratory tract could contribute to
resistance via enzyme production.
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 Cont’n

5. Target modification: Bacteria alter the

molecular targets of antibiotics, preventing binding
or action.
Mechanism: Mutations or acquired genes modify
target sites, such as ribosomal subunits (for
macrolides) or PBPs (for beta-lactams). E.g., In S.
pneumoniae, altered PBPs reduce binding of
penicillin, and ribosomal methylation by ermB
confers macrolide resistance, likely present in the
patient’s MDR strain.
• Target modification is a key resistance
mechanism in gram-positive bacteria, limiting
first-line treatment options.
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 Cont’n

6. Biofilm Formation: Bacteria form biofilms, structured

communities encased in a protective matrix, reducing
antibiotic penetration and efficacy.
Mechanism: Biofilms create physical barriers and slow
bacterial metabolism, making cells less susceptible to
antibiotics. They also facilitate HGT within the community.
E.g., In the patient with chronic bronchitis, S. pneumoniae
biofilms in the respiratory tract may have protected resistant
strains from antibiotics used in prior treatments, contributing
to MDR development.
• Biofilms are common in chronic infections, complicating
treatment and promoting GR0UP
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resistance.
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 Cont’n

7. Selection Pressure: Antibiotic exposure kills susceptible

bacteria, allowing resistant strains to survive and dominate
the population.
Mechanism: Repeated or inappropriate antibiotic use (e.g.,
broad-spectrum agents, incomplete courses) selects for
resistant mutants or acquired resistance genes. E.g., The
patient’s multiple antibiotic treatments for bronchitis likely
exerted selective pressure, favoring MDR S. pneumoniae
strains with resistance to penicillin and macrolides.
• Selection pressure is the driving force behind resistance
proliferation, amplified by healthcare practices like
overprescribing.
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 Question 4
CASE STUDY
A 22-year-old female schoolteacher was brought to
the emergency room after a 2-day history of
headache and fever. On the day of admission the
patient was confused and highly agitated. Purpuric
skin lesions were present on her trunk and arms.
Gram stain of CSF showed many gram-negative
diplococci, and the same organisms were isolated
from blood and CSF.

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 Cont’n

1. What is the most likely organism responsible for

this fulminant disease?
2. Describe the cultivation conditions necessary for
the identification of this species.
3. What is the epidemiology of this disease?
4. Which treatment (antibiotic) should be
administered?
5. What virulence factors have been associated
with this species?
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 Answers

1). Most likely organism responsible for

the fulminant disease.

Neisseria meningitidis.
Neisseria meningitidis spreads via inhalation of
respiarotory droplest from a carrier or a patient in
early stages of the disease and transmission is
favoured by close contact between individuals for
example school.

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 Cont’n

• It is pilliated, the pili allows attachment of the

organism to the nasopharyngeal mucosa where it
is harbored both in carriers and in individuals
with meningococcal disease.
• The bacteria will invade the blood-stream
(bacteremia) from the nasopharynx, resulting in
meningitis and deadly sepsis (called
meningococcemia).

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 Cont’n

• The classic clue to an invasive meningococcal

infection is the appearance of the purpuric
skin lesion.
• The rash is due to the release of endotoxin from
the meningococcus, causing vascular necrosis,
inflammatory reaction and hemorrhage into the
surrounding skin.

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 Meningococcemia

• The intravascular multiplication of Neisseria

meningitidis in abrupt onset of spiking fever, chills,
arthralgia (joint pains), and muscle pain as well
as the purpuric rash.
• The organism can seed from the blood to other sites,
for example, crossing the blood-brain barrier and
infecting the meninges leading to meningitis.
• Malaise can evolve into severe headache, a rigid neck,
vomiting, and sensitivity to bright lights—symptoms
characteristic of meningitis and fulminant
meningococcemia.
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 Cont’n

Ilustrationsof the pathogenesis of N. meningitidis

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Fulminant meningococcemia / Waterhouse Friderichen syndrome

• This is septic shock.

• Bilateral hemorrhage into the adrenal glands
occurs, which causes adrenal insufficiency.
Abrupt onset of hypotension and tachycardia
occurs, along with rapidly enlarging purpuric
rash. (dissemination intravascular coagulation)
and coma may develop.
• Death can occur rapidly.

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 Cont’n

• The gold standard for diagnosis of systemic

meningococcal infection is the isolation of
Neisseria meningitidis from a usually sterile
body fluid, such as blood and cerebrospinal fluid
(CFS).
• In performing a gram stain of the CSF, a gram-
negative diplococci shaped like a kidney, which
always appear in pairs.

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 Cont’n

2). Cultivation conditions for identification of

Neisseria meningitidis.
• Neisseria grow best on blood agar that has been heated so that the
agar turns brown (called chocolate agar) and incubated at 37°C in
an atmosphere of 5% carbon dioxide and the pH of 7.4 to 7.6. it
produces transparent or grey, shiny colonies.
• The classic medium for culturing Neisseria is called the Thayer-
Martin VCN media. This is chocolate agar with antibiotics, which
are included to killing competing bacteria.
• V stands for vancomycin, which kills gram-positive organisms

• C stands for colistin, which kills all gram-negative organisms.

• 08/19/2025
N stands for nystatin, which GR0UP
eliminates
FIVE fungi. 70
 3). Epidemiology of meningococcal disease.

Epidemiology: Is the study of how diseases

spread and the impact populations .

Global distribution

• Widely occurs in Sub-Saharan Africa from

Senegal to Ethiopia where large epidemics are

due to serogroups like A increasing in the

developing countries while in developed

countries are serogroups B,C,W,Y

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 Cont’n

 In developed countries the incidence is low ranging

from o.5-5 cases per 100,000 population annually and

in Developing countries areas like Africa , incidence

can exceed 100-1000 per 100,000 during epidemics.

 Risk groups: Crowded settings (e.g., dormitories, military

barracks), immunocompromised individuals (HIV patients)

are at higher risk; Viral respiratory infections (e.g., H.

influenzae )

 Age: Young adults (15-24 years), children under 5 (infants).

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 Cont’n

 Transmission: Spread occurs via respiratory droplets or

close contact with carriers. Asymptomatic nasopharyngeal

carriage is common (5-10% of the population).

 Serogroups: Common serogroups causing disease are A, B,

C, W, Y, with regional variations e.g., serogroup A in Africa,

B, C, W, and Y in developed countries (America & Europe). W

reported increasing in Africa and globally

 Seasonality: Outbreaks peak in winter/spring in temperate

regions and dry seasons in tropical areas.

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 Cont’n

Prevention.
Through routine vaccination so as to reduce cases
of targeted serogroups.

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 (4).Antibiotic treatment for meningococcal meningitis

For causative organisms not yet identified:

Start initial appropriate empirical broad spectrum
therapy
• Ceftriaxone 2 g IV or IM every 12 hours for 10-14
days.
• If ceftriaxone not available/not improving; use
chloramphenicol 1 g IV every 6 hours for up to 14
days (use IM if IV not possible)
• Once clinical improvement occurs; change to 500-750
mg orally every 6 hoursGR0UP
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to FIVE
complete the course. 75
 cont’n

For causative organism identified:

Neisseria meningitidis (up to 14 day course)
• Benzylpenicillin IV 5-6 MU every 6 hours

Or
• Ceftriaxone 2 g IV or IM every 12 hours

Or
• Chloramphenicol 1 g IV every 6 hours (IM if IV not
possible)
Once clinical improvement occurs
• Change to chloramphenicol 500-750 mg orally every 6
hours to complete the course.
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 cont’n

5). Virulence factors associated with Neisseria

meningitidis
 Polysaccharide capsule: Primary virulence factor,
inhibits phagocytosis and complement-mediated
killing. Different serogroups (A, B, C, W, Y) are
defined by capsule composition.
 Pili: Facilitate attachment to nasopharyngeal
epithelial cells, aiding colonization and invasion.
 Lipooligosaccharide (LOS): Endotoxin causing
systemic inflammation, septic shock, and purpuric
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lesions due to endothelial damage.
 cont’n

 Opacity proteins (Opa, Opc): Promote adhesion to

and invasion of host cells.
 IgA protease: Cleaves IgA antibodies, evading
mucosal immunity.
 Iron acquisition systems: Enable the bacterium to
scavenge iron from host proteins, supporting survival.
 Factor H-binding protein: Inhibits complement
activation, enhancing immune evasion.
 Outer membrane proteins porins (PorA and PorB)
formerly called proteins1 appear to promote invasion
into epithelial cells
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 cont’n

6. Prophylaxis for meningococcal meningitis.

 Vaccination (preventive prophylaxis):

• Conjugate vaccines protect against serogroups A, C, W,

Y and are recommended for adolescents, college
students, and travelers to endemic areas.
• Serogroup B vaccines target serogroup B and are
used in high-risk groups or outbreak settings.
• Routine vaccination schedules vary by country but
often include doses at ages 11-12, with boosters at 16-
18.
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 cont’n

 Post-Exposure Prophylaxis: (chemoprophylaxis)

• For close contacts (e.g., household members,

healthcare workers exposed to respiratory
secretions), rifampin (600 mg every 12 hours for 2
days), ceftriaxone (250 mg IM single dose), or
ciprofloxacin (500 mg orally single dose) in adults is
recommended to eradicate nasopharyngeal carriage.
• Prophylaxis should be administered within 24-48
hours of exposure.

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 References:

1. Carroll, K. C., Butel, J., & Morse, S. (2015).

Jawetz Melnick and Adelbergs Medical
Microbiology 27 E: McGraw-Hill Education.
2. Subhash Chandra Parija. (2012). Textbook of
Medical Microbiology & Immunology (2nd
Edition). Elsevier: A division of Reed Elsevier
India Private Limited.

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 End

Thank you
For listening

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