GOMBE STATE UNIVERSITY

SCHOOL OF POSTGRADUATE STUDIES

DEPARTMENT OF MICROBIOLOGY

COURSE TITLE: ADVANCE BACTERIOLOGY

COURSE CODE: MICB 805

BACTERIAL PATHOGENICITY AND OTHER

EMERGING DISEASES

BY

ZARMA MARYAM HALIRU

PG21/MSC/PHEM/1015

INTRODUCTION
Infectious diseases are the leading cause of death worldwide. Recently, significant evidence has
emerged which indicates that markedly different microbial pathogens use common strategies to
cause infection and disease. For example, many diverse bacterial pathogens share common
mechanisms in terms of their abilities to adhere, invade, and cause damage to host cells and
tissues, as well as to survive host defences and establish infection (Wilson et al., 2002). This
process of causing disease is termed as Pathogenesis. Pathogenesis is a multi-factorial process
which depends on the immune status of the host, the nature of the species or strain (virulence
factors) and the number of organisms in the initial exposure. Many of these commonalities of
infection appear to be related to the acquisition of large blocks of virulence genes from a
common microbial ancestor, which can be disseminated to other bacteria via horizontal transfer.
The horizontal transmission of large blocks of virulence determinants is also directly attributable
to the constant emergence of new strains of bacterial pathogens, many of which are resistant to
multiple antibiotics (Wilson et al., 2002).
Pathogenicity
Pathogenicity is the capacity to initiate disease. It requires the attributes of transmissibility or
communicability from one host or reservoir to a fresh host, survival in the new host, infectivity
or the ability to breach the new host’s defenses, and virulence, a variable that is multifactorial
and denotes the capacity of a pathogen to harm the host. Virulence in the clinical sense is a
manifestation of a complex bacterial–host relationship in which the capacity of the organism to
cause disease is considered in relation to the resistance of the host (Wilson et al., 2002).). The
process of pathogenesis involves various steps beginning with the transmission of the infectious
agent (bacterial) to the host, followed by colonization of the site. After the colonization of host,
the bacteria remain adherent at the site of colonization then invades the host system. After
surviving the host immune system it is ready to cause the disease.

Steps Involved In the Pathogenesis of the Bacteria:

1. Transmission
2. Colonization
3. Adhesion
4. Invasion
5. Survival in the host
6. Tissue Injury
Transmission
Potential pathogens may enter the body by various routes, including the respiratory,
gastrointestinal, urinary or genital tracts. Alternatively, they may directly enter tissues through
insect bites or by accidental or surgical trauma to the skin. Many opportunistic pathogens are
carried as part of the normal human flora, and this acts as a ready source of infection in the
compromised host (e.g. in cases of AIDS or when the skin barrier is breached). For many
primary pathogens, however, transmission to a new host and establishment of infection are more
complex processes.

Colonization
The establishment of a stable population of bacteria on the host’s skin or mucous membranes is
called colonization. Successful colonization also requires that bacteria are able to acquire
essential nutrients—in particular iron—for growth. For many pathogenic bacteria, the initial
interaction with host tissues occurs at a mucosal surface and colonization normally requires
adhesion to the mucosal cell surface. This allows the establishment of a focus of infection that
may remain localized or may subsequently spread to other tissues.

Adhesion
For bacteria pathogenesis, adhesion is an essential preliminary to colonization and then
penetration through tissues. Adhesion is necessary to avoid innate host defense mechanisms such
as peristalsis in the gut and the flushing action of mucus, saliva and urine, which remove non-
adherent bacteria At the molecular level, adhesion involves surface interactions between specific
receptors on the mammalian cell membrane (usually carbohydrates) and ligands (usually
proteins) on the bacterial surface. The presence or absence of specific receptors on mammalian
cells contributes significantly to tissue specificity of infection. Nonspecific surface properties of
the bacterium, including surface charge and hydrophobicity, also contribute to the initial stages
of the adhesion process. Several different mechanisms of bacterial adherence have evolved, all
utilizing specialized cell surface organelles or macromolecules, that help to overcome the natural
forces of repulsion that exist between the pathogen and its target cell. Many bacteria express pili
(or fimbriae) which are involved in mediating attachment to mammalian cell surfaces. Different
strains or species of bacteria produce different types of pili which can be identified on the basis
of antigenic composition, morphology and receptor specificity.
Invasion
Invasion is penetration of host cells and tissues (beyond the skin and mucous surfaces), and is
mediated by a complex array of molecules, often described as ‘invasins’. These can be in the
form of bacterial surface or secreted proteins which target host cell molecules (receptors).
Once attached to a mucosal surface, some bacteria, e.g. Corynebacterium diphtheriae or
Clostridium tetani, exert their pathogenic effects without penetrating the tissues of the host.
These produce biologically active molecules such as toxins, which mediate tissue damage at
local or distant sites. For a number of pathogenic bacteria, however, adherence to the mucosal
surface represents only the first stage of the invasion of tissues. Examples of organisms that are
able to invade and survive within host cells include Mycobacteria, Salmonella, Shigella and
others. The initial phase of cellular invasion involves penetration of the mammalian cell
membrane and many intracellular pathogens use normal phagocytic entry mechanisms to gain
access. Inside the cell, they become surrounded by host cell-derived membrane vesicles. Many
intracellular pathogens escape from these vesicles into the cell cytoplasm where they multiply
rapidly before spreading to adjacent cells and repeating the process of invasion. The availability
of specific receptors on host cells defines the type of host cells that are involved. As a result,
some pathogens can invade a wide range of cell types whilst others have a much more restricted
invasive potential.

Virulence determinants
Both primary and opportunistic pathogens possess virulence determinants or aggressins that
facilitate pathogenesis. Possession of a single virulence determinant is rarely sufficient to allow
the initiation of infection and production of pathology. Many bacteria possess several virulence
determinants, all of which play some part at various stages of the disease process. In addition,
not all strains of a particular bacterial species are equally pathogenic. For example, although six
separate serotypes of encapsulated Haemophilus influenzae are recognized, serious infection is
almost exclusively associated with isolates of serotype b (hence Hib vaccine). Moreover, even
within serotype b isolates, 80% of serious infections are caused by six out of > 100 clonal types.
Different strains of a pathogenic species may cause distinct types of infection, each associated
with possession of a particular complement of virulence determinants. Different strains of E.
coli, for example, cause several distinct gastrointestinal diseases, urinary tract infections,
septicemia, meningitis and a range of other minor infections. Many pathogens produce an
impressive armoury of virulence determinants; however, their expression is coordinated or
regulated by several nutritional and environmental factors. Among virulence regulators are the
availability of nutrition (e.g. iron), oxygen, suitable temperature or other growth requirements.
Importantly, differences in virulence between similar organisms may be due to additional cryptic
phenotypic or genotypic variations. For example, some virulence factors are only expressed
when indirect contact with host cells. Virulence genes can move between bacteria via special
genetic vehicles e.g. plasmids, bacteriophage and transposons. The horizontally transferred
virulence factors (e.g. toxins) may or may not transform the recipient bacteria into betteradapted
or more virulent pathogens.
Mechanism of Bacterial Pathogenicity
Pathogenic bacteria utilise a number of mechanisms to cause disease in human hosts. Bacterial
pathogens express a wide range of molecules that bind host cell targets to facilitate a variety of
different host responses. The molecular strategies used by bacteria to interact with the host can
be unique to specific pathogens or conserved across several different species. A key to fighting
bacterial disease is the identification and characterisation of all these different strategies. The
following are number of common mechanisms used by bacterial pathogens to cause infectious
disease.

Capsule
Some bacteria overproduce and excrete copious amounts of high molecular weight
polysaccharides, also called exopolysaccharides, when isolated from clinical samples. This
extracellular sugar coating is termed capsule. Different species of bacteria utilise diverse sugars
to produce the capsule. Capsule production is one of the major virulence factors utilised by
bacteria to evade clearance from an infectious site. Specifically, the capsule provides bacteria
with protection from the host immune response as well as antibiotics. Some capsules have also
been shown to have immunomodulatory effects. The capsule protects bacteria from phagocytosis
by not allowing opsonising antibodies to be recognised by phagocytic host defence cells (for
example, macrophages and neutrophils). This “frustrated phagocytosis” leads to enhanced
inflammatory response as the macrophages and neutrophils produce more inflammatory
cytokines in an attempt to clear the bacteria. The enhanced inflammatory response leads to
increased tissue damage as more neutrophils and macrophages are recruited to the site of
infection. The most notorious species of bacteria that produce capsules are Streptococcus
pneumoniae (pneumococcus), Neisseria meningitidis (meningococcus), and Pseudomonas
aeruginosa. ()
Cell Wall
Bacteria can be divided into two major groups based on differences in cell wall structure: Gram
positive and Gram negative bacteria. The cell wall of both Gram positive and Gram negative
bacteria contain toxic components that are potent virulence factors and have central roles in the
pathogenesis of bacterial septic shock, a frequently lethal condition that involves collapse of the
circulatory system and may result in multiple organ system failure. Septic shock is the result of
the combined action of cytokines, complement components, and coagulation cascade
components. Bacterial cell wall derived constituents can induce the host to produce or activate
these mediators. Indeed, the proximate triggering event of septic shock is the release of
lipopolysaccharide (LPS) or other toxic bacterial cell wall components into the circulation.
Bacterial LPS (also known as endotoxin) is a large amphophilic molecule embedded in the outer
membrane of Gram negative bacteria and is usually considered to be the principal component
responsible for the induction of septic shock that often accompanies severe infections with these
microbes. Bacteria frequently implicated in septic shock include Gram negative microbes such as
Escherichia coli, P aeruginosa, and meningococci, and Gram positive bacteria such as
Staphylococcus aureus, Staphylococcus epidermidis, and streptococci. Interestingly, the
aforementioned group of Gram positive bacteria have emerged as the most prevalent cause of
hospital acquired infections, and as such, play a significant part in nosocomial sepsis (Wilson et
al., 2002).
The toxic cell wall components of both Gram positive and Gram negative bacteria act largely via
the initiation of an inflammatory response through the stimulation of monocytes and
macrophages and the subsequent release of pro inflammatory cytokines, especially tumour
necrosis factor-alpha (TNF-α) and interleukin-1.

Toxins
Toxins are analogous to biological weapons in that these are proteinaceous or non-proteinaceous
molecules produced by bacteria to destroy or damage the host cell. Examples of non
proteinaceous toxins are LPS (endotoxin) for Gram negative organisms and teichoic acid for
Gram positive organisms. Bacterial exotoxins can be roughly categorised into four major types
based upon their amino acid composition and function: A-B toxins, proteolytic toxins, pore
forming toxins, and other toxins. Several different species of bacteria contain A-B toxins
including P aeruginosa, 14 E coli, Vibrio cholerae, Corynebacterium diphtheriae, and Bordetella
pertussis. A-B toxins have two components: the A subunit which possesses the enzymatic
activity; and the B subunit which is responsible for binding and delivery of the toxin into the host
cell. In addition to the A-B toxins, others include: immunoglobulin A (IgA) protease-type
proteins, heat stable toxins that activate guanylate cyclase, and toxins that modify the host cell
cytoskeleton. The common theme emerging from the study of these bacterial toxins is that
bacteria are able to utilise many different methods to disrupt host cell signalling pathways and
structural integrity to establish and maintain infection (Wilson et al., 2002).

Adhesins
A key step in the host-pathogen interaction is adherence of the pathogen to host surfaces. These
surfaces include skin, mucous membranes (oral cavity, nasopharynx, urogenital tract), and
deeper tissues (lymphoid tissue, gastric and intestinal epithelia, alveolar lining, endothelial
tissue). Numerous mechanical forces produced by the host act to wash microbes from these
surfaces: saliva secretion, coughing, sneezing, mucous flow, peristalsis, and blood flow. A
common trait of microbial pathogens is the expression of factors that bind to molecules on
various host tissue cells and render the microbe resistant to these mechanical washing forces.
Once bound or “adhered” to a specific host cell surface, the pathogen is then able to initiate its
specific biochemical processes that will result in disease including proliferation, toxin secretion,
host cell invasion, and activation of host cell signalling cascades. Microbial adherence factors are
called adhesins and can be made from polypeptides (proteins) or polysaccharides (carbohydrates
or sugars). Protein adhesins are separated into two groups: fimbrial and afimbrial. Fimbriae (also
known as pili) are appendages that protrude as hair-like structures from the bacterial surface and
are composed of proteins that are tightly packed into an array shaped like a helical cylinder. A
single protein usually serves as the major fimbrial subunit, however other protein subunits also
play structural roles at the tip and the base. Frequently, the fimbrial tip serves to bind the host
receptor. Gram negative bacterial pathogens in particular rely on fimbriae for adherence.
Examples include E coli (for both urinary tract infections and gastroenteritis), V cholerae, P
aeruginosa, and Neisseria species. Afimbrial adhesins refer to proteins that serve as adherence
factors, but do not form the long, polymeric fimbrial structure. The afimbrial adhesins generally
mediate more intimate contact with the host cell that occurs over a shorter range than with
fimbriae. Gram negative (Yersinia pseudotuberculosis, enteropathogenic E coli, Neisseria spp),
Gram positive (Staphylococcus spp, Streptococcus spp) and mycobacterial pathogens express
afimbrial adhesins (Donnenberg, 2000).
Invasion
A major advance in bacterial pathogenesis in recent years has been the identification of genes
that allow pathogens to invade host non-phagocytic cells. Once adhered to a host surface, some
pathogens gain deeper access into the host to perpetuate the infection cycle. This pathogenic
principle, termed invasion, can be divided into two types: extracellular and intracellular.
Extracellular invasion occurs when a microbe breaks down the barriers of a tissue to disseminate
in the host while remaining outside of host cells. This is a strategy used by group A. β-
haemolytic streptococcus and S aureus. 13 These species secrete several enzymes that degrade
host cell molecules: hyaluronidase (cleaves proteoglycans in connective tissue), streptokinase
and staphylokinase (breaks down fibrin clots), lipase (degrades accumulated host oils), and
nuclease (digests released RNA and DNA). The haemolysins (which punch holes in host cells)
expressed by these species lyse not only erythrocytes but other cell types as well and may also
contribute to their spread in host tissues. Pseudomonas aeruginosa secretes an enzyme, elastase,
which degrades extracellular molecules and aids tissue invasion associated with keratitis, burn
tissue necrosis, and cystic fibrosis.13 Extracellular invasion allows these pathogens access to
niches in tissues where they are able to proliferate, disseminate to other sites in the body, express
toxins, and initiate inflammatory responses. There is a growing body of evidence that suggests
that extracellulary invading pathogens may also enter host cells and use both the extracellular
and intracellular pathways during infection (Donnenberg, 2000).
Intracellular invasion occurs when a microbe actually penetrates the cells of a host tissue and
survives within this environment. A number of Gram negative, Gram positive, and mycobacterial
pathogens have been shown to have the ability to enter host cells and both phagocytic and non-
phagocytic cell types can serve as targets for invasion (Bermudez and Sangari, 2000). Some
pathogens have an obligate intracellular lifecycle which absolutely requires a mammalian cell for
growth. These include Chlamydia spp, Rickettsia spp, and Mycobacterium leprae. Other
pathogens are facultatively intracellular, using their ability to enter and survive within host cells
as a means of proliferation or spreading to other tissues. A major advance in bacterial
pathogenesis in recent years has been the identification of genes that allow pathogens to invade
host non-phagocytic cells. Remarkably, these invasion genes, present in several different
pathogens, were found to encode an evolutionarily related type III protein secretion pathway that
serves to inject signalling proteins from the microbe into the host cell. The injected proteins then
activate host cell signalling pathways that cause the host cell to internalise the microbe. These
entry mechanisms are well characterised in Salmonella spp and Shigella spp (Donnenberg,
2000).

INTRACELLULAR LIFESTYLES
Several bacterial pathogens have evolved to survive and replicate within host cells after invasion.
The range of host cell types in which pathogens can survive include non-phagocytic cells (such
as epithelial and endothelial) and professional phagocytes (such as macrophages and
neutrophils). The ability to survive and replicate inside of phagocytic cells is particularly
remarkable since these cells possess mechanisms to destroy ingested bacteria. These killing
mechanisms include the production of reactive oxidative intermediates, the lowering of pH of
bacteria-containing vacuoles, and the activation of degradative proteases. The strategies that
bacteria use to avoid killing via these mechanisms are becoming increasingly well-characterised
(Wilson et al., 2002). There are three general intracellular niches in which pathogens reside:
within an acidic, hydrolytically competent phagolysosomal vacuole; inside a vacuole which has
not fused with a lysosome; and in the host cell cytosol. Coxiella burnetti is an example of a
pathogen which is able to reside in the toxic environment of a phagolysosomal vacuole, and it
has been shown that low pH is required to intiate its intracellular replication.1 Mycobacterium
spp, Salmonella spp, Legionella pneumophila, and Chlamydia trachomatis are included in the
group which reside in non-lysosomal vacuoles. The vacuoles which are occupied by these
pathogens are referred to as “specialised” or “remodelled” as they are usually morphologically
different than other cellular vacuoles and contain a characteristic combination of surface markers
(Wilson et al., 2002). Shigella flexneri, L monocytogenes, and Rickettsia rickettsii are pathogens
which reside in the host cell cytosol.1 50 these bacteria share a common strategy of
enzymatically degrading the surrounding vacuole and spreading intracellulary via use of the host
cell cytoskeleton.
Bacteria which survive intracellularly may replicate and spread to cells in the local area of
infection or migrate to other areas of the body. Chlamydia and Rickettsia lyse the host cell
membrane, releasing infectious bacteria which attach to and invade adjacent cells (Wilson et al.,
2002). In addition to host cell lysis, Shigella and Listeria utilise a pathway of cell-to-cell spread
which involves extension of the infected cell into an adjacent cell.13 Invagination occurs where
the infected cell has protruded into the adjacent cell, followed by membrane fusion and
formation of a bacteria-containing vacuole in the adjacent cell. Bacteria residing in macrophages
and neutrophils may use these cells as vehicles to spread systemically via the blood or lymphatic
circulatory systems. Salmonella typhi, Yersinia spp, and Brucella spp are thought to move
between tissues in this manner.
Figure 2: An overview of bacterial mechanisms for pathogenicity.
A) Upon encountering a human host, a bacterial pathogen may illicit several host responses and
use a variety of mechanisms to evade the host defences. The bacterial components that interact
with the host include: (1) capsules that act to “frustrate” phagocytosis and protect the pathogen
from macrophage and neutrophil engulfment, (2) lipopolysaccharide (LPS) and cell wall
components which can cause septic shock, (3) toxins that can serve to damage host cells and aid
invasion, and (4) adhesins which facilitate binding of the pathogen to host surfaces. The degree
to which these various mechanisms play a part in the pathogenesis of an infection depends on the
bacterial species or strain, the site of pathogen entry, the immune status of the host and other
similar factors. (B) Once adhered to a host surface, a bacterial pathogen may further invade host
tissues. Pathogens may “burrow” further into a tissue by expressing and secreting proteases and
glycanases that digest host extracellular matrix proteins and polysaccharides. In addition, a
pathogen may also invade the host tissue cells and gain access to the intracellular environment.
This can be facilitated by the natural phagocytosis mechanisms of macrophages and neutrophils
or by induced uptake where the pathogen signals the host cell to engulf adhered bacteria. A
common strategy for pathogens to induce uptake is the use of a type III secretion system which
injects bacterial signaling proteins into the host cell. Within the host cell, the pathogen may
reside within a phagolysome (a phagosome which has fused with a lysosome), a phagosome
which has not fused with a lysosome, or within the host cell cytosol.

EMERGING DISEASES
Emerging infectious diseases are diseases that either have never occurred in humans before,
previously occurred but only affecting a limited number of people in affected places, or have
occurred throughout history but only recently identified as distinctly due to an infectious agent
while re-emerging infectious diseases are those that were once major public health problems
globally for a significant portion of the population (Testimony et al., 2020).
MAJOR FACTORS CONTRIBUTING TO EMERGING AND RE-EMERGING
INFECTIOUS DISEASES
There are various factors contributing to the emergence and re-emergence of infectious diseases
as highlighted below. Infectious disease emergence pathways and other multiple factors that
contribute to the emergence or resurgence of these infectious agents do so by means of multiple
human associated activities.
 Human Demographics, Behavior, and Vulnerability
Globally, there is explosion in the world population especially in the developing
countries with dwindling social amenities as well as public health facilities in the face of
scarce resources. The inadequacy of social amenities results in the acquisition and
spreading of these infectious diseases. There is poverty ravaging the teeming populations
of the developing world (Omilabu, 2016). Majority of the jobless engage in all sorts of
anti-social activities such as prostitution, drug addiction as well as abuse of drugs
especially antibiotics. There are also changes in lifestyle, with most people having a
preference for imported food items, many of which are known to be contaminated by
some food-borne pathogens e.g Salmonelosis, E.Coli 0157:H7, mad cow disease etc.
Many of these imported foods are associated with cancers because of the processes prior
to importation. Poverty leads to an increase in the population of those with weakened
 immune systems leading to their vulnerability to infectious diseases namely HIV/ AIDS,
Tuberculosis etc. (Omilabu, 2016).
 Technology and Industry
The advancement in technology has led to mass food production. Most of these food
products are being sold out. There is usually contamination of such food items with some
deadly microorganisms such as Campylobacter, Clostridium, and E.coli0157:H7etc.
Many of the animals from these sources are already abused with antibiotic treatment on
the farm thus generating antibiotic resistant strains bacteria. There is explosion of newly
produced drugs in the market many of which prolong immunosuppression. The advances
in technology are also encouraging more organ transplants and blood transfusion. The
inadequacy and shortcomings of screening kits for inherent pathogens from donors is
becoming a very serious health issue (Omilabu, 2016).
 Economic Development, Land use, Changing Ecosystem
Plays a vital role in the maintenance and sustenance of the infectious diseases. Human
encroachment into wilderness through afforestation and deforestation results in the
acquisition of these pathogens leading to jungle transmission of these pathogens. The
infectious diseases acquired (Lyme, Hantan Pulmonary syndrome, Yellow fever, Dengue,
West Nile, Lassa, Lujo, Ebola, SARS, Influenza etc) are found in bush dwellers e,g.
hunters, forest guards, adventurers, miners, etc. Changes in the eco-system also promote
heavy breeding of vectors and animal reservoirsthat often appear to tolerate these
infections with little evidence of disease (Figure 4) carrying the disease pathogens.
Global warming also accounts for the upsurge in the spread of Malaria, Dengue,
Filariasis and Leishmaniasis. Cattle grazing of farmlands always causes the
contamination of water sheds e.g. Cyclosporidium (Omilabu, 2016).
 Microbial Adaptation And Evolution
Microorganisms are not static and evolve even at their own pace. These agents mutate
after some cycles of replication. The agents mutate faster following introduction of drugs
(drug pressure). This is to allow them to perpetuate themselves. The antagonist will force
the agents to develop series of proteins to counter the influx of the chemicals. The genes
are the bedrock of their mutations. The gene sequence determines the proteins produced.
There is increased antibiotic resistance with increased antibiotics use or abuse. Other
 pathogens (fungi, helminths, protozoa and viruses) are capable of developing resistance
to drugs used against them. Some examples are Vancomycin resistant E.coli,
Vancomycin-resistant Staph. Aureus, Penicillin- and Macrolide-resistant Strep.
Pneumonia, and multi drug-resistant Salmonella. Virulent species of some viruses are
commonly found which jump from animals to humans. Such viruses have been mutated
to such a level, e.g. SARS, Avian influenza, HIV etc. (Omilabu, 2016).
 Poor Hygiene and Sanitation
Classical public health and sanitation measures have long served to minimize
dissemination and human exposure to the spread of many pathogens. The pathogens
themselves often still remain, albeit in reduced numbers, in reservoir hosts or in the
environment, or in small pockets of infection and therefore, are often able to take
advantage of the opportunity to re-emerge if there is a breakdown in these preventive
measures. Faecal-orally transmitted infectious agents are on the increase in disease
frequency in low socio-economic countries. The appearance of re-emerging diseases
may, therefore, often be a sign of the breakdown of public health measures (waste
disposal) most especially in hospital settings and should be a warning against
complacency in the war against infectious diseases (Omilabu, 2016).

SIGNIFICANT EMERGING DISEASES IN NIGERIA

Hemorrhagic Fever
Ebola virus, a member of the family Filoviridae burst from obscurity with spectacular outbreaks
of severe haemorrhagic fever. While the outbreak of Ebola virus disease (EVD) is infrequent and
dates back to 1976 in Sudan and Zaire, it is a global health concern because of the associated
high infectivity and fatality, with the propensity to spread as an exotic virus. The 2014 - 2015
Ebola outbreak which is the largest in history is clear evidence of this, as the outbreak went
beyond the traditional East African countries of previous outbreaks, with spread to Spain, United
States of America, England, Italy and Nigeria. (Omilabu, 2016).
Yellow fever disease (YFD)
YFD is an acute viral hemorrhagic fever caused by the yellow fever virus, a member of the
family Flaviviridae, and transmitted by an infected female Aedes mosquito. The first recorded
yellow fever outbreak in Nigeria occurred in Lagos in 1864. This was followed by other
outbreaks in Lagos in 1894, 1905, 1906, 1925 and 1926. The next outbreak happened in Jos in
1969, infecting over 100,000 people, and then in 1987 and 1996, infecting over 120,000 people
in different parts of the country including: Jos, Azare in Bauchi state, Ogoja in Cross River state,
Oju in Benue state and Ogbomosho in Oyo state (Testimony et al., 2020).
Poliomyelitis
This is a highly infectious viral disease caused by the poliovirus, which belongs to the family of
Enteroviruses and results in muscle weakness or paralysis of the limbs, with very few other
symptoms except minor headaches, neck stiffness, and stiffness of the arms and legs . major
outbreak to happen in Nigeria was in 2007, involving 69 children in Northern Nigeria, and was a
direct consequence of the refusal of locals to vaccinate their children due to anti-vaccination
religious propaganda . In 2015, the WHO removed Nigeria from the list of polio-endemic nations
due to the high likelihood that wild poliovirus (WPV) circulation had been interrupted in
Nigeria. However, four new cases were discovered in August and September 2016 in Borno, and
were attributed to the destabilization of healthcare infrastructure as a consequence of the
protracted Boko Haram insurgency in North-East Nigeria. Following this isolated occurrence, no
new case has been reported to date (Testimony et al., 2020).

Avian Influenza
The emergence and re-emergence of influenza viruses with pandemic potential for both human
and veterinary public health is of great concern to humans globally. This is because the evolution
of influenza is a continuing process and the increasing emergence of the highly pathogenic H 5 N1
H7 N3 H7 N7 and H9 N3 viruses are of great concern to both veterinary and public health officials
in Nigeria. Highly concentrated poultry and pig farming provide optimal conditions for increased
mutation, re-assortment and recombination of influenza virus. The surveillance is now active in
Nigeria with designated laboratories including ours, capable of molecular detection of the
different strains (Omilabu, 2016).

HEPATITIS
While hepatitis Band C have been prevalent in many countries, hepatitis E virus (HEV) is a viral
disease which is caused by an emerging pathogen of the family Herpe viridae of RNA viruses.
HEV is an important enterically transmitted human pathogen with a worldwide distribution and
increased frequency in Nigeria. Epidemics are primarily water borne in areas where water
supplies are contaminated by HEV and can cause sporadic cases as well as large epidemics of
acute hepatitis. (Omilabu, 2016).

Hantavirus Pulmonary Syndrome

Hantaviruses are a newly emerging group of arthropod-borne viruses, belonging to the family
Bunyaviridae that have significant zoonotic specific potential. Hantaviruses transmitted from the
contaminated urine and faeces of infected rodents cause two important human diseases:
haemorrhagic fever with renal syndrome and Hantavirus pulmonary syndrome. Most epidemics
occur in areas with large populations of rodents and congestion such as Nigeria as initially
highlighted by Tomori et al (Trans R Sac Trap Med Hyg 1986; 80(6):1008-9) when they
demonstrated Japanese strains of haemorrhagic fever with renal syndrome (HFRS) virus in
Nigerian sera in 1986. (Omilabu, 2016).
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