Bacteria can be classified into three groups based on pathogenicity: primary pathogens that are known to cause disease when isolated from patients; opportunistic pathogens that cause disease in hosts with compromised defenses; and normal flora that rarely cause disease. Some bacteria previously considered non-pathogenic are now known to cause disease in compromised hosts due to their adaptability. Virulence factors like adherence factors, invasion factors, capsules, endotoxins, exotoxins, and siderophores help bacteria invade hosts, cause disease, and evade defenses. The immune system responds to bacterial infection through phagocytosis, antibodies, and the complement system, while bacteria have developed mechanisms like antigenic variation and inhibition of immune responses to ev

1. Adaption and immunity
Grace orina

2. • Infection is the invasion of the host by
microorganisms, which then multiply in close
association with the host's tissues. Infection is
distinguished from disease, a morbid process
that does not necessarily involve infection
(diabetes, for example, is a disease with no
known causative agent).

3. State three groups of bacteria in
relation to pathogenicity
• Probable agents of disease (e.g., when the cause of
diarrheal disease is identified by the laboratory
isolation of Salmonella spp. from feces)- When isolated
from a patient, frank or primary pathogens
• Opportunistic pathogens are those isolated from
patients whose host defense mechanisms have been
compromised. They may be the agents of disease (e.g.,
in patients who have been predisposed to urinary tract
infections with Escherichia coli by catheterization).
• Non-pathogens( normal florah), because they rarely or
never cause human disease. These are bacteria, such
as Lactobacillus acidophilus

4. Non pathogens
• May change
• why? because of the adaptability of bacteria
• Detrimental effect of modern radiation therapy,
chemotherapy, and immunotherapy on resistance
mechanisms.
• Some bacteria previously considered to be
nonpathogens
• known to cause disease.
• Example Serratia marcescens,, is a common soil
bacterium that causes pneumonia, urinary tract
infections, and bacteremia in compromised hosts.

5. Virulence
• Virulence is the measure of the pathogenicity
of an organism. The degree of virulence is
related directly to the ability of the organism
to cause disease despite host resistance
mechanisms; it is affected by numerous
variables such as the number of infecting
bacteria, route of entry into the body, specific
and nonspecific host defense mechanisms,
and virulence factors of the bacterium.

6. Host Susceptibility
• Resistance to bacterial infections is enhanced
by phagocytic cells and an intact immune
system. Initial resistance is due to nonspecific
mechanisms. Specific immunity develops over
time. Susceptibility to some infections is
higher in the very young and the very old and
in immunosuppressed patients.

7. Bacterial Infectivity
• Bacterial infectivity results from a disturbance
in the balance between bacterial virulence
and host resistance. The “objective” of
bacteria is to multiply rather than to cause
disease; it is in the best interest of the
bacteria not to kill the host.

8. Immune response to bacterial infection
• Phagocytosis – local and recruited macrophages, neutrophils clear up debris/
ingest bacteria
• The skin forms a mechanical barrier for entry of bacteria
• Sebum produces by the sebaceous glands contains antiseptic which kill
bacteria
• HCl acid in the stomach kills bacteria
• Lysozyme in tears destroys bacteria
• Some bacterial flora on the skin and intestines destroy pathogenic bacteria
• Abs neutralize bacterial endotoxins
• Abs act as opsonins enabling phagocytosis
• Abs prevent adherence of bacteria to target host cells
• Abs activate the complement system leading to bacterial lysis
• Abs clump bacteria leading to lysis
• Abs inhibit the uptake of Iron by bacteria preventing bacterial growth
• Abs inhibit bacterial mobility and their metabolic activity
• IgE attaches to mast cells stimulating production of histamines to bring about
inflammation which contributes to killing bacteria through fever

9. Immune response to viral infection
1.Cell mediated response
Cytotoxic T lymphocytes (CTLs) are generated and play a role in lysing
viral infected cells.
• with the help of CD+Thelper cells which supply IL-2, IFN gamma and TNF
alpha that help pre CTLs to mature and destroy viral infected cells
• 2. Immunoglobulin neutralization
• Ags from viruses can be presented by HLA class II molecules to stimulate B
cells to secrete antibodies of diverse isotypes such as;
• (a) mucosal IgA blocks attachment of intestinal viruses
• (b) Viral bound abs opsonizes the virus for phagocytes to ingest them and
may induce complement mediated viral damage
• (c) Abs agglutinate virions to remove them from circulation by help of
phagocytes
• (d) some abs neutralize viruses in blood and some bind the surfaces of
free viruses and limit their ability to infect.

10. Immune response to parasites such as
protozoa and helminthes
• (a) Innate immunity include;
• The skin which provides a physical barrier to entry of the parasites
• Sickle cell trait confers resistance to malarial attacks
• Lack of Duffy blood group Ags to avoid attachment of parasite to RBCs
• (b) Phagocytosis – monocytes, macrophages, neutrophils and NK cells ingest
and destroy parasites with the help of Abs as opsonins and the complement
• (b) Humoral immunity
• Abs react with Ags at the surface of the parasite neutralizing the parasite by
interfering with its essential functions or block its attachment to target cells/
by binding its toxins
• IgM abs agglutinate parasites limiting their spread to tissues and neutralizing
toxins
• Complement lysis can occur and Abs act as opsonins to facilitate phagocytosis
e.g. Trypanosomes are killed by antibody dependent cellular cytotoxity (ADCC)
mechanisms
• CTLs destroy some parasites through lysis
• Activated macrophages through lymphokines act as Antigen presenting cells
and facilitate lysis of parasites

11. Host Resistance
• Numerous physical and chemical attributes of the host protect
against bacterial infection.
• These defenses include the antibacterial factors in secretions
covering mucosal surfaces and rapid rate of replacement of skin and
mucosal epithelial cells. Once the surface of the body is penetrated,
bacteria encounter an environment virtually devoid of free iron
needed for growth, which requires many of them to scavenge for
this essential element.
• Bacteria invading tissues encounter phagocytic cells that recognize
them as foreign, and through a complex signaling mechanism
involving interleukins, eicosanoids,
• complement, mediate an inflammatory response in which many
lymphoid cells participate.

12. Bacterial evasion mechanisms
• Secretion of proteins that promote their attachment through
mucosal layers
• Some bacterial products degrade IgA e.g. proteases
• Some alter their surface proteins during infection by antigenic
variation
• Many live within phagocytic cells blocking endosomal function
• Some grow in lymphoid organs interfering with cell mediated
immunity
• Some secrete substances that inhibit chemotaxis and macrophage
migration
• Some secrete catalase enzyme that protect it from phagocytic
hydrogen peroxide
• Some secrete complement inhibiting factors which inhibit
complement reactions

13. Viral evasion of Host defense
• Some viruses block INF and block expression of HLA which limits the
presentation and stimulation of the immune response
• Herpes virus have a protein that blocks C3b from binding and blocks its
activities in destroying the virus
• Many viruses use Ag variation to keep the immune system at bay by
expressing different surface proteins
• Use of antigenic shift and drift to cause either drastic/subtle changes to
their coat proteins causing annual flu shoots
• Infecting cells of the immune system- leading to temporal reduction of
immunity e.g HIV infects T-lymphocytes, monocytes and macrophages,
such cytopathogenicity leads to the loss of CD+ve T-cells and impaired
functioning of infected cells
• Release of Ags and production of Ags at sites inaccessible to the immune
system
• Retroviruses infect macrophages, and use macrophage lysosomal enzymes
to initiate uncoating of the virus before replication to avoid deletion.
• Some viruses move from cell to cell without entering the extracellular fluid
and blood to escape the Abs.

14. Immune response to parasites such as
protozoa and helminthes
• (a) Innate immunity include;
• The skin which provides a physical barrier to entry of the parasites
• Sickle cell trait confers resistance to malarial attacks
• Lack of Duffy blood group Ags to avoid attachment of parasite to RBCs
• (b) Phagocytosis – monocytes, macrophages, neutrophils and NK cells ingest
and destroy parasites with the help of Abs as opsonins and the complement
• (b) Humoral immunity
• Abs react with Ags at the surface of the parasite neutralizing the parasite by
interfering with its essential functions or block its attachment to target cells/
by binding its toxins
• IgM abs agglutinate parasites limiting their spread to tissues and neutralizing
toxins
• Complement lysis can occur and Abs act as opsonins to facilitate phagocytosis
e.g. Trypanosomes are killed by antibody dependent cellular cytotoxity (ADCC)
mechanisms
• CTLs destroy some parasites through lysis
• Activated macrophages through lymphokines act as Antigen presenting cells
and facilitate lysis of parasites

15. Virulence Factors
• Virulence factors help bacteria to
• (1) invade the host,
• (2) cause disease, and
• (3) evade host defenses.

16. Types of virulence factors:
• Adherence Factors: Many pathogenic bacteria colonize mucosal
sites by using pili (fimbriae) to adhere to cells.
• Invasion Factors: Surface components that allow the bacterium to
invade host cells can be encoded on plasmids, but more often are
on the chromosome.
• Capsules: Many bacteria are surrounded by capsules that protect
them from opsonization and phagocytosis.
• Endotoxins: The lipopolysaccharide endotoxins on Gram-negative
bacteria cause fever, changes in blood pressure, inflammation,
lethal shock, and many other toxic events.
• Exotoxins: Exotoxins include several types of protein toxins and
enzymes produced and/or secreted from pathogenic bacteria..
• Siderophores: Siderophores are iron-binding factors that allow
some bacteria to compete with the host for iron,