Reservoir - A place where the pathogen ultimately originates, its habitat, such as a human, animal, water, plant, etc.
Source - The immediate Origin of an infections agent
Carrier - An individual that inconspicuously shelters a pathogen and spreads it to others
Asymptomatic carrier - An infected individual with no obvious symptoms (gonorrhea and genital warts)
Convelescent carrier - recovering patients without symptoms with viable microbe shedding (Diphtheria, up to 30 days)
Chronic Carrier - Carriage of the microbe for a long period after recovery (Tuberculosis, salmonella, typhi -several years)
Passive carrier - Uninfected individual that carry infections agents from infected persons to uninfected ones by hands or instrument.
Acquisition of infection - Communicable infectious disease. When pathogen is transmitted from host to host directly or indirectly.
- Gram negative rods such as E. Coli, Klebsiella, and Pseudomonas are most often cultured from patient specimens followed by staph and strep.
Reportable/ notifiable disease - Disease that, by law, must be reported to authorities.
- The CDC and WHO keep track of infectious diseases at the levels of local, district, state, and international.
Koch’s Postulates
Robert Koch proved
the germ theory of disease by developing a standard for determining causative
agents.
1- Find evidence of
a particular microbe in every case of disease.
2- Isolate that
microbe from infected subject and cultivate it artificially in a lab.
3- Inoculate a
susceptible healthy subject with lab isolate and observe the resultant
disease
4- Re-isolate the agent
from this subject
Koch’s
Postulates - Click to enlarge
Establishment of Pathogen
By virulence factors
microbe settle in a particular organ and continue to cause damage.
The scope of
injuries during this accounts for the typical stages of infection.
Stages in the Course of Infection and
Disease
1.
Incubation time - the time when you become infected with a
microbe;
there are no symptoms during this time. Incubation periods
are
different for different bacteria.
2.
Prodromal Stage - the time when the microbe begin to multiply
and
the
signs and symptoms begin to occur.
3.
Period of Invasion - period when the microbes are growing and
there
are
maximal signs and symptoms.
4.
Convalescent Period - time of recovery for the body as the
number of
bacteria
decrease.
5.
Terminal Stage - does not occur if there was a convalescent
period.
If,
however, our body could not recover then we become terminal and
die.
Stages in
the course of infection and disease - Click to enlarge
Pattern of Infection
1.
Localized infection - the bacteria remain limited to one area
of the body.
2.
Generalize or Systemic infection - the bacterial infection gets to
the fluid
(blood
etc) and spread to several areas.
3.
Focal Infection - the bacterial infection spreads from one
area to one
other
area.
4.
Mixed infection - infection by more than one type of microbe
(two
different
bacteria or bacteria and virus etc.).
5.
Acute Infection - the type of infection which is very severe.
The period
of
the infection is very short.
6.
Chronic Infection - the severity is low and the timing is
long. Gradual
increase
in severity.
7. Subacute
Infection - midway between acute and chronic.
The occurrence of infections with regard to location and sequence - click to enlarge
Warning Signals of Disease
1.
Sign - any measurable evidence of the infection which can be
seen by an
observer.
Ex. temperature, antibody's in the blood, number of blood
cells
etc.
2.
Symptom - something that is felt or seen but cannot be
measured.
Ex:
headache.
3.
Syndrome - collection of symptoms.
4.
Blood Signs:
a) Leukocytosis
- increase in the number of white blood cells
b) Leukopenia
- decrease in the number of white blood cells
c) Septicemia
- multiplication of microbe in the blood.
d) Bacteremia
- presence of bacteria in the blood.
e) Viremia
- presence of virus in the blood.
Microbial Nutrition
Nutrition is a process by which all organisms (micro/macro) obtain
substances from their environment to convert to metabolic uses.
All microorganisms require six bioelements:
Carbon
Hydrogen
Oxygen
Nitrogen
Phosphorus
Sulfur
To survive, grow and reproduce.
Microbial Nutrient
Nutrient categorized by:
A. Amount
B. Chemical Structure
C. Importance to the Organism
A. Amount
1. Macronutrients: Large amounts required and have principal roles in
bacterial cells structure and metabolism.
2. Microelements: Small amount required for maintenance of bacterial
structure and function.
B. Chemical Structure
1. Organic
Composed of Carbon, and Hydrogen.
2. Inorganic
Simple molecule that is composed of other elements beside C, and H2.
C. Importance to the organism
1. Essential
Nutrients are essential for
bacterial growth and survival.
2. Non-Essential
Nutrients are not essential for bacterial growth and survival.
Microorganisms are classified by
chemical form of their nutrient.
a. Hetrotrophs
Microorganisms obtain carbon in the form of organic matter from the
bodies of other organisms.
b. Autotrophs
Microorganisms obtain carbon from inorganic gas (carbon dioxide) and have
the special capacity to convert CO2 into organic compounds.
Epidemiology:
Epidemiology- The study of
disease in a population
Surveillance- Rate of occurrence, mortality, morbidity
and transmission of infections
Prevalence- Total number of existing cases with respect to the entire population
Incidence- Number of new cases over a certain time over healthy population
Endemic- A constant number of cased during a long period of time in a specific geographic locale
Sporadic- A few isolated cased in
a wide spread locale (unpredictable)
Epidemic- Prevalence of cases increased unexpectedly, number of cases
increase
Pandemic- The spread of epidemic
all over the world ex (AIDS)
Defense Mechanism of the Host
The interaction and
cooperation of three lines of defense provide complete protection against
infection
First line of defense: (general function- same type of protection for
all bacteria)
Any barrier that block
invasion at the portal entry (skin)
Natural immunity is the
result of the first line of defense and it is nonspecific
Three different kind of
barrier may involved in the first line of defense
Ex. Skin and mucous
membrane
1- Physical: Structure of
tissue will protect us and not allow bacteria to come in and cause infection.
If skin has damage infection can occur
2- Chemical: Secretion of
chemicals to protect (Silvia protection in mouth; acid production in stomach;
tears has lysozyome that protect eye sockets from bacteria)
3- Genetics: Genetic
differences in susceptibility or resistance
Second Line of defense: (general function)
This line is non specific
and is composed of more sensitive system for protective cells and fluids that
includes inflammation and phagocytosis:
Phagocytosis:
Microorganisms that enter
the host are engulfed by any variety of phagocytic cells. The main function
of phagocytic include:
1- Chemotaxis- Attraction
due to chemical stimulate phagostic cell , phagoctic cell will be attracted and
begin to migrate
2- Migration- Move to
microbe
3- Ingestion
4-Microbial killing-
Lysozome kills bacteria
Microbes that enter the
lymphatic, lung, bone marrow or blood stream are engulfed by any of variety of
phagocytic cells
Most Common type of phagocytoic cells:
Polymorphonuclear
leukocytes (PMN)
PMN are Granulocyte and phagocytic
Moncyte = macrophage
Many microorganisms
elaborate chemotactic factors that attract phagocytic cells
Monocyte- Make the macrophage
Neutrophil- Most present (55%)
Eosinophil- Can also
perform phagocytosis
Basophil- can not do perform phagocytosis and Involve in inflammatory response
Factors affecting phagocytosis:
1- Presence of antibodies
(opsonins)
that coat the surface of bacteria, facilitate their ingestion by phagocytosis
Opsonization
Attachment of antibodies
to the microbial surface call opsonization that assist phagocytosis by forming
a physicochemical handle which the phagocyte can immediately recognize and
grasp
2- Hyperosmolarity
inhibits phagocytosis
Inflammatory response:
Injury to the tissue
following multiplication of microorganism, elicit an inflammatory reaction
After tissue damage,
histamine is produced (histamine is proceeds by tissue damage)
Steps in inflammatory response:
Dilation of local
capillaries
Escape of plasma
Fluid accumulation
(edema) in the area
Formation of fibrin
network- Limiting the spreads of microorganism
Migration (chemotaxis) of
PMN FROM ENGULFING OF MICROORGANISM BY PHAGOCYTE
Third line of function (specific function)
It is acquired as each
foreign substance is encountered by specially adopted cells called lymphocytes
Line is specific and
provides long term immunity
Four main body
compartments that dominate in immune function
B cells and T- cells are involved
Located in spleen and lymph nodes
Bone marrow→ Spleen →
Lymph nodes
1- Must be activated;
phagocytic cells involved (this occurs in the second line of defense)
2- B-cells multiply and form
plasma cells and create antibody (does not stay
effective in the body for a long time)
3- Memory cells created, has
longest life span (several years)
protect against exposure to infection that has occurred before
T- Cells function – Cell mediated or cellular mediated immunity
Lymphocyte- Make B and T cells
involved in third line of defense (20-35%)
Mechanism of Specific Host Response
Very specific and includes:
1- Surveillance (search for
marker, performed by phagocytic cells)
2-Recognize
3- Destroy
The cells of immune system
can recognize what is self and what is not
Self- Cell- Carries distinctive molecules (marker) that identify it
as self. The body’s immune defenses do not normally attack tissue that carries
a self marker
Immune Response:
A complex variety of
response
1- Antibody- mediated
response (humoral)
2- Cell mediated response
(cellular)
3- Combination of both
Low Fever- 99-100
Medium Fever- 100-103
High Fever- above 103
- Fever protects against
bacteria, bacteria is sensitive to the heat. Slows rate of growth
- Low iron will also slow
down growth rate of bacteria
Antibody mediated response
B cells undergoes blast
formation and several division of blast cells from plasma cell that secret antibody
and memory cells that can react to the same antigen
Antigen (Ag)- Antibody
(Ab) reactions:
1- Opsonization- (Ab) tags
the (Ag) to make it more accessible for phagocytosis
2- Neutralization- Attack
to an active site of toxin or a receptor of a virus
3- Aggregate (clumping)
Ag; kill microbe
4- Fix (binding)
complement and cause destruction of cells
Characteristics of Antigen: (part of bacteria that can bind to the
antibody)
a. Foreignness--- non self; not similar to components of the body
b. Molecular size large protein MW>10,000 (less that 1,000 can not
function as an antigen);<1,000 MW (haptens)
are not antigenic
c. Chemical & Structural complexity—
Certain amount of
complexity; made from several things to make them complex (ex protein)
d. Antigenic determinants (epitope)—
The smallest unit of a
complex antigen that is able to bind to an antibody
Antibody structure
1- Antibody is an
immunoglobulin
2- Light (L) & heavy
(H) polypeptide chains
3- The amino terminal of H
chain participate in the antigen in binding sites
4- The simplest antibody
molecule has a Y shaped molecule; contain two identical parts (Fab) and Fe
Types of Antibody
IGG
(memory cells make IGG)
A. IGG- simplest form of
antibody; in blood circulation
2- secondary response
(memory cells)- exposed to
3- Important defense
against bacteria and viruses
4- Pass through placenta
B. IgM ( Plasma cells create IgM)
Most effective ( f times
for effective) type of antibody, and heaviest
1- Five H2L2 units
2- Primary response
3- Important in
agglutination, complement, fixation, & in defense mechanism against
bacteria and viruses
4- Can be produced by a
fetus with a infection
5- Has highest activity
C. IgA
1- Two H2L2
2- Main immunoglobulin in
secretion (milk, saliva, tear)
3- Protect mucous membrane
from attack by bacteria and viruses
D. IgE
1- Antigen- antibody
complex
2- Allergic response
E. IgD
- A receptor on B cells
-Act as antigen receptor
on the surface of certain B cells
-Monoclonal, and Polyclonal
Ab:
-Monoclonal antibody
arises by fusing a B cell with a single clone of cancer cells (ab with single
specificity to Ag)
- Polyclonal antibodies arisen
in an animal in response to a single
complex Ag.
Antibodies in serum
(antiserum)
Cell medeiated immunity (CMI): Function of the T cells.
A direct attack of T cell
upon a variety of foreign cells and cell markers
Steps in CMI:
1- Presentation of a Ag by
macrophage; just like - Bcells
2- Sensitization of T cell
and blast formation
3- Formation of:
a. T- Helper cells assist other T and B cells
b. T-suppressor cells (limit the action of other T and B cells;
regulate function of T cells)
c. Cytotoxic or killer cells (destroy large, complex foreign and
abnormal cells)
d. Delayed hypersensitivity cells (reactions with foreign antigens
cause a form of allergy)
4- T Cells secrete a
series of chemicals called lympokinse
the destroy antigen or stimulate reaction
Reference 21-13 and 21-12
for examples
Complement or factor C: (Blood Protein)
Complex chemical defense system
that destroys certain pathogens and act as an
immune mediating system
1- Composed of 20-30 blood
proteins; inside 9 compartments (in order of when they were discovered)
2- Operates on cascade
reaction (one component activated, then second; so on and so fourth)
Cascade reaction:
Once component activates
the next in line, which activate the next
3- Originates from liver
cells keratocyte, lymphocyte, and monocyte
4- Two major pathways:
a. Classical pathway involves activation of complement by specific
antibody (It is initiated when antibody, called complement fixing antibody
attached to antigen on the surface of a membrane.
b. Alternative pathway involves non-specific reaction to infections (can
be initiated to wide variety of microbes, tumors and cell walls of bacteria).
Starts from C3 and goes to C9
5- Result of complement
activation is a huge enzyme called, the membrane
attack complex. Those can k kill bacteria cells and viruses by digesting
holes in their other membrane
6- Numbered C1-C9 in order
of their discovered
Having memory cells mean the body have become immune to an infection
Resistant and Immunity
The term immunity
indicates that those properties of the those that confer resistance to a
specific infectious agent
Innate or Native Immunity - Resistance state at the time of birth;
based on your genetic make up
- Species immunity
- Racial immunity
- Individual immunity
Acquired Immunity- The resistance obtained during the life of the
individual
- Natural: An immune state
obtained by natural means (ex. infection or placental transfer)
- Artificial: Immune state
produced by the introduction of immunizing materials (active) or of immunoglobulins (antibodies) that have been prepared
for this purpose (passive)
- Active- antibodies are
produced by the individual’s immune mechanism
- Passive- antibodies are
received from an outside source (e.g. colostrums or placental transmission
from the mother to her off spring, breast feeding)
Immunization-Producing immunity by medical intervention (general
term)
Vaccination- Production of a long lasting immunity following
an antigenic stimulus; (active immunity, body is exposed to the antigen)
1- Killed cell or
inactivated cell (used as the vaccine) entire cell used
2- Live or attenuated cells
bad
method weak; bacteria can get strong again
3-Subunit or part of
microbe only part of cell used- ex:
viral surface protein
4-Neutralized toxin-
Passive vaccine, antibody against toxin (ex. Tetanus shot) passive
5-Cloned Ag or recombinant
attenuated microbes- cloning of proteins (best vaccine )
Immune testing:
1- Agglutination test
Ab cross linked whole cell
antigen, forming three dimensional complexes that settle our and form visible
clump
2- Double diffusion
precipitation test Diffusion of Ags and Abs in a soft agar gel
Diffusion of Ags and Abs
in a soft agar gel forming zone of precipitation where they met
Hypersensitivity or Allergy
Immune response results in
reactions that are harmful to the host
Function of the immune
systems harms host (over reaction of the
immune system)
Types of Hypersensitivity
Type I
Immediate (anaphylactic) hypersensitivity:
Fast within a few minutes
(very fast)
First exposure, no
symptoms
Second exposure, host experience
symptoms IgE procuded
An Ag induces IgE with
bind to basophyls mediator
Histamine and
prostaglandin
Atopy:
1- Hay Fever- Seasonal
reaction to pollen
2- Asthma
3- Atopic dermatitis
eczema
4- Food allergy
5- Drug allergy
Anaphylaxis
1- Cutaneous
2- Systemic
Type II – Cytotoxic Hypersensitivity
Ab directed at cell
surface antigens activates C to damage the cells
IgG or IgM and
C are the primary mediator of this type of hypersensitivity
B cells is involved
Ex. Blood transfusion,
body reaction when bad blood is received
Type- III
Immune complex hypersensitivity
Deposition of immune
complex which activate the complement and cause inflammations
IgG involved; production
of IgG will bind to antigen and form the complex.
Binding can occur in
heart, joints and kidney; comes from blood that contains complement
Function of immune system
causes problem
Ex: Complication following Strep
infection -Rheumatic fever,
Acute Glomerulnephritis
Type IV
Cell mediated (delayed) Hypersensitivities
A Function of T lymphocyte
(B
cell is not involved)
It
starts hours or days after contact with Ag
Activated by the T -Cells
Ex.(1) Poison Oak, Poison ivy,(2)
rejection of organ
Medically Important Cocci
Pyogenic cocci: (cause pus forming infection )
3 Types:
1- Syaphyloccocci ( gram
positive)
2- Streptoccocci ( gram
positive)
3-Neisseria ( gram
negative)
Staphylococcus
Characteristic:
1- non-motile
2-non-spore forming
3-irregular clusters
4-faculative anaerobe
5-salt tolerant
6- Catalase- positive
7- Fermentative
8- pigmented
arge colonies
Staphylococcus aureus (most pathogen of group)
Virulence factors
1- Coagulase- Coagulates
plasma and blood( MOST USEFUL DIAGNOSTIC ENZAYME )
2- Halurindiase- Digests
ground substance around the cells (dissolve cement of cells)
3- Staphylokinase- Digests
blood clots
4- Nuclease- attack DNA
5-Cytotoxin:
-Hemolysin- Lyse red blood
cells X toxin; B hemolysis
-Luekocidin- Alter the
permeability of neutrophils , can kill with blood cells (phagocytic cells)
- Entrotoxin- act upon
gastronintestinal tract, (cause food poisoning)
-Toxic shock syndrome
toxin-toxemia in women due to infection of vagina associated with wearing
tampons (tampon allow bacteria that cause bacteria to grow faster)
- Exfoliative toxin-
separates the epidermal layer from the dermis
Target of infection: Skin and
gland
Systemic infection:
Bone and joint
Epidemiology:
Common human associates
Poor hygiene and
nutrition, tissue injury, persisting primary infections, diabetes mellitus and
immunodeficiency states increase
S. aureus infections
Clinical manifestations
1- Local or contiguous
infections
Skin
- folliculitis
denotes a superficial infection ( the mildest skin infection)
- a boil or furuncle extends
into the subcutaneous area (more severe than folliculitis)
- a carbuncle
invades dipper tissue; it tends to be multiple and contiguous especially in the
neck and upper back ( most sever skin infection)
- impetigo involve
encrusted pustules on superficial layers skin; it is highly contagious and
occurs mostly in preschool children (streptococci also may cause impetigo)
Eye
- conjunctivitis
Lungs
-pneumonia (common in
children under age 1)
Wounds
-trauma or surgical sites,
especially in the abdomen
Disseminated infections
(1) Blood stream or
lymphatic disseminated infections (infection spread all over the body)
- occur away from the
infection site
- are chronic and
difficult to cure
(a) Osteomyelitis, especially in the diaphysis
of long bones
(b) Pyoarthritis with permanent cartilage
damage, especially in the hip
(c) Acute
bacterial endocarditis in drug abuser or
within 2 months after heart surgery
(2) Toxin-associated infections
(a) Scalded skin syndrome
due to an exfoliative toxin that splits the epidermis at the stratum granulosum
(b) Toxic shock syndrome
due to pyogenic toxins (TSST); occurs mostly in females using tampons is characterized
by high fever with vomiting and diarrhea, collapse of peripheral circulation,
and scarli form rash
(c ) Food poisoning due to
an enterotoxin preformed in food to 6 hours after ingestion of contaminated
food (local infection)
(e) Enterocolitis;
following broad spectrum antibiotic therapy for other bacterial infections cause
cramps, diarrhea, fever, and dehydration
1- Treatment
-Isolate orgamisms and
perform antibiotic sensitivity tests (because widespread resistance)
- Give oral antibiotics
for 10 days for localized infections
-Give parental antibiotics
for 4 to 6 weeks for disseminated infection
-Drain abscesses; remove
any foreign body, if possible
-Severe toxic shock
syndrome may require intravenous(IV) fluids measures to elevate blood pressure
- food poisoning is
self-limiting within 24 hours; no treatment is required
2- S. epidermidis
- cause urinary tract
infections, primarily in the elderly
-may cause subacute
bacterial endocarditis at least two months after heart surgery of after
gastrointestinal instrumentation or dental work when person is not wearing
gloves ( blood transmission)
- usually normal flora of
the skin
2- Prevention
- Hand washing is a key to
prevention in a hospital environment
-Hospital problems occur
primarily in operating rooms and nurseries
Streptocpccus
Normal resident or agent
of disease in human or animal
Characteristic:
1. Spherical Shape
2. Long bead like chains
e. Non spore forming and
none motile
f. Facultative anaerobes
g. Ferment sugar with the
production of lactic acid
h. Colonies usually small,
and non-pigmented
i Catalase- negative
h. A peroxidase system for
inactivation of hydrogen peroxide
Calassification:
Rebecca Lancefield (1930)
Cell wall
Carbohydrates abs WITH DIFFERING
SPECIFICTIES
Another classification on the base of their reaction in blood agar
A, B, C and some D are Beta
HEMOLYTIC
Streptoccoccus pneumoniae
Viridians (mitis and pneumoniae)
Are alpha hemolysis
producer
Group A
Streptoccoccus pyogenes (B
hemolytic)
Cause throat infection
Inhabitait of the
throat,nasopharynx and skin of humans
Virulance factors:
1- Capsule
2- C- carbohydrate- protect bacterium from being dissolved by the host lysozyme
2- C- carbohydrate- protect bacterium from being dissolved by the host lysozyme
3- M protein- main component
of fimbriae
All are antiphagocyitic
and adherence factor
4- Streptolysin O (SLO)
and streptolysin S (SLS)
Both produce B hemolysis
5- Erythogenic or pyogenic
toxin
Responsible for scarlet
fever and induces fever and red rashes
6- Streptokinase
Digest in the fibrin clot
and may play a role in invasion
7- Hyalurinidase
Promote the
spreading of bacteria by digestion of intracellular glue
Targets of infection
1- Skin or the mucus
membranes of the throat primary lesion ( skin infection- strep impetigo or
pyoderma = itching papules that break
open and form a highly contagious yellow
crust)
Pharyngitis or tonsillitis
(strep throat)
Redness, edema,
enlargement of tonsils
2- Lymph and blood
(systemic infections)
3- Vagina (puerperal
fever)
4- Join, heart, and
subcutaneous tissues (delayed inflammatory reaction- rheumatic
fever)
5- Kidney (acute
gomerulonephritis)
6- Tissue between skin and
muscle Necrotising Faceitis
(Flesh eating disease)
Treatment:
Penicillin and its
derivatives
Erythromycin or
cephalosporin
Alpha Hemolytic Streptococci: The Viridan Group
Most numerous and
residents of the oral cavity
S. mits, S. mutans, and S. sanguis
Dental procedures can lead
to:
Bacteremia
Meningitis
Abdominal infection
Sinusitis
Wound infections
And subacute endocarditis
Dental caries because of
streptococci mutans
And streptococci sanguis
Streptococcus pneumoniae:
Significant human pathogen
Characteristics:
Encapsulated
Capsules contain a
polysaccharide antigen called the specific soluble substance (SSS) that varies
chemically between the pneumococcal types and stimulates different Abs of
varying specificity
Target of Infection:
Adult:
1-pharynx
2-Lung (lovar peumoniae)
Symptoms: chills, shaking,
fever
Young children:
1- Upper respiratory tract
2- Meninges (meningitis)
3 middle ear (otitis
media)
Treatement:
Penicillin, clindamycin,
erythromycin and cephalosporin
Neisseriaceae:
Resident of the mucous
membrane of worm blooded animals
Two species are primary
human pathogens
1- Neisseria
2- Moraxella
Neisseria:
-Distinguishing feature is
the morphology
-Bean-shaped and paired
-Capsule on the pathogens
-Pilli (slow down phag)
-Strict parasite
-Aerobic
-Catalase positive
Neisseria gonirrhaeae
-Sexually transmitted
disease (STD)
Albert Neisser 1879
Site of infection:
Genital tract, eye, rectum
and throat
Symptom: Yellow creamy pus
with painful urination
Virulence;
Pilli-promote attachment
of cocci to each other an epithelial tissue to each other and epithelial tissue
Pilli also seem to slow
pahgocytosis by macrophage and neutrophiles
-Protease-cleaves the
secretory antibody( IgA)
Epidemiology and
pathology
Strictly human pathogen
Rank in top 5 STD
600,000 to 700,000/ year
in the USA
Several categories of
gonorrhea male, female and children
Treatment
1- Intramuscular injection
of procaine pencillin G
2- Oral ampicillin and
probenecid
Gonorrhea is reportable
Neisseria meningoccous:
Neisseia meningitides is a
serious human pathogen
Important virulence
factors:
1- a polysaccharide
capsule( nine different strains of a capsular antigens exist, serotypes A,B,
and C are responsible for most infections
2- Pilli
3- IgA protease
4-Lippoplysaccharide
(endotoxin) released for cell wall
Epidemiology and Pathogenesis
:
The continuing reservoir
of infection is human Neisseria meingitidis is the second most
frequent cause of meningitis
in young children
Serious complication due to
meningococcemia bacteria entering the blood vessel rapidly permeate the
meninges and produces symptoms of meningitis
Symptoms:
Fever,weakness, headace,
stiff neck. Convulsions and vomiting
Treatment:
Penecillin G
Prevention therapy with
rifamphin or tetracycline
Other gram negative
cocci:
1- Branhamella catarrhlis-common
member of throat flora, and can cause opportunistic infection
2- Moraxella, a
short rods that colonies mammalian mucous membrane
Bacilli of Medical Importance
Gram positive bacilli:
a. Aerobic: Bacillus
b. Anaerobic: Clostridium
2- Non spore-forming
Gram positive spore-forming bacilli:
Motile
Rod-shape
Endospore
Extreme resistance to
heat, drying and radiation
Ex. Bacillus, Clostridium
Bacillus anthracis:
Blocked-shaped angular
rods
Largest bacteria
Zoonatic disease of domesticated
animal
Central spore
Virulence factors:
Capsule
Exotoxins
Very important in medical
microbiology
Robert kock used this
organism for developing his postulate, and Louis Pasteur used the disease to
prove the usefulness of vaccination.
Depending upon the portal
entry
1- Cutaneous anthrax---skin---through small cut
2- Pulmonary anthrax---inhaling airborne spores
Exotoxins produce a
toxemia with cardiovascular shock
Treatment
Penicillin or tetracycline
Bacillus cereus:
A common air-borne and
dust- borne contaminant
Multiply in cooked food
(starchy food and meet )
Spore survive short
periods of heating
Spore germinates and
release entrotoxins
Ingestion of toxin
containing food causes nausea, vomiting, abdominal cramps and diarrhea
No specific treatment
The Genus Clostridium:
Gram positive
Spore forming
Heat resistant
Requirement of oxygen
Catalase
Inhabitant of human and animals
Single, pair and chain
arrangement
Exotoxins play an
important role in various clostridial disease
Several species are
important
Types of infections
1- Wound and tissue
infections, including myonerosis, antibiotic-associated colitis and tetanus
2- Food intoxication of
the perfringens and botulism varieties
Clostridium Prifringes----soft tissue and wound infection (Gas
gangeria)
Extent and symptom of
infection
Two forms: (wound infection)
1- Anaerobic cellulites:
Target—previously injured
necrotic tissue
Toxin and gas production
Localized infection
2- Myonecrosis:
Most distractive
Target--- injured tissue
(often large muscle)
Diffuse into nearby tissue
and cause necrosis there. This damage tissue then be a source continuation of
growth of bacteria
Treatment
Removing of the infected
tissue (this is very difficult in the intestine or body cavity infection)
Large dose of a
broad-spectrum cephalosporin
Passive immunization with
polyvalent antitoxin
Clostridium tetani:
Common resident of
cultivated soil and gastrointestinal tracts of humans and animals
Spore usually enter the
body through accidental cut
Tetanus neuromascular
disease--- Lockjaw
Spores cannot become
established unless tissue at the site of the wound is necrotic and poorly
supplied with the blood
Neurotoxin (tetanospasmin)
responsible for the major symptoms
Treatment:
1. Immediately receives
antitoxin therapy with Human tetanus Immune Golbulin (TIGH). Tetanus antitoxin
from a horse is also acceptable with a chance of allergic reaction
2. Remove the infected
tissue
3. Control the infection
with Penicillin
4. Administration of
muscle relaxants
Clostriduim food poisoning:
C. perfringens- Bacteria is eaten with uncooked meat and fish,
producing toxin in the intestine, not usually fatal
C. botulinum (improperly home- canned food)
Spore withstands food
processing and germinates in stored food and produce Toxin (botulin)
Food poisoning
a. Caused by poisonous
plants animals
b. Caused by microbes
1- Food toxication
(toxin)
2- Food infection
(bacteria)
Most common food poisoning
in the USA is Staphylococcal food intoxication
Other common: Salmonella,
Clostriduim perferingen, Shigella
Irregular, non spore forming bacilli:
Corynobacterium
Mycobacteria
Nocardia
Corynebacterium
Corynebacterium
diphtheriae
Aerobic curved rod and
palisade arrangement
Epidemiology
400 years
ago---significant cause of mortality and morbidity
Today mortality declined
to 0.1% in 1,000,000
Many healthy human carrier
Pathology:
The main pathogenicity
factor is production of diphtherotoxin
This exotoxin is produced only
by strains of C diphtheriae that carry the gene for toxin production that obtained from bactriophage
during transduction
Clinical disease:
Diphteria--- a disease
occurs in two stages
a. local infection---
Toxin absorbed into the
mucous membrane of upper respiratory tracts (tonsils, pharynx, larynx, and
trachea) causes destruction of epithelium and causes superficial inflammatory
response and formation of a grayish “pseudo membrane)
Other symptoms—low grade-
fever, sore throat, nausea, vomiting and sever edema of the entire neck
b. Systemic infection:
Toxin is absorbed from the
throat to the blood - to heart (
myocarditis and nerve( paralysis ); patient could die from this infection
Treatments
Pseudo membrane can be
removed
Penicillin and
Erythromycin
DPT ( toxoid vaccine -prevention
Acid fast Bacteria (wax layer
in the cell wall)
Mycolic acid and waxes
Strict aerobes
Filamentous rod
Resistant to environment
Mycobacteria:
Several species are
important
Mycobacterium tuberculosis
1- Generally we get
infected easily, and develop resistance to disease (95%)
2- 5% of population will
develop disease
3- 85% of 5% population will
develop lung infection
Lung infection- lesion-
lesion in regional lymph nodes- Ghon complex-,healthy people will recover from
infection by fibrosis—calcification, and healing.
Unhealthy people will
develop TB through blood circulation
Diagnosis:
1- Chest X ray
2- Isolation Acid Fast
bacteria from Sputum
3- Tuberculin Skin Test (Mantoux
test)-
Exposure to small amount
of purified protein derivative (PPD)
4- Lab cultivation and
Diagnosis
Gram Negative Rod:
Non- spore former
Cell walls contain lypopolysacharide
that is endotoxin
1. Aerobic non
spore forming:
Pseudomonas aerugionsa
Opportunistic pathogens
May attack lung, skin,
burns, urinary tract eye and ear
2-Facultative Anaerobic
rods
:
Enterobacteriaceae:
Small, ofter motile,
Found in intestine----enteric
1- Coliforms---E.Coli,serratia (ferment lactose)
Normal flora that are rapid lactose
fermenters (coliform)
Non- coliforms
Do not or only weakly ferment
lactose (Proteus)
Coliform Bacteira: (can produce
sugar from lactic acid; non pathogen)
Ecoli
Klebsiella
Entrobacter
Citrobacter
Serratina
Non- Coliform Bacteria (non- pathogen)
Proteus vulgaris
Morganella
Pathogen:
Salmonella---salmonelosis
(Typhoid Fever)
Shigella---- Sigellosis
(Bacillary dysentery)
Yersinia—Bubnic plague
Virulence factor:
Flagella, Capsule, and
Firbriae
E. Coli
Most common in gut and
harmless
Pathogenic strains:
Virulence factor:
Toxin and fimbriae
Causes sever diarrhea
illness
Agent of infantile
diarrhea (greatest cause of mortality in babies) most common cause of Travelers
diarrhea
E coli type 157
Newest pathogenic strain
Mild gastroenteritis with
fever to bloody diarrhea
Can cause kidney damage
and failure
High risk in your children,
elderly and immune-compromised people
first discovered on 1982
The Spirochetes:
Long Rod
Spiral and motile
1. Treponema
Gram negative cell wall
with axial filament
Causes syphilis, bejel,
yaws, and pinta
Ttreponema palidum
A. Acquired Syphilis:
Limited to human host
Sensitive bacteria to
environmental condition and transmitted by sexual contact
Involve all tissues of the
body
Multiply at the sit of
entry--- spread to nearby lymph nodes—blood stream
2-10 weeks—hard chance (an
ulcer with a clean, hard base at the site of entry- primary lesion)
2-10 weeks later—secondary
lesion—red rash anywhere on the body
Both primary and secondary
lesions are highly infectious. Contagious lesion may recur within 3-5 years after
infection but thereafter the infected individual is not infectious
- 30% remain latent
-In the remainder, disease
progresses to tertiary stage, characterized to the development of glaucomatous
lesion in the skin, bones, liver and degenerative changed in CNS, and
cardiovascular system
B. Congenial syphilis:
A pregnant woman can transmit infection to the fetus during 10th -15th
week gestation
Some of the infected fetus
may die
Misscarriages
Problem with eye, teeth, nose and CNS
Treatment: Penecillin G
Prevention use of condom
2. Borrelia
( Arthoropod- borne spirochete)
Borrelia burgdorferi—lyme
disease
Human---accidental host
Principal host--- mouse
and deer
Transmission by tick
Symptom:
Early—skin lesion in 70% of infected patient -called erythema
chromicum migrans and flue like symptoms ( fever, chills, headache)
Late—Arthralgia and arthritis
Neurological manifestation—meningitis
Cardiac disease
Treatment: Tetracycline,
and penicillin
3. Vibrio (curved gram negative)
Spread by water and food
Uncommon in USA
Sporadic out break along
of Gulf of Mexico
Sometimes isolated from
shellfish
Vibro parahaemolyticus in sea
food
Microbiology of Drinking Water
Water need to be free of pathogen. Water can
pick up pathogen through ordinary exposure to air, soil, etc.
Most common pathogen in water:
Salmonella
Sigella
Bacteria Vibrio
Mycobacterium
Campylobacter
Virus
Hepatitis A
Norwalk Virus ( reovirus)
Fecal contamination :
Most common source of pathogens in drinking
water.
Monitoring Water
Water constantly surveyed for certain
indicator bacteria.
Indicator Bacteria -
Intestinal residents of birds and mammals that
can be identified more readily than individual pathogens
Coliforms
Streptococci
These bacteria survive in water without
multiplication.
High numbers indicate high levels of fecal
contamination.
Environmental Protection Agency (EPA)
Standard for water sanitation based on the
levels of coliforms.
Water Quality Assays:
1- Standard plate count
2- Measurement of dissolved oxygen
3- Colifrm Enumeration
a.
Most Probable Number( MPN )
b.
Membrane filter
Water and Sewage Treatment
Water Purification
Storage, Sedimentation, Settling, Aeration
and disinfection
Sewage Treatment:
Sewage processed to remove solid matter,
dangerous chemical and microorganism.
Bioremediation:
Using microorganisms to breakdown or remove
toxic waste in water and soil
Most important bioremedial microbes: Pseudomonas,
Bacillus and toxic - eating Fungi
Medically important Bacteria of unique Morphology
Helicobacter Pylori
Rickettsias
Chlamydia
Mycoplasma
Helicobacter Pylori
Unusuall Spiral in human and animal
Microaerophilic
Pollar fellagella
Grow in acidic environment
Causes inflammation of lining of
Stmomach called gastritis
Implicated in 90% of stomach and
duodenalulcer
Cofactor in the decelopment of a
common type of stomch cancer called adenocarcinoma
Transmision: person to
person by oral- oral or oral – fecal
Treatment: antibiotic and
antiacid
Rickettsias:
Gram negative rod or cocci
Obligate intracellular
Transmission by insect
Rickettsia rickettsii:
Gram negative rod, multiply in endothelial
cells of lining of blood vessel , causing necrosis
Rocky Mountain spotted fever
Zoonosis carried by dog and wood
tick
Symptoms: Spotted, migratory rash,
Fever, chills, headache
Complications:
Hemorrhage, heart damage, CNS
damage
Treatment: Tetracycline
Rickettsia prowazekii:
Typhus
Carried by lice
Symptoms: High fever, chills,
headache,
Rush
Treatment: Tetracycline
Chlamydia:
Gram negative coccobacilli
Obligate intracellular
2 forms:
Elementary body which is
infectious
Intracellular reticular body –
reproductive form and pathological effect
Chlamydia trachomatis:
Eye infection and STD
Eye disease is the infection of
eyelid and cornea, can cause blindness
STD is non gonococcal urethritis
in male and cervicitis and infertility in female
Chlamydia psittaci:
Cause disease in bird (parrots)
Cause human respiratory infection
(Parrots Fever)
Mycoplasma:
Lack cell, wall have strole and
highly pleomorphic
Not obligate parasite but require
special lipids from host membrane
Mycoplasma pneumonia:
Contain sterols for protection
Causes atypical pneumonia
Symptoms:
Fever chest pain and sore throat
Symptoms:
Fever chest pain and sore throat
Viruses in infection and disease:
Virus Particle- Needs cell to
live;
Structure of virus:
Consists of Covering and Central
Core
Covering: Capsid, envelope not
found in all viruses
Central Core: Nucleic acid
molecule DNA or RNA and Matrix Proteins enzumes; not found in all viruses
DNA-double stranded except
parvovirus (or)
RNA-single strand except reovirus
- will only have DNA or RNA will
not have both
Target cell
Scope of infections
Latency/ oncogencity (can cause
cancer)
Viral Replication
1- Adsorption: Virus attaches to
hose
2- Penetration-
Lysogeny (Latent) State- Virus go
to bacterial DNA and become dormiant will not damage cell; can come out and
begin to grow
Lytic State- grow and burst out
of the cell
3.Synthesus structural parts
4-Assembly-
5- Release
DNA viruses:
Enveloped
1-Pox virus
2- Herpes virus
3- Hepanavirus
Non enveloped:
1- Adenovirus
2-Papovavirus
3-Parvoirus
Pox virus—Infect
epithelial of respiratory tracts circulation and lymph nodes
Skin pustules----pock or pox
Largest virus
Symptoms: fever, malaise, later
rash in pharynx and
Small pox, and variola
Minor—mild
Major – 25 times more virulent
Vaccine—cow pix virus
The Herpesviruses: (herpes viruse hominis)
Herpes= Creeping
Herpes simplex type 1
(Fever blister)
- hide in the Ganglion area,
until activated
Type 2= Genital infections
- Latent in the ganglion of the
lumbosacral spinal nerve trunk
Herpes zoster = Chickenpox
and shingle
Cytomegalovirus= salivary
glands
Epstein-Barr Virus=
Lymphoid tissue
Herpus virus 6= T Cell and
B cell
Herpus virus 7- T cell
Herpus virus 8- T cells
Herpes simplex type 1 &
type
2
Enveloped
Structrue:
Large virus –150-200 nm diameter
Envelope with glycoprotein spike
Icosahedral capsid
Core—double strand DNA
Replication in host nucleus
Viral release by cell budding
The exact mechanisms of latency
are not known, the virus remain inside trigeminal ganglion ( type 1 ) and Lumbar sacral
ganglion( type -2) in a non-dividing
stage for a variable time , recurrent infection is triggered by different
stimuli:
Fever
UV radiation
Menstrusation
Stress
And mechanical injury
After reactivation virus migrates
to the body sites and produce local skin or membranes lesion
Types of HSV-1 infection:
1. Gingivostomatitis- most
primary infection; infection of the oropharynx- inflammation of the oral mucosa
(gum, tounge,soft palate and lips)
2. Herpes labialis- fever blister
or cold sore on the lips or adjacent skin
Herpes Keratitis (ocular herpes)
Primary and recurrent infection
of eye
Cornea is the site of infection
The chronic case can lease to
visual loss
Encephalitis- complication in
newborns infected at birth – brain infection
Severe CNS damage
Fatal of neonate and fetus
(50%-80%)
Disseminated herpes- inpatient
with immunodeficiency
Herpetic Whitlow
Finger tip infection
Diagnosis and Treatment
Tissue culture for virus
cytopathic effect is essential for diagnosis
Acyclovir ( can stop the growth
of virus)
Varicella-Zoster Virus (VZV)
Chickenpox (varicella) and zoster
(shingles) chickenpox is the primary infection, and zoster is the later
recurrence of infection by latent virus
a- Vesicular rash on the fact and
truck (primary)
b- Latency in the dorsal ganglia
c-the one site pattern in shingle
(reactivation)
Transmission by droplets
Treatment:
Uncomplicated is self limited
Drug for systemic disease is
intravenous
Acyclovir, interferon, and
vidarabine
The use of aspirin is not
recommended because of the risk of Reye syndrome ( a disease that strikes the brain,
liver and kidney fatalities are common.
Children given aspirin therapy have a higher risk for the disease)
Cytomegalovirus (CMV):
Named from the characteristic
cytopathic
Effects (nuclear and cytoplasmic
inclusion bodies)
High infection rate in children,
pregnant woman and drug abuser
Spread with close contact with
saliva, mucus, urine, and semen
Congenital infection causes
disturbance of liver, spleen, brain, and eyes
Disseminated disease in AIDS and
transplant patients
Treatment: If you are healthy
immune will cure; if you have low immunity
Treatment: Gancyclover; best for treatment of
chickenpox
Epstein- Barr Virus (EBV)
Infect lymphoid and glandular
tissue
Transmitted by saliva, oral
contact
95% of all persons develop some
kind of infection asymptomatic
Cause of monoucleosis a “kissing
disease”
Common in college students
Can cause cancer
None enveloped DNA
virus
Adenovirus:
Transmission:
•
Transmitted by fecal to oral contact, waterborne
transmission and inhalation of aerosols also possible.
•
There are many different types of adenovirus and they
all survive adverse conditions from chemicals and pH levels and rely on the
host for survival and replication
•
Examples: conjunctivitis,
ear infections,
tonsillitis,
and croup
Pathology:
•
Most cases involve respiratory tract, GI tract and eye
•
Most people are infected with some type of strain
before the age of 15
•
50 to 80 percent of tonsils removed contain some form
of adenovirus
•
In some cases the virus can live inside the host for up
to 2 years, it can be excreted from the stool and urine
Diagnosis:
•
viral culture, adenovirus-specific viral antigen
assays and polymerase chain reaction assays are most commonly used
Prevention:
Hand hygiene is the most
important preventative measure along with adequate amounts of chlorine in
swimming pools
RNA virus
More kinds of RNA virus than DNA
virus
Segmented-
Non- Segmented virus
Postitive Sense
Negative Sense
Retroviruses:
1- Most unusual virus
2- Oncogenic (some viruses are
transforming agent regulate certain genes and convert normal cells into cancer
cells
3- Capable of reprogramming a
hosts DNA
4- Unusual enzyme called reverse
transcriptase which can convert a singe stranded RNA into double stranded viral
DNA
RNA- AIDS virus
Enzyme can change RNA into DNA (
reverse transcriptase enzyme )
Classification:
Human T- cell leukemia virus
(HTLV)
HTLV I, II and III
Type I & II are associated
with human leukemia or lymphoma, and type III is the agent of AIDS
Type III- agent of AIDS
Since it was determine that HTLV
III LYMPHADENOPATHY VIRUS (LAV) AND (AIDS) retrovirus (ARV) are all the same
virus, a unified names HIV-1
Epidemiology:
AIDS have been reported in every
country (30-40 million)
1 million in the USA
Transmission:
Sexual Intercourse
Transfer of blood of blood
products
The virus can be isolated from
urine, tears, sweat, and saliva, but these fluids are considered an unlikely
source of infection
The mother milk can be a source
of neonatal infection
AIDS is defined as severe immunodeficiency Disease arising from
infection with HIV-1
Symptoms:
Opportunistic infections,
persistent fever,
ARC (AIDS related complex) is
considered a stave in the development of the disease
AIDS Pathology
1- HIV initially enter special
cells on the membranes called dendritic cells
2- It grows and she from the
cells with out killing them
3- It can multiply in a
macrophages, skin, lymph organ, bone marrow, and blood
4- Infect and destroys many of
cells need to destroy microbes including the helper
Class of lymphocytes, monocytes,
macrophages and even B lymphocytes
Can infect brain cells,
macrophage,
Diagnosis and Treatment
1- Secondary infection and
cancers
2- The enzyme- linked immunabsorbent
assay (ELISA) is highly
sensitive but can lead to false positive
3- Western blot, which is most specific test and can rule out false positive
There is no cure for AIDS.
The available therapies prolong life or diminish symptoms by stopping the
growth of virus .
Drug:
AZT (retrovir) blocks the
replication of virus
DDI (videx)
Both drugs are synthetic
nucleotide and incorporate into the DNA molecules during reverse transcription
Rhabdovirus- Rabies
•
The Rhabdovirus is a negative stranded RNA genome that
is uniquely bullet shaped.
•
The name is derived from the Greek word rhabdos
meaning rod referring to the shape of the virus.
•
They typically carry genes for five proteins.
•
Rhabdoviruses have a broad host range affecting both
animal and plant kingdoms.
•
Rhabdoviruses infect cells and generally enter via a
bite or a wound infected with saliva.
Rabies:
•
Rabies is a viral disease that causes acute
encephalitis (inflammation of the brain) in warm-blooded animals Initially, the
virus replicates at the site and then infects the CNS tissue.
•
Rhabdovirus causes lethal encephalitis resulting in
approximately 50,000 human deaths per year. The rabies virus is classified as
Lyssavirus genus, in the family Rhabdoviridae.
•
Orthomyxovirus-Influenza Virus:
All orthomyxovirus are viruses, isolated strains and are
named after the virus type (A,B,C), the host and location of initial isolation,
the year of isolation, and the antigenic designation of the hemagglutinin and
neuraminidase
•
Influenza is an acute respiratory tract infection that
usually occurs as epidemic by influenza virus
•
Just three types of influenza virus are known : A,B and
C
•
•
Major outbreaks of influenza
•
are associated
with influenza virus type A or B.
•
Infection with type B influenza is usually milder than
type A.
•
Type C virus is associated with minor symptoms.
Antigenic Drift and Shift
Type A: antigenic shift
Type B: antigenic Drift
Virus like agent---
Prions- atypical chemical and physical properties
10- 20 years before you feel
symptom
Agents of spongiform
Encephalopathies or neurodegenerative dementias
Human diseases with prions:
1- Kuru
2- Creutzfeldt- Jacob disease
3. Gerstmann Straussler-
Scheinker disease
4. Faal Familial Isomina (FFI)
Aminal disease with prions:
Scrapie--- found in sheep and
goats
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