Lesson 5 - Bacterial Infection

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SUBJECT CODE: BHCM 3163

SUBJECT NAME: PRINCIPLE OF HEALTHCARE &


DISEASE PREVENTION

WEEK: 3 (LESSON 5)
TOPIC: BACTERIAL INFECTION

PREPARED BY:
MS. ZAYAN NABILAH
Course
Learning
Outline
Bacteria
Two kingdoms of bacteria:

•Eubacteria – “true” bacteria

•Archaebacteria – oldest
organisms on earth, live in
extreme conditions
Bacteria are:
•Unicellular
•Prokaryotic…which means?
Fact: Each square centimeter of
your skin averages about 100,000
bacteria. A single teaspoon of topsoil
contains more than a billion
(1,000,000,000) bacteria.
Bacteria Characteristics
• Some bacteria are aerobic, meaning
that they require oxygen in order to
survive. Other bacteria are anaerobes,
meaning that they do not require
oxygen to survive.
• Most bacteria are harmless and offer
beneficial functions to living things and
humanity.
Bacteria contain:
•a singular, circular
piece of DNA
•tiny circular pieces
of DNA called
plasmids
•ribosomes
Bacteria
reproduce:

Asexually
(mitosis)
using binary
fission.
Bacteria reproduce:
sexually using
conjugation.
Bacteria exchange
plasmid DNA.

This is how bacteria


become antibiotic
resistant.
Bacteria have cell walls made of:
•peptidoglycan (polysaccharide linked
with chains of amino acids).
•this may be covered with an outer
membrane of lipopolysaccharide
(chain of sugar with a lipid attached).
Some bacteria:
• have a gelatinous layer called a
capsule surrounding the cell wall.
• form thick-walled endospores around
chromosomes when they are
exposed to harsh conditions
(drought, high temperatures) - these
types cause botulism
Some bacteria have:
• flagella for
locomotion.
• pili (short, thicker
outgrowths that
help cell to
attach to
surfaces)
• Bacteria can be moved by air and water
currents, and on any surface such as
clothing, hands, or any object.
Three bacterial shapes:
1. Rod shaped are called bacillus(i)
2. Sphere shaped are called coccus(i)
3. Spiral shaped are called
spirillum(I)
Gram stains:
• Important in medicine because
provides information for treatment of
bacterial disease.
•Bacteria stain either gram positive
(purple) or gram negative (pink).
•Gram positive tend to respond to
penicillin and like antibiotics.
•Gram negative respond to types of
antibiotics unrelated to penicillin.
Gram Stain Process:

Crystal violet dye Iodine


Purple Decolorizes
Alcohol Safranin
Pink Counterstain
A Gram Stain is
usually performed
on a smear
preparation that
has been heat
fixed. One
function of
fixation is to
secure (fix) the
cells to the slide.
Gram positive = purple because of large
amount of peptidoglycan in cell wall.

Polymer consisting of sugars and amino acids that forms a mesh-


like layer outside the plasma membrane of eubacteria.
Gram negative = pink because
lipopolysaccharide membrane is removed by
alcohol and thin peptidoglycan layer allows dye to
escape.

(LPS) is a large molecule consisting of a lipid and a


polysaccharide (carbohydrate) joined by a covalent
bond.
• work by preventing cell wall
formation, breaking up cell
membranes, or disrupting chemical
processes.

•Antibiotics cannot treat viral


infections.
There are three types of
bacteria based on how they
obtain energy: heterotrophs,
photosynthetic, and
chemoautotrophs.
This is the
anthrax
bacterium.
1. Most are heterotrophs:
a. Decomposers – feed on and recycle organic
material
b. Pathogens – parasitic, disease-causing
bacteria
• Either attack cells or secrete toxins
c. Nitrogen-fixing bacteria (Rhizobium)
• Found in nodules of soybeans, peanuts,
alfalfa, and clover
• Convert atmospheric nitrogen (N2) into
ammonia, called nitrogen fixation.
• Used in crop rotation
Decomposers
• Bacteria are decomposers, they break
down the chemical elements inside
other living or dead organisms. Some
bacteria live in the intestines of humans
and animals

Rhizobia bacteria convert nitrogen


gas into other
substances that help plants grow.
Pathogens Strep
throat

Streptococcus

Staphylococcus
Nitrogen-fixing
bacteria (Rhizobium)

Nitrogen fixing bacteria


in the nodules of roots
2. Some, like Cyanobacteria, are
photosynthetic.
•These are autotrophs that use the
sun’s energy to make food.

This bacteria has


chlorophyll and uses the
process of photosynthesis
to produce food very much
like a plant.
3. Chemoautotrophs
•Obtain energy by removing electrons from
inorganic molecules such as ammonia
and methane to make food.
•Examples: Nitrobacter and Nitrosomonas
- live in soil
- have a crucial role in nitrification (turn
ammonia into nitrates, the
form of nitrogen commonly
used by plants).
Some Good Bacteria
• Lactic acid bacteria have been used to ferment or
culture foods for at least 4000 years.
• Examples: products like yogurt and cheese

• Wastewater bacteria feed on everything from


solid human waste matter to last night's leftovers.
As the bacteria eat, they convert organic matter to
carbon dioxide, releasing electrons, the basic
element of electrical current.
Bacterial infections
• toxemia = toxins in blood circulation
• alimentary
– botulotoxin (Cl. botulinum)
– enterotoxin (Staphylococci)
• wound
– tetanotoxin (Cl. tetani)
• other
– diphtheratoxin (C. diphtheriae)
• regressive changes (liver, kidney, heart)
Bacterial infections
• bacteremia = bacteria in blood circulation
• time-limited
• elimination by immune system
• e.g.: digestion, tooth extraction,
tonsillectomy, catheter, cystoscopy…

!!! heart valves defect  infective


endocarditis  ATB cover !!!
Bacterial infections
• sepsis = bacteria > immune system
• fever + splenomegaly + lymphadenopathy
• streptococci, staphylococci

• metastasizing sepsis (septicemia)


• nasopharynx  menings (N. meningitidis)
• pulmonary abscess  brain abscess
• furuncle  bones + kidney (Staphylococci)
Staphylococci
• Gram+, common
• normally on skin + mucosa
• skin abscesses x sepsis
• nosocomial infections
• secondary infections (influenza)

• Staph. aureus + Staph. epidermidis


Staphylococci
• 1. skin lesions (wounds)
– furuncle  carbuncle (DM)
– impetigo
– panaritium
• 2. mastitis (breast feeding woman)
• 3. osteomyelitis + arthritis
• 4. enterocolitis + alimentary enterotoxicosis
• 5. acute infective endocarditis
• 6. toxic shock syndrome
Streptococci
• Gram+, common
• β-hemolytic (A-D, G)
– Str. pyogenes (A)
– Str. agalactiae (B) – mother´s vagina  newborn´s

meningitis
• α-viridans (H)
– subacute infective endocarditis
– Str. mutans – caries, pulpitis
• anaerobic (Peptostreptococci) – oral cavity
Streptococci
• Str. pyogenes (A)
• 1. local inf. – phlegmone, impetigo, wound inf.
• 2. angina (tonsilitis)  otitis, sinusitis
• 3. scarlet fever (erythrogenic toxin)
– angina + oral enanthema (raspberry tongue) + skin
exanthema (face, trunk)
• 4. erysipelas
– skin erythema (lower limbs, face) + toxemia
– lymphatic + blood vein thrombosis  lymphostasis 
edema  elephantiasis
Streptococci
• sequelae (Streptococcus A)
– M protein
– cross reaction (immune)
– acute glomerulonephritis
– rheumatic fever
Pneumococci
• Str. pneumoniae
• Gram+ diplococci
• children
– rhinitis, nasopharyngitis, sinusitis, otitis
• adults
– lobar pneumonia  meningitis
Neisseria
• Gram- diplococci
• N. meningitidis
• sporadic x endemic
• children, young adults, soldiers
• nasopharynx  menings
• !!! rapid course  death (hours) !!!
• meningeal syndrom + skin purpura + DIC
• Waterhouse-Fridrichsen syndrome
– meningococcal sepsis + DIC + bleeding in adrenals
(insufficiency)
Neisseria
• N. gonorrhoeae
• gonorrhoea – STD
• purulent inflammation + discharge
• M: urethritis  prostate, vesicles
• F: kolpitis, cervicitis  endometritis 
salpingo-oophoritis  sterility
• distant complication: arthritis (knee)
Escherichia coli
• Gram- rod
• normal in colon x other location - pathogenic
• enteropatogenic – diarrhoea (newborn)
• enteroinvasive – diarrhoea (adults)
• enterotoxigenic – travellers´ diarrhoea
• enterohemorrhagic - verotoxin
– hemorrhagic colitis
– hemolytic-uremic syndrome (children)
Salmonella
• S. typhi – typhoid fever
• food  bowel  liver  gallbladder  bowel
• ileum
• 1. hyperplasia of RES in ileum – typhoid cells
• 2. mucosal necroses upon Peyer patches
• 3. ulcerations
• 4. reparation  scar
• complications
– bowel perforation/hemorrhage
– chronic carriage (gallbladder)
Salmonella
• S. paratyphi – paratyphoid fever

• S. enteritidis, S. typhimurium
• gastroenteritis + enterocolitis
• alimentary
• vomiting + diarrhoea
Campylobacter + Helicobacter
• Campylobacter jejuni
• infants
• diarrhoea
• Helicobacter pylori
• asymptomatic
• etiology of:
– chronic gastritis
– peptic ulcer of stomach and duodenum
– gastric carcinoma
– gastric MALT-lymphoma
Vibrio
• V. cholerae – cholera
• water, food, ill man
• massive watery diarrhoea (15 l) !!!
• NO inflammation x enterotoxin
• dehydration  collapse

• cholera nostras - enterotoxins


Klebsiella
• K. pneumoniae
• pneumonia
• lung + liver abscesses

• K. rhinoscleromatis
• ulcerations of upper airways
Clostridium
• Cl. tetani – tetanus
• wound  toxins (blood, nerves)  spinal cord 
spasms of striated muscles (necroses)
• risus sardonicus + opisthotonus
• 10-50% mortality
• Cl. botulinum - botulism
• meal from tins (toxin)
• visual disturbances, muscle paralysis 
respiratory insufficiency + arrhythmias  death
Clostridium
• Cl. perfringens
• wound  emphysematous gangrene

• Cl. difficile
• pseudomembranous enterocolitis
• after ATB treatment
Mycoplasma
• NO cellular wall
• children + young adults

• M. pneumoniae
– pneumonia, otitis, sinusitis
• M. hominis
– non-gonococcal urethritis
• Ureaplasma urealyticum
– non-gonococcal urethritis
Rickettsia
• intracellular
• R. prowazeki – spotted fever (typhus exanthematicus)
• ill man  louse (Pediculus h. corporis)  skin wound
• endothelium (+ vasculitis)  blood circulation
• skin exanthema + petechiae
• encephalitis + myocarditis
  mortality (20-70%)
• recurrence (20 years) – Brill-Zinser disease (LN)
Rickettsia
• R. rickettsii – Rocky Mountain fever
• tick (Dermacentor)

• Coxiella burnetii - Q fever


• Australia
• animal milk, dust inbreathing
• atypical pneumonia
• liver + bone granulomas
Routes of Bacterial Infection
• Respiratory tract
• Gastrointestinal Tract
• Genitourinary tract
• Unnatural routes opened up
by breaks in mucous
membranes or skin
• Different levels of host
defense mechanisms are
enlisted depending on the
number of organisms
entering and their virulence.
Immune Response to Bacteria
• Extracellular Bacteria
– Humoral immune response
– Humoral antibodies produced by plasma cells
in regional lymph nodes and submucosa of
respiratory and gastrointestinal tracts
– The antibodies remove the bacteria and
inactivate bacterial toxins to protect the host
cell from invading organisms.
• Antibody neutralizes
bacterial toxins
• Complement activation
• Antibody and complement
split product C3b bind to
bacteria, serving as opsonins
to increase phagocytosis.
• C3a and C5a induce local
mast cell degranulation
• Other complement split
products are chemotactic for
neutrophils and
macrophages.
Immune Response to Bacteria
• Intracellular Bacteria
– Cell-mediated immune response (Delayed-type
hypersensitivity)
– Activate Natural Killer (NK) cells provide early
defense against bacteria.
• In delayed type
hypersensitivity,
cytokines secreted by
CD4+ T cells, such as
IFN gamma, activate
macrophages to kill
ingested pathogens
more effectively.
Bacterial Evasion of Host Defense
Mechanism
• Four Steps in Bacterial Infection
–Attachment to host cells
–Proliferation
–Invasion of host tissue
–Toxin-induced damage to host cell
Many bacteria have developed ways to overcome
some of these host defense mechanisms
Contribution of the Immune
Response to Bacterial Pathogenesis
• Disease can also be caused by the immune
response to the pathogen.
• Pathogen-stimulated overproduction of
cytokines can lead to symptoms of bacterial
septic shock, food poisoning, and toxic shock
syndrome.
Contribution of the Immune
Response to Bacterial Pathogenesis
• Bacteria that can survive intracellularly within
infected cells can result in chronic antigenic
activation of CD4+ T-cells, leading to tissue
destruction by a cell-mediated response with
characteristics of a delayed type hypersensitivity
reaction
• Cytokines secreted by CD4+ cells can accumulate,
leading to the formation of granulomas. The
concentrations of lysosomal enzymes in the
granulomas can cause tissue necrosis.
Diphtheria (Corynebacterium
diphtheriae)
• Gram positive, rod-like organism
• Bacterial disease caused by a
secreted exotoxin.
• Spread via airborne respiratory
droplets
• Exotoxin destroys underlying
tissue, forming a tough, fibrous
membrane compose of fibrin,
white blood cells and dead
respiratory cells
• Also responsible for systemic
manifestations.
Symptoms of Diphtheria
• Damage to different organs such
as the heart, liver, kidneys and
nervous system.
• Choking layer of bacteria and
dead cells in the respiratory
system, accompanied by an
unworldly stench
• Difficulty swallowing and
breathing
• Pus and blood discharge through
nostrils following death from
asphyxiation
More info on diphtheria……
• The exotoxin is encoded by the tox gene carried by phage
B (beta)
• Some strains can exist in the state of lysogeny.
• Exotoxin has two disulfide linked chains, a binding chain
and a toxin chain. The binding chain interacts with
ganglioside receptors on susceptible cells, facilitating
internalization of the exotoxin.
• Inhibitory effect of toxin chain on protein synthesis leads
to toxicity.
• Removal of the binding chain prevents exotoxin from
entering the cell.
How We Treat This Bad Boy….
• Toxoid prepared by treating diphtheria toxin with
formaldehyde.
• Reaction with formaldehyde cross-links the toxin,
resulting in loss of toxicity and enhancement in its
antigenicity.
• Usually administered with tetanus toxoid and inactivated
Bordetelal pertussis in a combined vaccine that is given to
children 6-8 weeks of age.
• Immunization with toxoid induces production of
antibodies which bind to the toxin and neutralize its
activity.
The reaction that
results from the
vaccine
Photo Ops of Diphtheria (Smile!)
Tuberculosis (Mycobacterium
tuberculosis)
• Bacilli shaped organism
• Pulmonary infection by inhalation of
small droplets of respiratory
secretions containing a few bacilli
• Inhaled bacilli are ingested by
alveolar macrophages and multiply
intracellulary by inhibiting formation
of phagolysomes.
• Macrophages lyse and large numbers
of bacilli are released.
• Cell mediated response by CD4+ T
cells may be responsible for much of
the tissue damage of the disease.
• Most common infection of
tuberculosis is pulmonary
tuberculosis.
Symptoms of Tuberculosis
• Symptoms of TB depend on where in
the body the TB bacteria are growing.
TB bacteria usually grow in the lungs.
TB in the lungs may cause
– a bad cough that lasts longer than 2
weeks
– pain in the chest
– coughing up blood or sputum
(phlegm from deep inside the
lungs)
• Other symptoms of TB disease are
– weakness or fatigue
– weight loss
– no appetite
– chills
– fever
– sweating at night
Immune Response to Tuberculosis
• Cytokines produced by CD4+ T cells activate
macrophages, which kill the bacilli or inhibits their
growth.
• High levels of interleukin-2 (IL-2), produced by
macrophages, stimulates Th 1-mediated responses.
• IL-2 may also contribute to resistance by inducing
production of chemokines that attract macrophages to the
site of infection.
• CD4+ T cell mediated response mounted by those exposed
to M. tuberculosis controls the infection and protects
against later infection.
Treatment and Vaccines
• Tuberculosis is treated with
several drugs including isoniazid,
rifampin, streptomycin,
pyrazinamide, and ethambutol.
• Drug therapy must continue for at
least 9 months to get rid of the
bacteria since the intracellular
growth of M. tuberculosis makes it
difficult for the drugs to reach the
bacilli.
• Vaccine : attenuated strain of M.
bovis called BCG (Bacillus
Calmette-Guerin) Most effective
against extrapulmonary
tuberculosis. Not used in the U.S.
though. Sorry!
Tuberculosis Links! Yay!
• http://www.phppo.cdc.gov/PHTN/tbmodule
s/modules1-5/m1/anim.htm
• http://www.phppo.cdc.gov/PHTN/tbmodule
s/modules1-5/m3/photos/3photo3.9.htm
• http://www.phppo.cdc.gov/PHTN/tbmodule
s/modules1-5/m3/photos/3photo3.8.htm
• http://www.cdc.gov/ncidod/diseases/subme
nus/sub_tuberculosis.htm
Lyme Disease (Borrelia burgdoferi)
• Helical shaped bacteria
• Disease spread by bite from
an infected deer tick
• Enters the bloodstream and
spreads to different organs
in the body
• Arthritic symptoms and
neurologic symptoms can
develop. Most people
complain of headaches and
some people develop
meningitis or encephalitis.
Immune Response
• Antibodies to a protein associated with
the flagella of B. burgdorferi is usually
detected after infection and may
contribute to pathogenesis.
• Antigen-antibody complexes can
activate complement system, resulting
in direct lytic damage to the joints or
vasculature.
• Interleukin 1 (IL-1) said to be involved
in pathogenesis of Lyme disease, since
Borrelia has a cell wall containing
lipopolysaccharide (LPS) and LPS is a
well known inducer of IL-1
• Most humans develop antibodies to a
flagellar antigen, while mice develop
antibodies to two proteins on the outer
surface of the bacterial envelope.
How do we treat it?
• Lyme disease can be
successfully treated with
broad-spectrum antibiotics
such as penicillin and
tetracycline.
• A vaccine based on outer-
surface protein A suggests
that it offers significant
protection. The vaccine was
approved for use in January
1999.
Online Information on Lyme
Disease
• http://www.cdc.gov/ncidod/dvbid/lyme/ind
ex.htm
– This is just some general info on Lyme Disease
• http://phil.cdc.gov/Phil/detail.asp?id=2417
– This is a up close and personal picture of
Borrelia burgdorferi

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