-Pathogenic Bacteria-

Mechanisms of pathogenicity and diseases

Biol 385- Lebanese International University

 Bacteria

Gram-positives Gram-negatives

Cocci Bacilli

Staphylococcus Corynebacterium diphtheriae

Staphylococcus aureus
Staphylococcus epidermidis Bacillus anthracis

Streptococcus
Streptococcus agalactiae Listeria monocytogenes
Streptococcus pneumoniae
Streptococcus pyogenes
Clostridium botulinum
Clostridium perfringens
Clostridium tetani

Biol 385- Lebanese International University

 Bacteria

Gram-negatives Gram-positives

Cocci Bacilli Spirochete

Neisseria Enteric Bacilli Non enteric Bacilli

Neisseria gonorrhoeae
Neisseria meningitidis Escherichia Vibrio
Salmonella species
Helicobacter
Shigella species
Pseudomonas
aeruginosa

Biol 385- Lebanese International University

 Staphylococcus

Staphylococcal bacteria:
S. aureus
S. epidermidis

.Gram+, spherical shape, grapes.

These bacteria:
. are present on the skin and mucous
membranes of humans.
. have a capsule
. Both produce catalase Staphylococcus:
. are facultative anaerobes

Catalase Test:
(+) in the left tube
(-) In the right tube

Biol 385- Lebanese International University

 Staphylococcus aureus

S. aureus :
. aureus: as it forms golden colonies
. catalase positive like all Staphylococci
. the only staphylococci coagulase +
converts plasma fibrinogen to insoluble fibrin.
. the most virulent and best-known member of the genus

. Superantigen exotoxin: enterotoxin causing septic shock

S. aureus: S. aureus:
. Mb-disrupting exotoxins:
Golden colonies β hemolytic colonies
Leukocidins
Hemolysins (α, β and δ)
. Protein A: cell wall virulence factor

Coagulase Test:
(-) on the left for S. epidermedis
Biol 385- Lebanese International University
(+) on the right for S. aureus
S. aureus virulance factors:

a) Immunoglobulin binds on the cell wall, recruits Polymorph 1. S. aureus produces coagulase 2. Fibrin clot forms around
nuclear (PMN) White cells that will phagocyte the Bacteria pathogen protecting it
b) S. aureus protein A: a cell wall virulent factor against phagocytosis.
that prevents IgG to recruit PMN protecting S. aureus

Biol 385- Lebanese International University

S. aureus: cutaneous (skin) diseases and wound infection:

Folliculitis: infection of hair Impetigo: pustules that Furuncles : when folliculitis spreads to
follicles. become crusted. involve subcutaneous tissue.

- Bullous impetigo:

Biol 385- Lebanese International University

A localized form
of Staphylococcal
Scalded Skin Syndrome
(SSSS).
- It is caused by
exfoliative Toxins .
that split desmosomes. Lesions of scalded skin syndrome:
toxin production that causes the
Skin to peel off in sheets.
S. aureus: Toxic shock syndrome
• It starts most commonly as a vaginal infection in menstruating women
using tampons.
• The disease is initiated with the localized growth of toxin-producing S. aureus in the
vagina or a wound, followed by release of the toxin into the blood.
• It is followed by a sudden onset of high fever, vomiting, diarrhea, red rash (macular
erythematous), and shock due to TSS-1 (Heat resistant protein).
• This is followed 1-2 weeks later by desquamation (skin peeling).
• Toxin production requires an aerobic atmosphere and neutral pH.
• TSS-1 is a superantigen:
• Stimulate release of cytokines (IL-1)
• Producing leakage of endothelial cells at low concentration
• Cytotoxic effect at high concentration
Macular erythematous caused
• Death is caused by hypovolemic shock leading to multiorgan failure by TSS-1: a superantigen

S. aureus: Food poisoning caused by Toxin that may lead to septic shock.

Biol 385- Lebanese International University

 Staphylococcus epidermidis

. White colonies on agar

. Catalase positive like all Staphylococci
. Coagulase negative

Disease:
Bacteremia, infection of implants (heart valves) S. epidermedis:
white colonies on agar
Pathogenesis:
cell envelope factors facilitate their attachment to plastic surface: catheters.

S. epidermidis:
Biol 385- Lebanese International University heart valves infections and endocarditis
 Streptococcus

3 streptococcal bacteria:
Streptococcus pyogenes
Streptococcus agalactiae
Streptococcus pneumonia

. Gram-positive, spherical shape, non-motile have a capsule.

. Most are facultative anaerobes.
. streptococci are catalase-negative

Streptococcus :
Gram+, spherical shape, chain organisation

Biol 385- Lebanese International University

 Streptococcus pyogenes

S. pyogenes
1. The most virulent member of this group.
2. Catalase-negative: does not survive well in the
environment.
3. β-hemolytic: complete hemolysis.

Pathogenesis :
Have M and F protein: mediates adherence
Exotoxins: streptolysin O and S, streptokinase
Pyrogenic exotoxins: A, B and C

S. pyogenes: cell wall structure organisation

Biol 385- Lebanese International University

Streptococcus pyogenes: skin diseases

Streptococcal gangrene: destruction of the fibrous

Impetigo caused by S. pyogenes in older children: tissue deep in the skin that covers the muscle.
isolated pustules that become crusted (”flesh eating bacteria”)

Biol 385- Lebanese International University

Streptococcus pyogenes: other diseases

Pharyngitis caused by S. pyogenes Scarlet fever caused by S. pyogenes with Erythematous rash on the
erythematous (red) with a grayish-white exudate. chest ( left photo) and Strawberry tongue (right photo): with red
The tonsils and lymph nodes are enlarged. spots on a yellowish-white colored tongue

Biol 385- Lebanese International University

Streptococcus pyogenes: other diseases

Nodules because of rheumatic fever caused by

S.pyogenes: Subcutaneous nodules appear at
the joint

Biol 385- Lebanese International University

 Streptococcus pneumoniae

• S. pneumoniae colonizes the oropharynx and is able to spread to the middle ear or/ and to
the lungs. It may pass into the blood reaching the brain and causing meningitis
• Produces pneumolysin (a pore forming toxin) that causes localized damage by creating
pores
• Has polysaccharide capsule that protects it from phagocytosis. This capsule can be
purified and used in vaccination.

Streptococcus agalactiae

• β-Hemolytic
• Disease: Leading cause of meningitis : meningitis is an inflammation of the
membrane that covers the brain and spinal cord.

Biol 385- Lebanese International University

 Corynebacterium diphteriae

• Gram positive pleomorphic rod, non-motile, no spores, unencapsulated

• Facultative anaerobe.
• They normally colonize the skin, upper respiratory tract, gastrointestinal tract, and
urogenital tract in humans.

• The symptoms of diphtheria usually begin two to seven days after infection. Symptoms of
diphtheria include fever of 38 °C (100.4 °F) or above, chills, fatigue, bluish skin coloration
(cyanosis), sore throat, hoarseness, cough, headache, difficulty swallowing, painful
swallowing, difficulty breathing, rapid breathing, foul-smelling and bloodstained nasal
discharge, and lymphadenopathy.[8][9] Symptoms can also include cardiac arrhythmias,
myocarditis, and cranial and peripheral nerve palsies.

Corynebacterium diphteriae:
Shape and Gram staining

Biol 385- Lebanese International University

 Corynebacterium diphtheriae
Pathogenisis:
Diphtheria exotoxin is an A-B toxin . Receptors of this exotoxin are present particularly on heart and nerve
cells. Its catalytic region (the A subunit): inactivating elongation factor eEF2 therefore inhibiting protein
synthesis and causing severe disease in the heart and nervous system.
Disease:
- Opportunistic pathogens, cause diphtheria
Infection of the throat (upper respiratory tract).
- Cutaneous diphtheriae
. Acquired by skin contact with other infected persons
. Colonize the skin and enter into subcutaneous tissue through breaks
in the skin;
. A papule (a small pimple) develops first, then evolve to chronic,
nonhealing ulcer.
. Sometimes S. aureus or S. pyogenes are also present in the wound

Exudative pharyngitis: diphtheria white

Pseudo-membrane composed of bacteria
white blood cells, fibrin and dead cells covering
the tonsils. This pseudo-membrane adheres firmly
and is difficult to dislodge.
Cutaneous diphtheriae Biol 385- Lebanese International University
 Bacillus anthracis

Gram positive, rod-shaped, forms endospores, have a capsule,

Facultative anaerobes

Virulence factors:
- Capsule helps organism to resist phagocytosis.
- Exotoxin produced only when the bacteria is growing
in animal tissues.
Disease:
- Anthrax (cutaneous, gastrointestinal, inhalation)
- Anthrax is an enzootic disease.

B. anthracis: morphology and spores

Biol 385- Lebanese International University

 Bacillus anthracis
Spores may be acquired:
- through wounds,
- by inhalation,
- or by ingestion.
The disease that develops depends upon the mode of transmission:
- Pulmonary spores are inhaled and germinate in the lungs where they multiply causing edema and will spread to
cause fatal septicemia or meningitis. This is the most serious form of the disease.
- Intestinal anthrax results from ingestion of spores.
- In humans: anthrax gives rise to skin infections---->Papule --> pustule --> necrotic ulcer (ischar) --> septicemia -->
meningitis or hemorrhagic pneumonia

Biol 385- Lebanese International University

C

Evolution of cutaneous anthrax (ischar). If not treated septicimia might be the next stage.
 Clostridium
3 clostridial bacteria:
Clostridium perfringens
Clostridium tetani
Clostridium botulinium
A- typical organism
- Anaerobic gram +ve sporeforming rods: unable to use O2 to detoxify H2O2
- The spore is terminal in C. Tetani
- In the various species: spore is central, sub-terminal or terminal
- Most are motile-peritrichous

B- Growth condition and culture

- Anaerobic conditions: agar or broth in anaerobic jar
- In thioglycollate medium
- They can ferment sugars and digest proteins

C- prevention and treatment

- Active immunization
- Proper care of wounds
- Use of antitoxin: The antitoxin can neutralize toxin only before fixation onto CNS
- Administration of penicillin
Biol 385- Lebanese International University
 Clostridium tetani Clostridium botulinum

Gram (+), spore-forming, anaerobic, rods shape Gram (+), strict anaerobes, Spore-forming, rod-shaped
Are widely distributed in soil and water Are widely distributed in soil, water,

Disease: Disease:
. Tetanus (Lock Jaw) . Botulism : flaccid paralysis
Pathogenesis: Pathogenesis
. A-B toxin: tetanospasmin
The botulinum toxin act at the neuromuscular junction and
. This neurotoxin reaches the CNS and binds to nerve cells that
prevent the transmission of signal from the nerve cell to the
control the contraction of skeletal muscle, and block the muscle
muscle Inhibiting the release of neurotransmitter called

Biol 385- Lebanese International University

relaxation
acetylcholine

C. tetani

C. botulinum
Tetanus (Lock Jaw)
spores

C. Tetani: mode of action of tetanospasmin.
This neurotoxin reaches the CNS and binds
to nerve cells that control the contraction
of skeletal muscle, and block the muscle
Relaxation leading to Tetanus (Lock Jaw).
Biol 385- Lebanese International University
C. Botulinum: mode of action of botulinum toxin.
Following ingestion, toxin is absorbed from the intestine
and transported via blood and lymph to the PNS.
The first symptoms include nausea, vomiting,
and diarrhea followed by symmetric, descending
paralysis (eyes, throat, neck, trunk, and then the limbs)
Paralysis of respiratory muscles results in death.
 Listeria monocytogenes

Gram positive rods, sometimes occur as diplobacilli, motile, facultative

anaerobes, Nonsporing and noncapsulated
Catalase positive

Pathogenesis:
- Infections are usualy foodborne
- Capable of growth at 4°C
- Escape from phagocytosis by secreting an exotoxin : listeriolysin O

Listeriosis disease includes:

- Lesions may be found in the liver, spleen, adrenals, respiratory tract, CNS, and skin. Meningitis with
septicemia and pneumonia and a high mortality rate may occur.
- Pregnancy renders an individual more susceptible to the infection, the effect on the mom is usually
minimal. It can be devastating for the fetus or newborn: This may result in abortion, stillbirth, premature
delivery, or death soon after birth.
- Listeria should always be suspected in patients with organ transplants.

Biol 385- Lebanese International University

 Listeria monocytogenes
Invasion mechanism:

3-Using actin Filament to move.

1-Ruffling Pseudopod formation to cross
from one cell to another

4- Invasion
2- Breaking
the endosome
by phospholipase
secretion

Biol 385- Lebanese International University

 Listeria monocytogenes
Transmission mode and diseases:

Rash caused by Listeria

Biol 385- Lebanese International University

 Enterobacteriaceae

- Classification – more than 40 different genera

• Escherichia
• Shigella
• Salmonella
- Morphology and General Characteristics
• Gram-negative, non-sporing, rod shaped bacteria
• Oxidase negative.
• facultative anaerobes
• Ferment glucose: Distinguishes among other fermentative and non-fermentative Gram negative bacilli

- Some are always associated with disease e.g., Shigella, Salmonella,

- Some are normal flora that can become opportunistic pathogens e.g., E. coli

Biol 385- Lebanese International University

 Enterobacteriaceae: E. coli

. Adherence

Adherence:
Enterobacteriaceae adheres on eukaryotic cells,
through interaction between fimbrial adhesins’ and
host cell receptors

Biol 385- Lebanese International University

 Enterobacteriaceae: E. coli

Enterotoxigenic (ETEC)
- is a common cause of traveler’s diarrhea and diarrhea in children in developing countries.
- it attaches, using pili, to the intestinal mucosa and then liberates enterotoxin. Mediated by heat-labile/ LT
(like cholera) and heat-stable exotoxins/ ST.
- the disease is characterized by a watery diarrhea, nausea, abdominal cramps and low-grade fever for 1-5 days.
- Transmitted through contaminated food or water.

Virulence factors
Enterotoxigenic (ETEC)

(epithelial cells
of the intestine)

Biol 385- Lebanese International University

 Enterobacteriaceae: E. coli

Enteropathogenic (EPEC)- childhood diarrhea

-The exact mode of pathogenesis is unclear, but watery diarrhea with large amounts of mucous without blood and
with low grade fever.
-This is a problem mainly in hospitalized infants (less than 1 year old).
- Organism adheres through pili to enterocyte plasma membrane.

Enterohemorrhagic (EHEC; hemorrhagic colitis)

- It attaches via pili to the intestinal mucosa and liberates the shiga-like toxin.
- The symptoms start with a watery diarrhea that progresses to bloody diarrhea with no fever or a low-grade fever.
It affects children < 5 years.
- This may progress to hemolytic-uremic syndrome, hemolytic anemia, and kidney failure because of Siga like toxine:
this is most often caused by serotypes O157:H7. This strain of E. coli can be differentiated from other strains of E. coli
by the fact that it does not ferment sorbitol in 48 hours (other strains do).
- Transmitted through undercooked meat, uncooked vegetables and fruits, Water, unpasteurized milk or fruit juices

Biol 385- Lebanese International University

Virulence factors
Enterohemorrhagic (EHEC)
 Enterobacteriaceae: E. coli

Enteroinvasive (EIEC)
. Present in the large intestin
. Cannot ferment lactose
. Adhere to epithelial cells, internalised by endosomes, rupture the endosome, use actin filament to invade
adjacent cells, leading to the epithelium destruction which dysentery like symptom
with fever and bloody stools (resembles to Shigella pathogenesis)

(EIEC) Adherence

Biol 385- Lebanese International University

 Enterobacteriaceae: E. coli

Summary of the pathogenicity of E.coli strains that cause gastroenteritis.

Various types of E. coli: differences in

pathogenicity
Biol 385- Lebanese International University

Summary of E.coli strains that cause gastroenteritis.
Enteropathogenic E. coli (EPEC)
Enterotoxigenic E. coli (ETEC)
Enterohemorrhagic E. coli (EHEC)
Enteroinvasive E. coli (EIEC)
Enterobacteriaceae: E. coli
Small intestine . Infant diarrhea
. vomiting,
. nonbloody stools
. ferment glucose and lactose
Small intestine . Traveler's diarrhea
. vomiting, Cramps, nausea
. Ferment glucose and lactose
Large intestine . bloody diarrhea with abdominal cramps;
. Ferment glucose and lactose
. Can ferment sorbitol slowly
Large intestine . fever, cramping. progress to dysentery: bloody stools
. Ferment glucose
. Cannot ferment lactose
Biol 385- Lebanese International University
 Enterobacteriaceae: E. coli
E. coli causing urinary tract infections :
- Originate from gastrointestinal tract
- Is the leading cause of urinary tract infections which can lead
to acute cystitis (bladder infection) and pyelonephritis (kidney
infection).

Biol 385- Lebanese International University

 Enterobacteriaceae: Salmonella typhi
. Source of most infections
- Ingestion of contaminated water, food, Poultry, eggs, and dairy products
- Need to be ingested with large number of organisms (106/8)
- fecal-oral contamination in children.
. Virulence factor: Antigenic variation

Antigenic variation of Salmonella:

. 2 form of Flagellar antigen: H antigen (flagellin protein)
might be expressed from 2 different genes
. O antigen: part of LPS ( saccharides) is not involved in this process
Biol 385- Lebanese International University
 Enterobacteriacae: Salmonella typhi

. Disease/ Symptoms

- Gastroenteritis (most common):

. Symptoms 6-48 hours after ingestion
. Nausea, vomiting, non-bloody diarrhea
. Elevated temperature, abdominal cramps, muscle cramps, headache
. Symptoms persist for 2 days to a week
For gastroenteritis the Salmonella multiply and their presence induces a strong inflammatory response
which causes most of the symptoms seen in gastroenteritis (mild to moderate fever with diarrhea and
abdominal cramps). The inflammatory response prevents the spread beyond the GI tract and
eventually kills the bacteria (refer to the next slide).

- Enteric (typhoid) fever:

. Gradually increasing fever
. Headache, muscle aches, malaise (general feeling of discomfort), and decreased appetite; gastrointestinal symptoms.
In enteric fevers (typhoid) the Salmonella disseminate into the blood before they multiply to high
enough levels to stimulate a strong inflammatory response (refer to the next slide).

Biol 385- Lebanese International University

 Enterobacteriacae: Salmonella typhi
How S. typhi causes disease?

Invasion of host intestinal cells by S. typhi:

-Salmonella adheres to intestinal epithelium (M cells).
-Salmonella multiplies within the endosome.

. For gastroenteritis the Salmonella multiply and

their presence induces a strong inflammatory response
which causes most of the symptoms seen in gastroenteritis
(mild to moderate fever with diarrhea and abdominal cramps).
The inflammatory response prevents the spread beyond
the GI tract and eventually kills the bacteria.

. In enteric fevers(typhoid) the Salmonella

disseminate before they multiply to high enough levels
to stimulate a strong inflammatory response.

Biol 385- Lebanese International University

 Enterobacteriacae: Shigella
How Shigella causes disease?

- Shigella destroy the vacuoles to escape into the cytoplasm.

From there they spread laterally : Cell-to-cell passage
(Polymerization of actin filaments propels them through the
cytoplasm.) to epithelial cells where they multiply but do not
usually disseminate beyond the epithelium: in the blood.
- causes shigellosis or bacillary dysentery:
there is an incubation of 1-7 days followed by fever,
cramping, abdominal pain, and watery diarrhea (due to the toxin,
Shiga toxin)
for 1-3 days. This may be followed by frequent,
scant stools with blood, mucous, and pus (due to invasion
of intestinal mucosa).

- transmission is via the fecal-oral route.

- the infective dose required to cause infection is very low
(100-200 organisms).

Shigellosis: the sequence shows How Shigella invade

Intestinal M cells?
 Vibrio cholerae

Vibrio species are :

- found in salt water and in the intestines of human
- Gram negative straight or curved rods with polar flagella
- Facultative anaerobes
- Oxidase positive
- Transmitted by:
. contaminated water and blood
. Raw or undercooked seafood harvested from contaminated waters.
. contaminated fruits and vegetables can transmit the disease.

People with type O blood group are more susceptible. V. cholerae: curved rods with polar flagella

Biol 385- Lebanese International University

 Vibrio cholerae

Net movement of ions and water across intestinal cells

Symptoms caused by cholera toxin
in the absence or presence of cholera toxin
Biol 385- Lebanese International University
 Pseudomonas aeroginosa

Morphology and structure :

- In pairs but similar to one cell (Pseudo/monas)
- Gram— bacterial
- Polar flagella; motile
- Obligate aerobe, opportunistic pathogen
- Have a capsule

P. aeroginosa : morphology

Biol 385- Lebanese International University

 Pseudomonas aeroginosa

Virulence factors of P. aeroginosa :

- Some strains appear mucoid due to polysaccharide capsule--
Some produce diffusible pigments: Pyocyanin (blue) that
catalyzes the production of H2O2 and O2-, fluorescin
(yellow), pyoverdine (yellow- green) that is a siderophore
- Presence of cytochrome oxidase (Distinguishes it from
Enterobacteriaceae)
- Have pili Adhesins and non-pilus adhesins
- Have Alginate (mucoid layer): Protects against phagocytosis
and facilitates adherence to host cells

P. aeroginosa producing pyocyanin P. aeroginosa : virulence factors

Biol 385- Lebanese International University
 Pseudomonas aeroginosa

. Endocarditis
- Observed primarily in drug abusers through drug
equipment's
- Anatomy of heart affected with valves abnormalities
- CNS infection ( as a complication)

. Ear infections (otitis)

. Skin infection

. Urinary infection (cystitis):

- Primarily in patients with long-terme Indwelling
- urinary catheters

Biol 385- Lebanese International University

 Helicobacter pylori

Morphology and biochemical characteristics:

- Small, gram-negative, curved rod
- urease + test
- Cannot use carbohydrate
- Oxidase and catalase positive

Morphology of H. pylori
and flagellar lopotrichous organisation
Diseases and clinical manifestations:
- Helicobacter pylori is associated with chronic superficial gastritis (stomach inflammation) and peptic ulcer
disease.
- Increasing evidence indicates that H pylori infection is important in causing gastric carcinoma and
lymphoma.
- Acute infection may cause vomiting and upper gastrointestinal pain. Chronic infection usually is asymptomatic
People with type O blood are more susceptible.

Virulance factors:
- Phospholipase (damages cell memebrane), Protease (hydrolysis digestive enzymes).
- Urease facilitates survival in the stomach by raising the pH, provides access to nitrogenous nutrients needed by the bacteria
for growth, and the NH4+ end product may cause cell damage and inflammation
Flagella – allow bacteria to penetrate through gastric mucous
Biol 385- Lebanese International University
 Helicobacter pylori

Strategies used by H. pylori to survive and grow in the stomach:

- To escape the low pH of the stomach, H. pylori uses the motility to
enter gastric mucus where a more favourable pH exists. H. pylori and ulcer formation:
- Once in the gastric mucus, it produces urease converting after adhering to host cells, H. pylori induces
Urea to ammonium (NH3) as well as CO2 increasing the pH. their destruction (urease, NH4+…) causing ulcer
Some H. pylori cells may move through the mucus and adhere formation
Biol 385- Lebanese International University
to the gastric epithelium….
46
 Helicobacter pylori

. Diseases: Diagnosis:
- Examination of gastric biopsy: definitive diagnosis
is made by culture
- Recently, non-invasive techniques such as the:
serologic tests (antibodies detection) have been developed
Treatment:
- administration of several antimicrobial agents,
including metronidazole, tetracycline, amoxicillin,
and clarithromycin
- No vaccine is yet available.

Biol 385- Lebanese International University

 Neisseria meningitidis

Gram negative, diplococcus, piliated, nonmotile

Ferment glucose AND maltose.

Pathogenesis:
Presence of capsule that prevent phagocytosis

Mode of transmission: N. meningitidis Gram-, diplococcus

Airborne droplet:

Attach to the epithelial cells of the Nasopharynx

Invade columnar epithelial cells of the Nasopharynx

Enter the blood stream

Reach CNS

Attach to meninges

Meningitis
Mode
Biol 385- Lebanese of transmission
International University of N. meningitidis
 Neisseria meningitidis

Disease:
. Meningitis:
- fever can evolve into severe headache,
- a rigid neck,
- vomiting and sensibility to bright lights.
- Coma can occur within a few hours
. Septicemia: blood infection
. Skin rash

Meningococcal skin rash

Biol 385- Lebanese International University
 Neisseria gonorrhoeae

Unencapsulated, piliated, nonmotile

Ferment glucose BUT not maltose, lactose or sucrose.
Transmission:
. Usually transmitted during sexual contact (females
tend to be more susceptible to the disease than men.

Disease:
. Salpingitis: inflammation of the fallopian tubes
. Purulent discharge in males Purulant discharge caused
Salpingitis caused
. Pharyngitis : inflammation of the throat or pharynx by N.gonorrhea
by N. gonorrhea
. Ophthalmia neonatorum: infection of the conjunctival
sac

Pharyngitis caused Ophtalmia neonatorum caused

by N. gonorrhea by N.gonorrhea
Biol 385- Lebanese International University
 Treponema pallidum
-Treponema is a Gram-negative, spirochete,
thin, motile, spiral shaped bacterium (corkscrew-shaped cells)
- Humans are the only source of treponemal infections.
- The bacteria lack necessary enzymes so they rely on the host to
survive.
- Once outside the mammalian host, they lose infectiveness.
- Lack classical LPS in the outer membrane .
- Produce lipoproteins that induce an inflammatory response.

- They are highly invasive pathogens and are sexually transmitted:

Treponema is a spiral shaped bacterium

Sexual contact
(corkscrew-shaped cells

Penetrating the skin due to their corckscrew shape

Pass into the blood

Biol 385- Lebanese International University

Tissue destruction
 Treponema pallidum

Disease:
Syphilis is caused by T. pallidum.
Primary syphilis : painless sores are the site of infection. The sores heal on their
own after 3 to 6 weeks. The disease is contagious.
Secondary syphilis : cutaneous rash, swollen lymph nodes, fever. The disease is
contagious.
Tertiary syphilis: problem controlling muscle movement, numbness, vision problem,
dementia. The disease is not contagious.

Primary syphilis : ulcer that contain bacteria Secondary syphilis :

cutaneous rash
 Mycobacterium tuberculosis

• The basic structure is composed of: Peptidoglycan

and a Waxy layer (mycolic acid).

• The mycolic acid component strongly stimulates

an inflammatory response that causes tissue
damage and remodeling.

• Lipid-rich cell wall responsible for many of the

following properties:
• Acid-fast staining: stained red with Atypical structure of M. tuberculosis cell wall
carbofluscin
• Slow growth
• Resistance to detergents
• Resistance to some antibiotics.
Biol 385- Lebanese International University
 Mycobacterium tuberculosis

Diseases and symptoms:

.Symptoms are almost always pulmonary: cough, hemoptysis, chest pain
.Systemic Symptoms include fatigue, weight loss, fevers, night sweats, …these symptoms probably
due to cytokines…especially TNF-alpha (Tumor Necrosis Factor)

Diagnosis:
. Extracted and partially purified proteins of these proteins derivatives (PPDs) are used as skin test
reagent to measure exposure to M. tuberculosis.
. Acid fast stain on sputum
. X ray of lungs

Tuberculin skin test using PPD as antigen

Tuberculosis, advanced – Acid-fast stain : M. tuberculosis stained
chest x-rays red with carbofluscin
Biol 385- Lebanese International University
from a sputum
Steps in the development of tuberculosis: Mycobacterium tuberculosis

Inhalation of bacteria
M. tuberculosis: enters the respiratory
airways through infectious particles Bacteria reach lungs,
(water droplets) penetrate to the enter macrophages
alveoli where they are phagocytized Dead
by alveolar macrophages. Bacteria reproduce phagocytes,
in macrophages necrosis
M. tuberculosis

Lesion begins to form

(caseous necrosis)
Activated
macrophages
Phagocytes,
T cells, and
Bacteria cease to
B cells
grow; lesion calcifies Lesion Bacteria coughed trying to
liquefies up in sputum kill bacteria
M. tuberculosis
prevents fusion of the phagosome Tubercles : rings of macrophages and
Spread to
with lysosomes. Macrophages secrete blood organs other inflammatory cells surrounding
cytokines that recruits T cells and NK infected cells. caseous (solid cheese-like
cells into the area of the infected macrophages material) in the middle
Death