S. pyogenes is a Gram-positive bacterium that commonly causes infections of the skin and throat. It is transmitted through direct contact with infected individuals. The bacterium produces several virulence factors like M protein, capsule, and streptokinase that help it evade the immune system and spread infection. Common diseases caused include pharyngitis, impetigo, and necrotizing fasciitis. Treatment involves antibiotics like penicillin.

1. SKIN
PATHOGENS
School of Medicine 331
TEAM NO. 1

2. BACILLUS ANTHRAX
School of Medicine – 331
Team no. 1

3. Morphology
• Gram +
• Spore- forming
• Rod shaped
• Aerobic
• Facultative anaerobic
• Capsulated (by plasmid )

4. Anthrax spore
• Central protoblast
dipicolinic acid
• Cortex
peptidoglycan
• Spore coats

5. Antigens
• Capsular antigen (not protective)
• Cell wall antigen (not protective)
• Somatic antigen (in bacterial body, protective)

6. Virulence factor
A. Bacterial capsule
o Non toxic, protection
A. Anthrax toxin complex
i. Protective antigen
ii. Edema factor
iii. Lethal factor

8. Host
• Herbivores ( cattle, sheep, horses)
• Rats, chickens, pigs
• Birds, buzzards

9. Cutaneous Anthrax
• Papule (primary lesion, 1-2 cm)
within 2 days
• Vesicle with edema( bacillus)
necrosis and ulcer
• Black eschar (malignant pustule)
1-2 weeks

10. Diagnosis
• Vesicular fluid, under eschar
single/ in pairs/in short chain/in long chain

11. Treatment
• Penicillin
• Ciprofloxacin and doxycycline

12. Prevention
• Vaccination in animals
• Human vaccination
Anthrax Vaccine Adsorbed (AVA)
3 subcutaneous injections (6 m period)
18-65 age

13. BORRELIA
BURGDORFERI
School of Medicine 331
Team no.1

14. Morphology
• Gram –
• Helical
• Motile
• Microaerophillic

15. Lyme disease
• Tick-borne disease by IXODID TRICK
• Skin
• Spreads locally
• Erythema migrans
• Rash
• Papule (5-50cm)
• Systemic complication

16. Transmission
• Zoonotic disease (Rodents, bear )
• Hard thick

17. STAPHYLOCOCCAL
SCALDED SKIN
SYNDROME
Gantuul N
Class-331
School of Medicine

18. Biology, Virulence, and Disease
Virulence factors include
• structural components that facilitate adherence to host tissues
and avoid phagocytosis
• a variety of toxins and hydrolytic enzymes
Diseases include
• toxin-mediated diseases (food poisoning, TSS, scalded skin
syndrome),
• pyogenic diseases (impetigo, folliculitis, furuncles, carbuncles,
wound infections)
• other systemic diseases
Hospital- and community-acquired infections with MRSA
are a significant worldwide problem.

19. Morphology
• Gram-positive cocci
• Nonmotile, nonsporing
• Noncapsulated
• Contain a microcapsule, which can be visualized by
electron microscope only, but not by a light microscope.
• The cocci are typically arranged in irregular grape-like
clusters.
• In smears taken from pus, the cocci are present either
singly or in pairs, in clusters, or in short chains of three or
four cells.

20. Virulence factors & Biological functions
Cell wall associated polymers and proteins
• Peptidoglycan- Inhibits chemotaxis of inflammatory cells
• Capsular polysaccharide- Inhibits phagocytosis and chemotaxis
• Teichoic acid- Mediates attachment of staphylococci to mucosal cell
• Protein A- Chemotactic, anticomplementary, and antiphagocytic; causes
platelet injury; and elicits hypersensitivity reactions
Enzymes
• Coagulase -The enzyme coats the bacterial cells with fibrin, rendering
them resistant to opsonization and phagocytosis
• Catalase -Produces nascent oxygen which causes oxidative damage to
host tissue
• Hyaluronidase- Hydrolyzes hyaluronic acids present in the matrix of the
connective tissues, thereby facilitating the spread of bacteria in the
tissues
• Penicillinase - Inactivates penicillins
• Nuclease - Hydrolyzes DNA
• Lipases- Hydrolyzes lipids

21. Virulence factors & Biological functions
Toxins
• Toxic shock syndrome toxin- Superantigen, stimulates
the release of large amount of interleukins (IL-1 and IL-2)
• Enterotoxin- Superantigen, acts by producing large
amounts of interleukins (IL-1 and IL-2)
• Exfoliative toxin- Splits intercellular bridges in the
stratum granulosum of epidermis of the skin
• Leukocidin toxin -Leukolysin is thermostable and causes
lysis of leukocytes
• Hemolysin- Causes lysis of erythrocytes

22. Epidemiology
• Normal flora on human skin and mucosal surfaces
• Organisms can survive on dry surfaces for long periods
• Person-to-person spread through direct contact or exposure to
contaminated fomites (e.g., bed linens, clothing)
• Risk factors include
• presence of a foreign body (e.g., splinter, suture, prosthesis, catheter),
• previous surgical procedure,
• use of antibiotics that suppress the normal microbial flora
• Patients at risk for specific diseases include
• infants (scalded skin syndrome),
• young children with poor personal hygiene (impetigo and other cutaneous
infections),
• menstruating women (TSS),
• patients with intravascular catheters (bacteremia and endocarditis) or shunts
(meningitis)
• patients with compromised pulmonary function or an antecedent viral respiratory
infection
• MRSA now the most common cause of communityacquired skin and soft-
tissue infections

23. • S. aureus causes disease through the production of toxins
or through the direct invasion and destruction of tissue.
• The clinical manifestations of some staphylococcal
diseases are almost exclusively the result of toxin activity
• SSSS
• staphylococcal food poisoning
• TSS
• other diseases result from the proliferation of the
organisms, leading to abscess formation and tissue
destruction

24. Staphylococcal Scalded Skin
Syndrome
• is characterized by the abrupt onset of a localized perioral
erythema (redness and inflammation around the mouth)
that spreads over the entire body within 2 days
• Slight pressure displaces the skin (a positive Nikolsky
sign), and large bullae or cutaneous blisters form soon
thereafter, followed by desquamation of the epithelium.
• The blisters contain clear fluid but no organisms or
leukocytes, a finding consistent with the fact that the
disease is caused by the bacterial toxin.
• The epithelium becomes intact again within 7 to 10 days,
when antibodies against
• the toxin appear

26. Treatment, Prevention, and Control
• Localized infections managed by incision and drainage;
antibiotic therapy indicated for systemic infections
• Empiric therapy should include antibiotics active against
MRSA strains
• Oral therapy
• Treatment is symptomatic for patients with food poisoning
(although the source of infection should be identified so
that appropriate preventive procedures can be enacted)
• Proper cleansing of wounds and use of disinfectant help
prevent infections
• Thorough hand washing and covering of exposed skin
helps medical personnel prevent infection or spread to
other patients

27. Bullous impetigo
• Is a localized form of SSSS.
• In this syndrome, specific strains of toxin-producing S.
aureus are associated with the formation of superficial
skin blisters.
• The disease occurs primarily in infants and young children
and is highly communicable.

30. Smallpox party

31. Variola

32. Pathogenesis
• Inhalation
• Direct contact
• Enter to host
• Replication
• Spread
• Viremia
• -clinical manifestation

33. Clinical manifestation
• After incubation period, onset of high fever (usually not
infectious)
• Malaise, prostration with headache and backache
• Rash develops 1-2 days later (infectious)
• First appears on tongue, mouth, oropharynx
• Spreads to face, forearms 2-3 days later
• Finally appears on trunk and legs
• Rash becomes vesicular then pustular
• Most infectious from rash onset to first 7-10 days of rash
• Death from smallpox occurs in 2nd week of illness due to
toxemia

34. Smallpox Rash
• Stages of rash: maculopapular → vesicular → pustular
• Smallpox rash has centrifugal distribution (i.e., most
dense on face, then extremities)
• Synchronous lesions (appear during a 1-2 day period
and evolve at the same rate)

35. FEVERRASH
Pre-
eruption
Papules-Vesicles Pustules Scabs
Onset of rash
Day
s
–
4
–
3
–
2
–
1
1 2 3 4 5 6 7 8 9 10 11 12 13 14 21
Source: WHO
Smallpox Rash and Lesion Developmen

36. Smallpox Rash Progression
43 5
7 9 13
Source: WHO

37. Smallpox
Rash
3rd Day

38. Smallpox
Rash
5th Day

39. Smallpox
Rash
7th Day

40. VARICELLA ZOSTER
VIRUS

41. • Smallest genome of all human hv
• Enveloped, dsRNA

42. • Virus contact w/ mucosa of RT ,conjuctiva
• Enters blood stream and lymphatic system to RES
• After 11-13 DAYS,secondary viremia occurs
• Spreads through the body and skin
PATHOGENESIS
varicella zoster virus infection

43. • Migrates along the sensory nerve fibers to cranial nerve
ganglia (latent)
• Reactivation- virus replicates and spreads along nerve
fiber to skin -> shingles

44. • - varicella (chickenpox)
• -herpes zoster (shingles)
Varicella zoster

45. PSEUDOMONAS
AERUGINOSA
Gantuul N.
Class-331
School of Medicine

46. Pseudomonas
• family pseudomonadaceae
• obligatory aerobic
• non-fermentative
• oxidase-positive
• motile by presence of one or two flagella
• ubiquitous bacteria, primarily saprophytic

47. Where is it found?

48. Unfortunately, they are also found…
• throughout the hospital environment
• in moist reservoirs
• food
• cut flowers
• sinks
• toilets
• floor mops
• respiratory therapy and dialysis equipment
• even in disinfectant solutions

49. Pseudomonas aeruginosa
• P. aeruginosa is the most important species associated
with human infection. It is a most common human
saprophyte, but it rarely causes disease in healthy
individuals. P. aeruginosa causes most of human
infections in immunocompromised human host.

50. Structure
• straight or slightly curved
• gram-negative bacillus
• 0.5–1.0 1.5–5.0 μm in size
• arranged singly, in pairs, or in short chains
• is motile by the presence of a polar flagellum
• strains may possess two or three polar flagella

51. Physiology
• aerobic respiration-utilizes CH
• the presence of cytochrome oxidase in is used to
differentiate them from the Enterobacteriaceae and
Stenotrophomonas
• Some species produce diffusible pigments that give
them a characteristic appearance in culture and simplify
the preliminary identification.

52. Virulence Factors
• Toxins
• exotoxin A, and exotoxins S and T
• Enzymes
• elastase, alkaline protease, phospholipase C, and rhamnolipid
• Cell wall components
• pili, loose slime layer, LPS, and pyocyanin

53. Cell Wall Components and Antigenic
Structure
• Pili - Adhesion of the bacteria to the epithelial cells
• Slime layer-protects the bacteria from phagocytosis and
against activity of many antibiotics, such as
aminoglycosides
• Capsule - inhibits antibiotics killing of the bacteria
• Lipopolysaccharide - endotoxic activity, sepsis
• Pyocyanin - Causes tissue damage, inflammation

54. Toxins
• Exotoxin A
• one of the most important virulence factor produced by P.
aeruginosa.
• like the diphtheria toxin
• acts by preventing synthesis of proteins in eukaryotic cells.
• is less potent than diphtheria toxin.
• is responsible for causing tissue damage in chronic pulmonary
infection, dermatonecrosis in burns wound, and destruction of
cornea in ocular infection
• also causes suppression of immunity in the infected host

55. Toxins
• Exotoxins S and T
• show adenosine diphosphate ribosyl transferase activity
• these toxins are believed to facilitate spread of bacteria and
invasion of tissues followed by necrosis by causing damage in the
epithelial cells.

56. Enzymes
• Elastase
• serine protease (LasA)
• zinc metalloprotease (LasB)
• destroy elastin present in elastin-containing tissues
• cause damage in parenchymal tissues of the lung and
produce hemorrhagic lesions
• facilitate spread of infection and damage of tissues in
acute infections (by degrading complement, chemotaxis)

57. Enzymes
• Alkaline protease
• responsible for destruction of tissue
• interferes with immune response of the host.
• Phospholipase C
• is a heat-labile hemolysin
• contributes to tissue destruction by breaking down lipids and
lecithin.
• Rhamnolipid
• is a heat-stable hemolysin
• contributes to breaking down of lecithin-containing tissues

58. • The most recognized are infections of burn wounds
• Colonization of a burn wound, followed by
• localized vascular damage
• tissue necrosis
• and ultimately
• The moist surface of the burn and inability of neutrophils
to penetrate into the wounds predispose patients to such
infections.
• Wound management with topical antibiotic creams

60. • Folliculitis is another common infection which result from
immersion in contaminated water.
• Secondary infections with Pseudomonas also occur in
people who have acne or who depilate their legs.
• P. aeruginosa can cause fingernail infections in people
whose hands are frequently exposed to water or frequent
“nail salons.”

61. STREPTOCOCCUS
PYOGENES
group A (beta-hemolytic)
MSS-331
Namuun

63. Streptococcus pyogenes
• Gram-positive
bacterium
• Occur in pairs
• Cells are 0.6-1.0
μm in diameter
• Further subdivided
by serotypes
http://textbookofbacteriology.net

64. Structure

65. Transmission
• Initially colonizes skin
and pharynx
• Person-to-person
spread
-Strains that cause skin
infections are spread via
skin contact
-Strains that cause
respiratory infections are
spread via respiratory
droplets
• The
immunucompromised
are especially
susceptible
http://www.cellsalive.ne

66. History of serotyping
• In 1928, Rebecca Lancefield published a method for
serotyping S. pyogenes based on its M protein, a
virulence factor displayed on its surface.
• In 1946, Lancefield described the serologic classification
of S. pyogenes isolates based on their surface T antigen.
• Four of the 20 T antigens have been revealed to be pili,
which are used by bacteria to attach to host cells.
• Over 220 M serotypes and about 20 T serotypes are
known

69. Capsule: antiphagocytosis. The capsule of group A
streptococci is composed of hyaluronic acid.
Group-specific cell wall antigen (Lancefield group
A)
Carbohydrate
A dimer of N-acetylglucosamine and rhamnose.
M protein: interfere with phagocytosis.
Lipoteichoic acid: binds to epithelial cells.
Protein F: a major adhesin of S. pyogenes, binding
with fibronectin.

70. Streptokinase (fibrinolysin)
Can lyse blood clots and may be responsible for the
rapid spread of the organism.
Used (IV injection) for treatment of pulmonary emboli,
coronary artery thrombosis and venous thrombosis.
Streptodornase (DNases A to D)
Decreases viscosity of DNA suspension. A mixture
of this and streptokinase is used in enzymatic debridement-
liquifies exudates and facilitates removal of pus and necrotic
tissue.
Hyaluronidase (spreading factor):
Destroys connective tissue and aids in spreading
infecting bacteria.
C5a peptidase
Prevents streptococci from C5a-mediated
recruitment and activation of phagocytes, and is important for
survival of S. pyogenes in tissue and blood.

71. Hemolysins
Streptolysin O: O2-labile; causes hemolysis
deep in blood agar plates. ASO
(antistreptolysin O) titer >160-200 units
suggests recent infection or exaggerated
immune response to an earlier respiratory
infection. However, skin infection does not
induce ASO.
Streptolysin S: O2-stable. Causes b-
hemolysis on the surface of blood agar
plates. Cell-bound, not antigenic. Produced
in the presence of serum. Kills phagocytes
by releasing the lysosomal contents after
engulfment.

72. Pathogenesis

73. Adherence to the epithelial cells
Invasion into the epithelial cells
mediated by M protein and protein F
important for persistent infections and invasion into
deep tissues
Avoiding opsonization and phagocytosis
M protein, M-like proteins, and C5a peptidase
Producing enzymes and toxins

74. Laboratory
DiagnosisSmears: useful for soft tissue infections or
pyoderma, but not for respiratory infections.
Antigen detection tests: commercial kits for rapid
detection of group A streptococcal antigen from
throat swabs.
Detection of group A streptococci by molecular
methods: PCR assay for pharyngeal specimens.
Culture: Specimens are cultured on blood agar
plates in air. Antibiotics may be added to inhibit
growth of contaminating bacteria.
Identification: serological and biochemical tests.
Antibody detection
ASO titration for respiratory infections.
Anti-DNase B and antihyaluronidase titration
for skin infections.

75. Treatment
• Penicillin
• Interferes with the
synthesis of a
peptide in the
bacterial cell wall
• Clindamycin
• Inhibits RNA-
dependent protein
synthesis
• Vancomycin
• For people allergic to
penicillin
• Vaccines
http://www.accessexcellence.org/AE/AE
“Staphylococcus aureus growth
is inhibited in the area
surrounding the invading
penicillin-secreting Penicillium
mold colony.”

77. Streptococcus
agalactiae

78. Streptococcus agalactiae
• Physiology and
Structure
Gram (+)
streptococci
Facultative anaerobe
β –hemolytic (1-2%
are nonhemolytic)
Classified by B
antigen

79. S. agalactiae
• contains type-specific capsular polysaccharides
which is the most important virulence factor
• can induce protective antibodies
• may colonize at lower gastrointestinal tract and
genitourinary tract

80. Epidemiology
• Site of colonization:
Lower gastrointestinal tract
Genitourinary tract
• 10% to 30% of pregnant women are carriers.
• 60% of infants born to colonized mothers
become infected with mothers’ organisms.

81. Clinical Diseases
• Pregnant women – UTI’s
• Infections in Men and Non-pregnant women:
• Generally older and/or compromised immunity
• Common infections:
Bacteremia
Pneumonia
Bone and joint infections
Skin and soft-tissue infections

83. Streptococcus agalactiae
• Diagnosis
• Culturing
• Antigen Detection
• DNA (PCR) test
• Treatment
• Penicillin G
• Pregnant women are
give IV 4 hours before
delivery

84. CLOSTRIDIUM
PERFRINGENS

85. •Clostridium perfringens, a gram-
positive endospore-forming
bacterium. The spores of these
species can be found in soil, on
human skin, and in the human
intestine and vagina.

86. Pathogenesis
• Because clostridia are not highly invasive,
infection requires damaged or dead tissue,
which supplies growth factors, and an anaerobic
environment. The low-oxygen environment
results from an interrupted blood supply and the
presence of aerobic bacteria, which deplete
oxygen. Such conditions stimulate spore
germination, rapid vegetative growth in the dead
tissue, and release of exotoxins. C. perfringens
produces several active exotoxins; the most
potent one, alpha toxin, causes red blood cell
rupture, edema, and tissue destruction.

87. Toxins:
1. alpha- toxin
2. 11 other
enzymes
Virulence:
Non-motile
Transmission
1.Soil
2. GI tract
Clinic:
1. Cellulitis
2. Clostridial
myonecrosis
Metabolism
• Anaerobic
Treatment
1. Hyperbaric
oxygen
2. Antibiotics
3. Removal of
necrotic tissue

88. 1. cellulitis/ wound infection 2. Clostridium myonecrosis

89. HUMAN PAPILLOMA
VIRUS

90. • dsDNA virus
• Keratinocytes
• Cancer / cervical
cancer- 16&18 type/
• Skin warts /1,2,4&7
types/
• Genital warts
/6,11,16&18 types/
• Respiratory
papillomatosis /6&8
types/

91. Transmittion Prevention
1. Prenatal
2. Genital infections
3. Hands
4. Shared objects
5. Blood
6. Surgery
1. Vaccines
2. Condoms
3. Wart removal
methods:
• Liquid nitrogen /freeze
them/
• Surgical
• Electrosurgery /laser/
• Podophyllin /for genital
warts/

93. HUMAN HERPES VIRUS
6

94. Unique Features of Herpesviruses
• Large, enveloped capsids containing double-stranded
DNA genomes
• Herpesviruses encode many proteins that manipulate the
host cell and immune response.
• Virus is released by exocytosis, cell lysis, and through
cell-to-cell bridges.
• Herpesviruses can cause lytic, persistent, latent, and (for
Epstein-Barr virus) immortalizing infections.
• Herpesviruses are ubiquitous.
• Cell-mediated immunity is required for control.

95. HUMAN HERPESVIRUSES 6
• Members of the genus Roseolovirus of the subfamily
Betaherpesvirinae
• HHV-6 is lymphotropic and ubiquitous.
• At least 45% of the population is seropositive for HHV-6
by age 2 years, and almost 100% by adulthood.
• In 1988, HHV-6 was serologically associated with a
common disease of children, exanthem subitum,
commonly known as roseola.

96. Pathogenesis and Immunity
• HHV-6 infection occurs very early in life.
• The virus replicates in the salivary gland, is shed, and
transmitted in saliva.
• HHV-6 primarily infects lymphocytes, especially CD4 T
cells.
• HHV-6 establishes a latent infection in T cells and
monocytes but may replicate on activation of the cells.
• Similar to CMV, the virus is likely to become activated in
patients with AIDS or other lymphoproliferative and
immunosuppressive disorders and cause opportunistic
disease.

97. Clinical Syndromes
• Exanthem subitum, or roseola, is caused by either HHV-
6B or HHV-7
• rapid onset of high fever of a few days’ duration
• rash on the trunk and face
• spreads and lasts only 24 to 48 hours
• HHV-6 may also cause a mononucleosis syndrome and
lymphadenopathy in adults and may be a cofactor in the
pathogenesis of AIDS.
• Similar to CMV, HHV-6 may reactivate in transplant
patients and contribute to the failure of the graft.
• multiple sclerosis and chronic fatigue syndrome.

98. RUBELLA
“GERMAN” MEASLES
Team 1

99. Classification
• Family: Togavirus (Togaviridae)
• Genera: Rubivirus
• Rubella virus

100. Structure
• Spherical
• 40-80nm
• Single-stranded RNA virus with spike-like
• Outer membrane – lipid bilayer specialized glycoproteins
(E1, E2)

102. Pathogenesis
• Transmitted
• Via direct
• Via droplet
• Target-cells of RS
• Transplacentally infected

103. Life cycle
• Replication is slow with a latency period 8-12 hours
• 12-16 hours : structural proteins appears
• Peak viral 36-48 hours
• Rash appears: 16-20 days

105. Host defenses
• Neutralizing and hemagglutination-inhibiting antibodies
• Cell-mediated immunity develop
• Reinfection can occur

106. Symptoms

107. Clinical aspects

108. Forchheimers spot

110. Diagnosis
• Suspected by rash
• Confirmed by serology

111. Prevention
• Vaccine
• Live attenuated MMR vaccine

112. Treatment
• There is no specific treatment
• Supportive care should be used

113. RUBEOLA
MEASLES
Team 1

114. Overview
• Measles, an acute infection caused by rubeola virus
• Measles (also called Rubeola-(from rubeolus, Latin for
reddish) ) is usually a disease of childhood (aged 3-10
years) and is followed by life-long immunity.
• Important cause of childhood mortality in developing
countries.
• Human is the natural host

115. Classification
• Family: Paramyxoviridae
• Genus: Morbillivirus
• Measles virus

116. Structure
• Pleomorphic spheres
• 100-250nm in diameter
• Single stranded RNA – 4.5 kDa
• Enveloped
• Hemagglutinin protein- binding virus to cell
• Fusion protein - viral penetration

118. Replication cycle
• Adsoprtion to the cell surface: via Hemagglutinin ---
CD46 molecule.
• Penetrates the cell surface and uncoats
• Virion RNA polymerase transcribes the negative-strand
genome to mRNA
• Specific viral proteins are formed
• Assembly to helical nucleocapsid
• Release of virus by budding

119. Pathogenesis
• Measles virus invades the cells lining the upper
respiratory tracts
• After 2-3 days of replication in these sites, a primary
viraemia widens the infection to the reticuloendothelial
system where further replication takes place.
• Secondary viraemia occurs and the virus enters skin,
conjunctivae, respiratory tract and other organs, including
the spleen, thymus, lung, liver, and kidney and further
replication occurs.
• Appearances of rash: (because of cytotoxic T cells attacks
measles virus infected vascular endothelial cells in the
skin).
• Formation of Multinucleated giant cells

120. Host defences
• Interferon and other initial defenses
• Specific cellular and humoral immune responces

121. Epidemiology
• Worldwide
• Incidence peaks in the late winter and early summer

122. Clinical Manifestation
• Coryza
• Conjunctivitis
• Fever
• Rash
• The typical maculopapular rash appears 1 to 3 days later.
• Complications include otitis, pneumonia, and encephalitis.
• Subacute sclerosing panencephalitis is a rare late
sequela.

126. Koplik’s spot

128. Diagnosis
• Clinical picture is diagnostic
• Isolating the virus by direct smear
• Detection of RNA with PCR
• Detecting specific IgM

129. Prevention /VACCINE/
• In 1963
• Decrease in incidence of disease