This document provides an overview of bacterial skin diseases and infections. It discusses several gram-positive bacteria like Staphylococcus and Streptococcus that can cause infections. It describes common skin infections from Staphylococcus like folliculitis and boils. It also covers Streptococcus and the skin infection of scarlet fever. The document further discusses gram-negative pathogens such as Pseudomonas, Vibrio, E. coli, Campylobacter, Helicobacter, and Neisseriae that can infect the skin. It provides details on diseases associated with these bacteria and their characteristics, transmission, pathogenesis and symptoms.

1. Diseases caused by bacterial
infections

2. Bacterial skin diseases

3. Introduction
Intact skin surface
– prevents
microbes from
entering the body
Normal microflora
– inhibit growth of
pathogens
Oil gland – secret organic acid and
lipids; reduce pH thus inhibit
growth of pathogens
Sweat gland
- Secret organic
substances;
reduce pH and
inhibit pathogen
growth

4. Staphylococci: Gram positive
cocci ( from Greek staphyle,
means bunch of grapes ) that
occur singly and in pairs, short
chains and irregular grape-like
clusters.

5. MMoorrpphhoollooggyy ooff SSttaapphhyyllooccooccccuuss

6. Enzymes
1. Coagulase
– Triggers blood clotting
– Used for detection of S. aureus
1. Hyaluronidase
– Breaks down hyaluronic acid, enabling
the bacteria to spread between cells
1. Staphylokinase
– Dissolves fibrin threads in blood clots,
allowing Staphylococcus aureus to free
itself from clots
6

7. Enzymes (cont.)
4. Lipases
– Digest lipids, allowing staphylococcus to grow on the
skin’s surface and in oil glands
5. b-lactamase
– Breaks down penicillin
– Allows the bacteria to survive treatment with b-lactam
antimicrobial drugs
6. Catalase
– able to convert hydrogen peroxide to water and oxygen
7

8. 1) Staphylococcal infections
1) Diseases : folliculitis,boil
Pathogens : Staphylococcus aureus, Pseudomonas
Transmission : touching, hospital personnel,
nasal droplets etc
Pathogenesis : invade the skin through hair follicle
How can hair
follicle
damaged??

9. Superficial folliculitis:
1)Clusters of small red
or pus-filled bumps that
develop around hair
follicles
2)Pus-filled blisters that
break open and crust
over
3)Red and inflamed skin
4)Itchiness or
tenderness
Deep folliculitis
1)A large swollen
bump or mass
2)Pus-filled blisters
that break open and
crust over
3)Pain
4)Possible scars once
the infection clears

10. 1) Staphylococcal infections
2) Diseases : scalded skin syndrome (infant), toxic
shock syndrome (adult)
Pathogen : Staphylococcus aureus
Transmission : touching, fomite, breastfeeding
Pathogenesis : the bacterial toxins travel through the
bloodstream, causing the upper skin layers
to separate and peel off

11. Symptoms :
1)Blisters
2)Fever
3)Large areas of skin peel or fall
away (exfoliation)
4)Painful skin
5)Redness of the skin, which
spreads to cover most of the body
6)Skin slips off with gentle
pressure, leaving wet red areas
Diagnosis :
1)Physical examination
2)Complete blood count (CBC)
3)Cultures of the skin, throat, nose and
blood
Treatments:
1)Antibiotics - through a vein
(intravenously) to help fight the
infection.
2)Fluids - through a vein to prevent
dehydration. Much of the body's fluid is
lost through open skin.
3)Moisturizing ointment to keep the
skin moist. Healing begins about 10 days
after treatment.

12. Streptococcus
1) Gram-positive spherical/ovoid
cocci arranged in long chains
2) Non-spore-forming, nonmotile
3) Can form capsules and slime
layers
4) Facultative anaerobes
5) Catalase Negative
6) Most parasitic forms are
fastidious and require enriched
media
7) Sensitive to drying, heat, and
disinfectants

13. 2) Streptococcal infection
1) Diseases : scarlet fever (scarlatina)
Pathogen : Streptococcus pyogenes
Pathogenesis : the bacteria produce erythrogenic toxins
Symptoms :
i) begin with rashes on the neck and face
ii) then the rashes spread to the chest and
back before the rest of the body
iii) sore throat
iv) fever (T > 38.5°C)
v) whitish or yellowish coating at tongue
and throat
vi) vomiting & loss appetite

14. Gram-negative pathogens

15. 1) Pseudomonas
2) Vibrios
3) E.coli
4) Campylobacters
5) Helicobacter
6) Haemophilus
7) Neisseriae
GRAM-NEGATIVE
BACTERIA

16. Pseudomonas
 obligate aerobic – rod shape
 motile – presence of flagella
normally found in water, soil and moist
environment
Culture morphology: round form, β-hemolysis,
fluorescent greenish color
Oxidase and catalase positive
Broad antibiotic resistance

17. P. aeruginosa
1)Opportunistic microorganisms – cause disease
when host defense is low:
Disruption of mucus membrane and skin
Usage of intravenous or catheters.
2) Can cause nosocomial infection, UTI,
meningitis, pulmonary infection,
dermatitis, GTI.

18. P. Aeruginosa enzymes
Enzymes Functions
Protease Cause tissue damage and help
bacteria spread
Phospholipase C Lyses hemoglobin
Exotoxin A Cause tissue necrosis (disrupt protein
synthesis)
Exoenzymes S & T Cytotoxic to host cells

19. Vibrio sp.
1) Coma shape
2) Non-spore forming
3) Highly motile – single flagella
4) Facultative anaerobes
5) Tolerate alkaline condition

20. Cholera
1) Acute diarrheal illness caused by
infection of intestine with V.
cholera
2) Transmitted via oral-focal route
3) Can multiply freely in water

21. Pathogenesis of V. Cholera
1) Cholera disease begins with ingestion of
contaminated water or food with cholera bacteria.
2) The bacteria that survive the acidic conditions of the
stomach colonize in the small intestine.
3) The cholera toxin (CT) is responsible for the severe
diarrhea characteristic of the disease.
4) If untreated, the disease rapidly result in dehydration
and death

22. Cholera Toxin (CT)
a) CT is a proteinaceous enterotoxin
b) Bind to host cells - mediates the formation of cAMP
c) The increase in cAMP levels bring about the
secretion of electrolytes (chloride and bicarbonate)
from the mucosal cells into the intestinal lumen
d) The change in ion concentrations leads to the
secretion of large amounts of water into the lumen,
known as diarrhea
e) If not treated, the infection can cause tubular
necrosis and renal failure – leads to death

23. Cholera Toxin (CT)

24. Signs and symptoms
Diarrhea Stomach pain Mild fever
Vomiting Dry mucosal membrane

25. E. coli
1) Commonly present in intestine
2) Can cause infections in human and animals
3) Some strains are not pathogenic, but some
of them are highly pathogenic
4) Detection of E. coli in water indicates
pollution and contamination. Maybe it is
caused by water treatment or other
problems.

26. Characteristic of
E. coli
1) Facultative anaerobes – non-spore
forming
2) Motile – have flagella
3) Non-capsulated
4) Non-fastidious
5) Grow on bile-containing media
(MacConkey)

27. Symptoms of Intestinal Infection
Due to E. coli
 abdominal cramping
 sudden, severe watery diarrhea that may
change to bloody stools
 gas
 loss of appetite/nausea
 vomiting (rare)
 fatigue
 fever

28. Campylobacter jejuni

29. Campylobacters
jejuni
1) Gram-negative, very slender, curved rods.
2) Motile, no spore, no capsule.
3) Catalase-positive, but are micro-aerophilic and
optimum growth is achieved in an atmosphere
containing 5% oxygen and 10% carbon dioxide.
4) Oxidase-positive.
5) The optimum temperature for growth for the
thermophilic campylobacters is 42°C, and they do
not grow at temperatures below 30°C.

30. Campylobacteriosis
1) caused by bacteria of the
genus Campylobacter
2) The illness typically lasts about one week
3) Outbreaks of Campylobacter have most often
been associated with unpasteurized dairy
products, contaminated water and poultry.
4) The organism is not usually spread from one
person to another, but this can happen if has
direct contact with the stool of infected person.

31. Campylobacter Virulence Factors
1) Flagellin - bacteria's motility
2) Produce toxins - LPS (endotoxin) and exotoxin
3) Superoxide dismutase - rid of the reactive oxygen
species superoxide which could harm the cell's DNA or
membrane factors
4) Siderophores – to take away iron from iron-transport
protein

32. What can be done to
prevent Campylobacter
infection?

33. Helicobacter pylori

34. Characteristic of
Helicobacter pylori
1) Gram-negative, rod curved
2) Very motile – flagella
3) Microaerophilic
4) Grow at body temperature –
37°C

35. How is helicobacter
pylori transmitted??

36. Diseases caused by
Helicobacter pylori
1) Cause stomach and duodenal ulcers

37. 2) Stomach cancer

38. Helicobacter pylori pathogenicity

39. Diagram of H. Pylori Infection

40. Diagnostic of H. Pylori Infection
1) Blood antibody test. A blood test checks to see
whether your body has made antibodies to H.
pylori bacteria. If you have antibodies to H. pylori in
your blood, it means you either are currently infected
or have been infected in the past.

41. Diagnostic of H. Pylori Infection
2) Urea breath test. A urea breath test checks to see if you
have H. pylori bacteria in your stomach. This test can show if
you have an H. pylori infection. It can also be used to see if
treatment has worked to get rid of H. pylori.

42. Diagnostic of H. Pylori Infection
3) Stool antigen test. A stool antigen test checks to see if
substances that trigger the immune system to fight an H.
pylori infection (H. pylori antigens) are present in your feces
(stool). Stool antigen testing may be done to help support a
diagnosis of H. pylori infection or to find out whether treatment
for an H. pylori infection has been successful.

43. Diagnostic of H. Pylori Infection
4) Stomach biopsy. A small sample (biopsy) is taken
from the lining of your stomach and small intestine
during an endoscopy.

44. Mycobacteria

45. Mycobacteria
• Name from Myco and
Bacteria, Fungus like
bacteria
• Because it forms mould
like growth on liquid
cultures
• Types:
1) M. Tuberculosis – TB
2) M. Leprae – Leprosy

46. Mycobacterium tuberculosis
• Cannot be stained with gram-staining
• Acid fast bacteria
• They have mycolic acid in their cell wall
which makes them acid fast
• Difficult to decolorise with organic acids

47. Acid Fast Bacteria

48. Mycobacterium tuberculosis
 Obligate aerobes
 Grow slowly – generation time 15 hours
 Colonies appear in two weeks
 Optimum temperature is 37 deg
 Solid media most commonly used – LJ
media

50. Pathogenicity and virulence
• Its pathogenicity is due to complex lipids
like mycolic acid in cell wall. This makes it
– Acid fast
– Resistant to antibiotics
– Resistant to disinfectants like acid and alkali
– Resistant to immune system
– Resistant to destruction by macrophages

51. Tuberculosis

52. Common symptoms include:
1)coughing that lasts longer than 2
weeks with green, yellow, or bloody
sputum
2)weight loss
3)fatigue
4)fever
5)night sweats
6)chills
7)chest pain
8)shortness of breath
9)loss of appetite

53. Lab diagnosis for M. tuberculosis
• Sample – sputum for pulmonary, biopsy for
extrapulmonary sites
• Stain – Ziehl-Neelsen stain
• Culture – Lowenstein-Jensen media
• PCR – polymerase chain reaction

54. Mycobacterium leprae
1) Causes leprosy - has a long
incubation period
2) gram-positive - Slightly curved rods
3) Singly or in groups
4) thick waxy coating
5) affects the skin, the peripheral
nerves, mucosa of the upper
respiratory tract and also the eyes

55. What Are the Symptoms of Leprosy?
1) Infect the skin and the
nerves outside
the brain and spinal cord
2) It may also strike
the eyes and the thin
tissue lining the inside of
the nose.
3) Symptoms: disfiguring
skin sores, lumps, or
bumps, loss of feeling in
the arms and legs,
Muscle weakness

56. Leprosy Complications
1) glaucoma.
2) Disfiguration of the face (including permanent
swelling, bumps, and lumps).
3) Kidney failure.
4) Muscle weakness.
5) Permanent damage to the inside of the nose,
6) Permanent damage to the nerves outside the brain
and spinal cord, including those in the arms, legs,
and feet.
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