3. Properties
• Club-shaped also V- or L-shaped
• Beaded appearance
• Methachromatic granules (Albert staining)
• Nonmotile
• no capsule
• Facultative anaerobic.
• Classified in CNM group.
4.
5.
6.
7.
8.
9. Biotypes
(based on colony shape, biochemical properties and virulence)
Gravis
Mitis
Intermedius
Belfanti
10.
11. Clinical finding
• Common diphtheria (Nasopharyngitis)
Incubation period of 2–5 days.
Fibrinous exudate “pseudomembrane”
Sore throat, fever, Enlargement of neck lymph nodes and
neck edema. Irregulatory of cardiac rhythm, difficulties
with vision, speech and swallowing.
Corrosion of myelin sheaths in the central and peripheral
nervous system leading to degenerating motor control
12.
13.
14.
15. Clinical finding
• Cutanous diphtheria
(a secondary infection)
• Antibody production: Blocking the fragment
B and so preventing entry into the cell.
16. Transmission
• Humans the only natural host
• C. diphtheriae reside in the upper respiratory
tract
• Transmitted by airborn droplet
• Infection at the site of a pre-existing skin
lesion
18. Invasivness
• Cord factor
A glycolipid inhibits eukaryotic cell oxidation.
• Nuraminidase
Removes N-acetyl nuraminic acid from musine
membranes.
19. Exotoxin
(Encoded by gen tox from a temperate phage)
Fragment B. Binding of the toxin
Fragment A. Enzymatic activity
A
B
20. Nicotinamide adenine dinucleotide phosphate (NAD)
Exotoxin
(A fragment)
Nicotinamide ADP
Reaction with EF2
ADP-EF2
Protein synthesis
inhibition
21. Testing immunity
(Schick’s test)
• Intradermal injection (0.1 mL):
I. Cause inflammation (4-7 days later): No
antitoxin in patient
II. No inflammation: Antitoxin is present
(Immune person)
22. Laboratory diagnosis
• Microscopic observation (differentiation from streptococcal and
vansant nasopharyngitis)
• Isolating the organism
Loffler’s medium
a tellurite plate
Tinsdal medium
• Demonstrating toxin production
Animal inoculation
Eleck test
ELISA
• PCR to detect tox gene
23. Treatment
• Tracheostomy in children (to prevent croup)
• Antitoxin
20000-100000 unit (Intra muscular)
• Penicillin or erythromycin
24. Prevention
• Vaccination
A combination of diphtheria toxoid, tetanus toxoid,
and killed pertusis organism.
Given at 2, 4 an 6 months of age, with a booster at
1 and 6 years of age and then each 10 years
afterward. (DPT or DT)
The toxoid is prepared by treating the exotoxin
with 0.3% formaldehyde.
25. Listeria monocytogenes
• Small rod like “chinese character”
• No capsule, Facultative aerobic.
• Tumbling movement. Movement in 25 c
• Growing in 4c
• Small and smooth colony on blood with a
narrow zone of beta-hemolysis
• Biochemical tests: Fermentation, Catalase +
Oxidase +
26. Disease
• Meningitis and sepsis in
1. The fetus or newborn as a result of
transmission across the placenta or during
delivery.
2. Immunosuppressed adults
(especially renal transplant patients)
• The infected mother: asymptomatic or
influenzalike illness/ Abortion
27.
28. Transmission
• The organism is distributed worldwide in
animals, plants and soil.
• Transmission to human by contact with
animals or their feces
unpasteurized milk
contaminated vegetables.
Endogenously from gasterointestinal tract.
30. Lab. diagnosis
• Microscopic observation: Diphtheroids
• Isolation by culture:
Blood and CSF samples on blood agar
Colonies: Small, gray colonies with a narrow
zone of beta hemolysis
31. Treatment
• Penicillin
Resistant are rare
Prevention
• Cell-mediated immunity is active but no
immunization
• Limiting the exposure of immunosuppressed
patients to potential sources
34. Properties
• A large rod with square ends.
• Frequently in chains
• A unique anti-phagocytic capsule is composed
of D-glutamate.
• Non-motile (other members of the genus are
motile.)
35.
36.
37.
38.
39.
40. Transmission
• Spores persist in soil for years. Infection from
animal products (hides, bristles and wool),
contact with sick animal.
• Portals of entry: skin, mucous membranes,
and respiratory tract.
41. Clinical findings
• A typical lesion: A painless ulcer with black,
necrotic eschar. Local edema.
• Untreated cases progress to bacteremia and
death.
• Woolsorter’s disease (pulmonary anthrax) is a
life threatening pneumonia (by inhalation of
spores).
42.
43.
44.
45. Pathogenesis
• Invasiveness
• Exotoxin
• Anthrax toxin, has 3 components:
- Protective antigen
- Lethal factor: In the presence of protective antigen is
rapidly fatal for mice. The action is unknown
- Edema factor (an exotoxin): An adenylate cyclase
dependent on protective antigen for its binding and
entry into the cell.
46. Lab. diagnosis
• Samples: Exudate, Blood, sputum.
• Direct smear: Large rods in chains. Spores not
seen in smears of exudate.
• Culture and biological/biochemical tests
(Sensitivity to penicillin (String of pearls test),
Fermentation, gelatin hydrolysis, Motility)
• No serological tests are useful
47.
48. Prevention
• Preventing soil contamination
• Sterilizing dead animals and animal products .
• Protecting persons at risk of exposure with
special clothes.
• Vaccination with cell-free vaccine for persons
at high risk.
51. Bacillus cereus
• Disease
Food poisoning
Rare infections: Meningitis, Osteomyelitis, …
• Transmission
Spores on grains survive during steaming and
rapid frying. Spore germinated when rice is
kept warm.
Portal of entry is the gastrointestinal tract.
52. Pathogenesis
• B. cereus produces 2 enterotoxins. Their actions
is unclear.
Clinical findings
1. Emetic syndrome
A short incubation period (4 hours) with nausea and
vomiting similar to staphylococcal food poisoning.
2. Diarrheal syndrome
Involves a long incubation period (18 hours) with diarrhea
and resembles clostridial gastroenteritis.
53. Lab. diagnosis
• Not usually done
Treatment
No antibiotic is given. Only symptomatic treatment
Prevention
Grains (specially rice) should not be reheated
55. Clinical findings
• Incubation period: 4-5 days – several weeks
• Violent muscle spasms in the site of infection
and then jaw)
• Lockjaw (trismus) due to rigid contraction of
the jaw muscles, which prevents the mouth
from opening: a characteristic known as “risus
sardonicus”’.
• Low blood pressure
• Respiratory failure
60. Transmission
Spores are widespread in soil.
The portal of entry is a wound site.
Germination of spores is favoured by necrotic
tissue and poor blood supply in the wound.
61. Pathogenesis
• Tetanus toxin (tetanospasmin)
It is carried intra-axonally (retrograde) to the
central nervous system, where it binds to
ganglioside receptors and blocks release of
inhibitory mediators (e.g. glycine, Gamma-
aminobutiric acid) at spinal synapses leading
to hyper reflection and spastic paralysis.
62.
63. Diagnosis
• History of wound and clinical picyure
• There is no microbiologic or serologic diagnosis.
• Organisms are rarely isolated from the wound site.
Treatment
• Antitoxin does have a low effect
• Penicillin
• Respiratory support
• Muscle relaxants
64. Prevention
• Immunization with toxoid in childhood (2, 4, 6, 12
months ages) and every 10 years thereafter.
• When trauma occurs deeply:
1. Wound should be cleaned and debrided.
2. Tetanus toxoid booster should be given.
3. Tetanus immune globulin should be given.
4. Penicillin administered.
66. Transmission
• In soil ---> Alkaline vegetables/meat --->
canned/vacuum-packed ---> Spore
germination ---> Toxin production --->
ingestion
67. Pathogenesis
• Botulinus toxin
Observing from the gut ---> Carrying via the
blood to peripheral nerve synapses --->
Blocking release of acetylcholine --->
Paralysis
72. Pathogenesis and clinical findings
• Alpha toxin: Lecithinase
• Glycogen metabolism: Gas in tissues:
Crepitation
• Treatment
Penicillin
Wounds should be debrided
H2O2
74. Lab diagnosis
• Smear of tissue and exudate samples: large
positive rods.
• Cultured anaerobically identified with
fermentation reactions
75. Food poisoning
• Transmission: Soil and food. Survives cooking and
grows to large numbers in reheated food, especially
meat.
• Pathogenesis: An enterotoxin (a protein in the spore
coat)
• Clinical findings:
Incubation: 8-16 hours, then watery diarrhea with
cramps and little vomiting. Resolves in 24 hours.
80. Pathogenesis
• Antibiotic (Clindamycin and ampicillin) supress
drug-sensitive normal flora, allowing C.
difficile to multiply: produce toxin.
• Toxin mechanism is unclear
81. Clinical findings
• Diarrhea
• Pseudomembranes (yellow-white plaques) on
the colonic mucosa.
• Visualised by sigmoidoscopy.
82. Lab diagnosis
• Toxin detectable in stool affecting on cell
cultured cells.
• Inhibition of cytotoxicity by specific antibody.
