Actinomycetes

1. ACTINOMYCTES
1
• Gram-positive, pleomorphic non–
spore- forming, non–acid-fast
anaerobic or Microaerophilic bacilli.
•
• Actinomyces are very closely related
to Nocardia species; both were once
considered to be fungal organisms.

2. • A. israelii – the
commonest
• A .meyeri
• A.naeslundii
• A.odontolyticus
• A. viscosus
ACTINOMYCOSIS

3. • Normal flora of the oropharynx, GI tract, and female
genital tract.
• This is not an exogenous infection; therefore, no
person-to- person spread of the pathogen occurs
ACTINOMYCES IS A
NORMAL FLORA
DR.T.V.RAO
MD
8

4. RISK Factors
4
• Having a dental disease or recent dental
surgery (for jaw abscess)
• Aspiration (liquids or solids are sucked into
lungs) (for lung abscess)
• Having bowel surgery (for abdominal abscess)
• Swallowing fragments of chicken or other bones (for
abdominal abscess)
• For women: having an intrauterine
contraceptive device (IUD) in place for many
years (for abscess affecting the reproductive
organs)

5. MORPHOLOGIC FEATURES
 . Depending upon the anatomic location of lesions,
actinomycosis is of 4 types:
 cervicofacial,
 thoracic,
 abdominal,
 and pelvic
 Cervicofacial actinomycosis. This is the commonest
form (60%) and has the best prognosis.

7. • This is the most common and
recognized presentation of the
disease.
• Actinomyces species are
commonly present in high
concentrations in tonsillar crypts
and gingivodental crevices.
Many patients have a history of
poor dentition, oral surgery or
dental procedures, or trauma to
the oral cavity.
• Chronic tonsillitis, mastoiditis,
and otitis are also important risk
factors for actinomycosis.
CERVICOFACIAL ACTINOMYCOSIS
7

8. • Periostitis or osteomyelitis
can develop if the infection
extends to facial and
maxillary bones.
• The mandible appears to be
one of the most common
osteomyelitis sites.
CERVICOFACIAL REGION
1

9. • The infection usually
develops after GI
mucosal integrity is
broken from surgical
procedures or trauma.
INTESTINAL ACTINOMYCOSIS
9

10. PELVIC ACTINOMYCOSIS
• Intrauterine contraception devices, usually for longer
than 2 years.
• Pelvic actinomycosis may develop from extension
of intestinal infection, commonly from indolent
Ileocecal disease.
• Patients present with an indolent history of vaginal
discharge, abdominal or pelvic pain, menorrhagia,
fever, weight loss, and prolonged use of an
intrauterine
2
0

11. EXAMINATION OF DISCHARGES
• Examination of
drained fluid under
a microscope
shows "sulphur
granules" in the
fluid.
• They are yellowish
granules made of
clumped organisms
2
2

12. Microscopy
 Irrespective of the location of actinomycosis, the following features are:
 1. Inflammatory reaction is a granuloma with central
suppuration with formation of abscesses in the centre of
lesions and at the periphery chronic inflammatory cells, giant
cells and fibroblasts are seen.
 2) The centre of each abscess contains the bacterial colony,
‘sulphur granule’, characterised by radiating filaments (hence
previously known as ray fungus) with hyaline, eosinophilic,
club-like ends representative of secreted immunoglobulins.

15. • Grow well in enriched
media with brain-
heart infusion and
may be aided in
growth by an
atmosphere of 6-10%
ambient carbon
dioxide.
CULTURING OF
ACTINOMYCES
1
5

16. • Treatment classically
begins with IV
penicillin for 2–6
weeks, followed by oral
therapy with penicillin or
amoxicillin for 6–12
months..
TREATMENT OF ACTINOMYCOSIS
1
6

17. Granulation Tissue:It is granular
and pink appearance of the
tissue in ahealing tissue and in
secondary union of wounds.

18. 1
8
GRANULATION TISSUE
Macrosopy

19. GRANULATION TISSUE

20. 2
0

21. 2
1

22. 2
2

23. Gross:
 Floor of lesion contain pink eosinophilic granulations
,composed of vascular connective tissue, edge are
sloping & bluish white.
Microscopy:
 Surface of ulcer –mixture of blood,fibrin & inflammatory
exudates.
 Zone below granulation tissue –composed of
proliferating fibroblast, newly formed small vessels &
varying no. of inflammatory cell.

25. chronic granulomatous disease
characterised by production of polyps
and other manifestations of hyperplasia
of nasal mucosa(predominantly).
The etiological agent is
Rhinosporidium seeberi.

26. Rhinosporidium seeberi:
Initially believed to be a sporozoan, but
later considered to be a fungus and has
been provisionally placed under the
Family -Olipidiaceae,
Order -chytridiales of phycomyetes by
ASHWORTH.

27. Spore is the ultimate infecting
unit.
It measures about 7 microns,
about the size of a red cell.
It is also known as a spherule.
It has a clear cytoplasm with 15
- 20 vacuoles.
It is enclosed in a chitinous
membrane which protects the
spore from hostile
environment.
It is found only in connective
tissue spaces and is rarely
intracellular.

28. 1)mature
sporangium.
2)spores(sporan
giospora/endos
pores.)
3)Immature
sporangium.

29. 1)mature
sporangium.
2)spores(sporan
giospora/endos
pores.)
3)Immature
sporangium.

30. Common sites affected:
Nose - 78%
Nasopharynx
Tonsil
Eye - 1%
Skin - very rare
Also affects the lips, palate, uvula,
maxillary antrum, epiglottis, larynx,
trachea, bronchus, ear, scalp, vulva,
vagina, penis, rectum, and the skin.

31. Lesions in the nose can be
polypoidal, reddish and
granular masses.
They could be multiple
pedunculated and friable.
They are highly vascular
and bleed easily.
Their surface is studded
with whitish dots
(sporangia)
They can be clearly seen
with a hand lens.
The whole mass is covered
by mucoid secretion.

32. The largest sporangia are usually in a
subepithelial location.
The size of the globular sporangia
depend on the stage of maturation.
Young trophic forms (immature
sporangia) are spherical ,10-100
micrometer in diameter and have a
central basophilic nucleus.
These develop into mature sporangia by
a process of progressive enlargement
and endosporulation.

33. Increased vascularity is due to the
release of angiognenesis factor from the
rhinosporidial mass.
Rhinosporidial spores stain with
sudan black, Bromphenol blue etc.

34. These spores are also
passed in the nasal
discharge.
Special stains:
R. Seeberi is visualized
by fungal stains such as
PAS, Gomori's
methenimine silver and
mucicarmine.

35. Microscopy

37.  Microscopy:
 Polypoidal structure lined by respiratory epi, with
underlying edematous stroma, showing numerous
sporangia with endospores.
 Large thick walled sporangia with endospores
surrounded bymixed inflammatory infiltrates.

38.  Diagnosis is based on the fine-needle aspiration cytology (Giemsa
stained) or histopathological demonstration of the characteristic
thickwalled sporangia in various stages of development and containing
numerous sporangiospores.
 R. seeberi can be easily identified in sections stained with hematoxylin
and eosin with many sporangia.


39. Treatment::
anti-rhinosporidial effect is
dapsone (4,4-
diaminodiphenyl sulphone)
which appears to arrest the
maturation of the sporangia
and to promote fibrosis in the
stroma, when used as an
adjunct to surgery.

40. Tuberculosis
 Tissue response in tuberculosis represents classical
example of chronic granulomatous inflammation in
humans.
 CAUSATIVE ORGANISM. Tubercle bacillus or Koch’s
bacillus (named after discovery of the organism by
Robert Koch

41. Caseating granulomatous
lymphadenitis

42. Morphology of a tubercle

44. Miliary tuberculosis lung

45.  Gross:
 Greyish white area of lung-focus of lesion.
 Presence of hilar LN ,blackish mark &enlarged.
 C/S-stuuded with grey white tubercles

46.  Microscopy:
 Central necrosis
 Epitheloid cells in centre with langhans type giant cell
surrounded by lymphocytes &fibroblast.
 Langhans type giant cell seen with nuclear arranged in
ring pattern.