Pathogenesis,pathology and diagnosis of Cryptococcosis,Histoplasmosis, Epizootic lymphangitis in horses(Histoplasma farciminosum),Zygomycosis, Pythiosis and Rhinosporidiosis in man and animals. All of the information are collected , it's not a research work but i think it will help the students to know about the basic information.

2. Pathogenesis,pathology and diagnosis of
Cryptococcosis,Histoplasmosis, Epizootic
lymphangitis in horses(Histoplasma
farciminosum),Zygomycosis, Pythiosis and
Rhinosporidiosis in man and animals.
Course no and title:VPATH
615,Pathology of Fungal
Rickettsial and Chlamydial
Diseases.
Name: Md Fayezur Rahaman.
Roll No:16VPATHJJ04M
Reg No: 37164
Department of Pathology

3. Cryptococcosis.

4. Causal Agent:
Cryptococcus neoformans

5. Pathogenesis
 Enters through lungs - inhalation of Basidiospores of C neoformans.
 Enters deep into lungs, Men acquires more infections, and women
less infected.
 Self limiting in most cases.
 Pulmonary infections can occur.
 Present as discrete nodules - Cryptococcoma.
 Can manifest with involvement of ,Skin,
mucosa,organs,Bones,and as Disseminated form.
Can mimic like Tuberculosis,

6. PATHOLOGY
 Most infections with C. neoformans occur in the lungs.
However, fungal meningitis and encephalitis, especially as a
secondary infection for AIDS patients.
 C. neoformans can cause meningoencephalitis.In the lungs, C.
neoformans cells are phagocytosed by alveolar macrophages.
C. neoformans seen in the lung of
a patient with AIDS: The inner
capsule of the organism stains red
in this photomicrograph.
Cryptococcus

7. Laboratory Diagnosis.
 CSF : Microscopic observation under India Ink preparation.
 Direct microscopy - Gram staining.
 Cultures on Sabouraud dextrose agar.
 Serological tests for detection of Capsular antigen.
 CSF findings mimic like Tuberculosis.
 Blood cultures.
 ELISA
C. neoformans stained by Gram
stain

8. Histoplasmosis

9. Causal Agent:
Histoplasma capsulatum.

10. Pathogenesis:
Infection by this dimorphic soil fungus
occur by inhalation.
Organism reach alveolar spaces where it multiplies in
mononuclear phagocytes.
mononuclear phagocytes then enter into various organs and at
last the symptoms are displayed.

11. Pathology:
Gross lesions:
 Lesions resemble tuberculosis for similar clinical and pathological
features.
 Chronic cough, chest pain,night sweat, malaise, loss of weight etc.
Microscopic lesions:
 Yeast-like forms in tissue section.
 A clear space or artifactual “holo” may be evident due to the retraction of the
basophilic fungal cell cytoplasm from the poorly stained cell wall.
 Necrotizing granuloma : Heal by fibrosis.
 In skin numerous parasitized macrophages containing yeast – like
organism.

12. Diagnosis:
 Histoplasmin skin test- positive with
negative tuberculin test.
 Antigen tests performed on blood,urine, or
CSF.
 In chronic infection special stains are
usually necessary to identify the
organisms and the Methenamine- Silver
stain is the best.

13. Epizootic lymphangitis in
horses

14. Causal Agent:
Histoplasma farciminosum
Pathogenesis:
1st after the initial invasion of the skin, the organism spreads through the
lymphatic vessels to the regional lymph nodes, and in more advanced
cases involves the internal organs . When mucosal lesions occur, most are
confined to the upper respiratory tract and eyes . The nasal infection is
usually accompanied by mucopurulent discharge containing large numbers
of the fungus.

15. Pathological lesions:
• The initial lesion is an open granulomatous wound along
the course of alymphatic vessel.
• In ophthalmic form of the Infection may occur as
conjunctivitis or a naso-lachrymal infection.
• Initial infection is characterised by a watery discharge
from one or both eyes and some swelling of the eyelids,
followed by the development of papules and ulcerating
button-like growths on the conjunctiva .

16.  The respiratory form of the disease is characterised by
lesions which are mostly confined to the upper
respiratory tract. On the nasal mucosa, the lesions
 Typical nodules of liquefied foci have also been recorded
in the pleura, spleen, liver and bone marrow .

17. Diagnosis:
i. Clinical signs and symptoms.
ii. Serological tests
a) Fluorescent antibody technique
b) Agar gel immunodiffusion tes
c) Enzyme-linked immunosorben
Assay(ELISA)
d) Haemagglutination test

18. ZYGOMYCOSIS

19. Causative agents:
Rhizopus, Rhizomucor, Mucor...

20. Pathogenesis:
1. Rhinocerebral zygomycosis: Infections usually begin
in the paranasal sinuses following the inhalation of
sporangiospores and may involve the orbit, palate,
face, nose or brain.
2. Pulmonary zygomycosis: Infections result by
inhalation of sporangiospores into the bronchioles and
alveoli, leading to pulmonary infraction and necrosis
with cavitation.
3. Gastrointestinal zygomycosis: Primary infections
probable result following the ingestion of fungal
elements and usually present as necrotic ulcers.

21. 4.Cutaneous zygomycosis:
Local traumatic implantation of fungal elements through the
skin, especially in patients with extensive burns, diabetes or
steroid induced hyperglycemia and trauma.
5.Disseminated zygomycosis:
May originate from any of the above, especially in severely
debilitated patients with haematological malignancies, burns,
diabetes or uraemia.
6. Central Nervous System alone:
Traumatic implantation leading to brain abscess.

22. Pathological lesions:
1. The infecting fungi have a predilection for invading vessels of the arterial
system, causing embolization and subsequent necrosis of surrounding
tissue.
2. Due to Pulmonary zygomycosis infraction and necrosis with cavitation can
be seen.
3. Necrotic ulcers will be found due to gastrointestinal Zygomycosis.
4. Plaques, pustules, ulcerations, deep abscesses and ragged necrotic
patches due to cutaneous zygomycosis.

23. Diagnosis
1. Clinical Material: Skin scrapings from cutaneous lesions; sputum and
needle biopsies from pulmonary lesions.
2. Direct Microscopy: (a) Scrapings, sputum and exudates should be
examined using 10% KOH & Parker ink. and (b) Tissue sections should be
stained with H&E and GMS. Examine specimens for broad, septate, thin-
walled hyphae and irregular branching.
3. Culture: Inoculate specimens onto primary isolation media, like
Sabouraud's dextrose agar.
4. Serology: There are currently no commercially available serological
procedures for the diagnosis of zygomycosis. Although some laboratories
have developed ELISA tests for the detection of antibodies to Zygomycetes.
septate,
thin-walled
hyphae and
irregular
branching.
H&E STAINING

24. Pythiosis

25. Causal Agent:
Pythium insidiosum

26. Pathogenesis:
Pythiosis is caused by invasion of the organism into wounds
either in the skin or in the gastrointestinal tract.
Then it grows slowly in the stomach and small intestine
Eventually forming large lumps of granulation tissue, It can
also invade surrounding lymph nodes.

27. Pathological lesions:
1. In horse lesions are most commonly found on the lower limbs,
abdomen, chest, and genitals. They are granulomatous and itchy,
and may be ulcerated or fistulated. The lesions often contain
yellow, firm masses of dead tissue known as kunkers.
2. In cats pythioisis is almost always confined to the skin as hairless
and edematous lesions. It is usually found on the limbs, perineum,
and at the base of the tail.[16] Lesions may also develop in the
nasopharynx.

28. Diagnosis
1. GMS staining is required to identify the hyphae
in slides.
2. Biopsies of infected tissues are known to be
difficult to culture but can help narrow the
diagnosis to several different organisms.
3. A definite diagnosis is confirmed using ELISA
testing of serum for pythiosis antibodies, or by
PCR testing of infected tissues or cultures.

29. RHINOSPORIDIOSIS

30. Causal Agent: Rhinosporidium seeberi
Pathogenesis:
Organism invade into the nasal mucosa
Inflammation occurs.
Polyps occur.

31. Pathology
Gross lesions:
1. Polypoid granulomatous lesions in nasal septum.
2. Polyps are irregular in size may occlude the nasal passage.
Microscopic lesions:
1. There is granulation tissue containing plasma
cells,lymphocytes,focal collection of histiocytes and neutrophils.
2. Polyps show spherical organism with a thick double controlled
wall.
3. Endospores are released by the ruptures of cell wall of
sporangium.

32. Diagnosis:
1) Clinical sign symptoms.
( Strawberry like Nasal Polyps)
2)Rhinosporidium seeberi is visualized by fungal
stains such as PAS stain.

33. THANK YOU ALL