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: 37164Department of Pathology

Cryptococcosis.

Causal Agent: Cryptococcus neoformans

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,

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

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. ELISAC. neoformans stained by Gram stain

Histoplasmosis

Causal Agent: Histoplasma capsulatum.

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.

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.

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.

Epizootic lymphangitis in horses

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.

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 .

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 .

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

ZYGOMYCOSIS

Causative agents: Rhizopus, Rhizomucor, Mucor...

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.

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.

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.

Diagnosis1. 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

Pythiosis

Causal Agent: Pythium insidiosum

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.

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.

Diagnosis1. 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.

RHINOSPORIDIOSIS

Causal Agent: Rhinosporidium seeberi

Pathogenesis: Organism invade into the nasal mucosa

Inflammation occurs.

Polyps occur.

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.

Diagnosis:

1) Clinical sign symptoms. ( Strawberry like Nasal Polyps)

2)Rhinosporidium seeberi is visualized by fungal stains such as PAS stain.

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