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20 Cards in this Set

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I. Systemic Mycoses: PRIMARY FUNGAL PATHOGENS
*
What are the MAJOR points for pathogens in this section?
1) Disease results from inhalation of spores

2) Geographic distribution specific to fungus

3) Classic dimorphism
ENVIRONMENTAL FORM (mold)
TISSUE FORM (yeast or other specialized form)

4) The host immune response that is protective consists of cell- mediated immunity.
- Cd4+ T cells are generated against fungal products
- immune T cells activate phagocytic cells to kill fungi
- Tissue macrophages become activated and fuse to "wall off" fungi from surrounding host tissue by forming a granuloma which prevents the fungus from causing disease
- BUT if the host becomes immunocompromised, the granuloma may dissociate, releasing live fungi into the host tissues

5) It may become latent like TB and form granulomas

6) Disease is much more severe in the presence of HIV infection

7) Exposure determined by skin test (DTH)

8) Not transmitted from person to person

9) Laboratory culture of mold are hazardous
What are three examples of PRIMARY FUNGAL PATHOGENS?
1) HISTOPLASMA CAPSULATUM
2) BLASTOMYCES DERMATITIDIS
3) COCCIDIOIDES IMMITIS
1) HISTOPLASMA CAPSULATUM

How frequent is this pathogen?

What regions of the country are highly endemic?

In how many people does the infection become progressive and require therapy?
This is widely distributed throughout the temperate, subtropical and tropical zones of teh world.

The Ohio and Mississippi Valley regions are highly endemic.

Less than 1% of infections become progressive and require therapy.
What are the properties/ characteristics of HISTOPLASMA CAPSULATUM?
1) it has DIMORPHIC growth, growing in HYPHAL form in the environment and in YEAST form in infected tissue

2) HYPHAL characteristics - septate branching hyphae that bear spores (2-6 micrometers in diameter)
MACROCONIDIA with characteristic morphology are also produced

3) Yeast are OVOID, 1.5 - 2 micrometers, found within macrophages and are CAPSULAR in appearnace

4) *An IMPORTANT attribute for virulence is it's ability to grow within macrophages, surviving in the phagocytic vacoule
INFECTIONS/ PATHOGENSIS
1) Inhaled spores (microconidia) reach the small bronichioles or alveoli and germinate after 2- 3 days

2) The yeasts then proliferate within the macrophages which migrate to the mediastinal lymph nodes, spleen, and liver, and then proliferate for 9- 15 days prior to onset of host cell mediated immune responses.

3) Yeasts are usually found INTRACELLULARY, but can also be found EXTRACELLULARLY in cases of overwhelming histoplasmosis

4) Epithelial cells can also be infected, which can serve as a resevoir of infection

5) Acute pulmonary histoplasmosis is found in immunocompetent hosts

6) Disseminated histoplasmosis is a rare and severe form of histoplasmosis. You may get this in AIDS

7) May also get CHRONIC PULMONARY HISTOPLASMOSIS as an opportunistic disease often mistaken for TB- - structural defects in the lung allow fungal colonization in abnormal pulmonary spaces
EPIDEMIOLOGY/ DIAGNOSIS
1) Soil is a native habitat and PERSON TO PERSON TRANSMISSION DOES NOT OCCUR

2) Skin testing surveys show that the central US is a major endemic area. Northern Texas is at the lower edge of the endemic area, but organisms exist around the world

3) POSITIVE histoplasmin test indicates exposure, but it does not necessarily indicate active infection

4) For DISSEMINATED histoplasmosis, a Wright stained smear of peripheral blood is almost always positive for intracellular yeasts within macrophages. The organism may also be isolated from blood cultures

5) For CHRONIC pulmonary histoplasmosis, a chest x- ray, CF test, sputum culture, and Wright stain of the sputum contribute to the diagnosis

6) Fungal stain of infected tissue and identification in the laboratory are used for diagnosis

7) Organisms can be cultured on special media; and you need a demonstration of dimorphism for identification
PREVENTION/ TREATMENT
Avoid environmental exposure.

Use ANTIFUNGAL treatment for disemminated disease.
2) BLASTOMYCES DERMATITIDIS
*
What is the CLINICAL SIGNIFICANCE OF BLASTOMYCES DERMATITIDIS?
B. dermatitidis causes a high frequency of clinical disease compared with mild and asymptomatic infections among people infected in epidemics and is a primary fungal pathogen.

Though blastomycosis occurs mainly as a sporadic infection in immunocompetent hosts, many epidemics and cases of opportunistic infection in AIDS patients and other immunocompromised hosts have been described.

Cell mediated immunity is vital in controlling growth.

Blastomycosis is a common infection of dogs in endemic zones, and canine infections are often sever or lethal.
PROPERTIES/ CHARACTERISTICS OF B. DERMATITIDIS
DIMORPHIC

FILAMENTOUS hyphal forms with associated aerial spores are produced in the laboratory cultures at room temperature.

Cultures appear cottony

At 37 degrees, cultures grow as yeasts, 5- 30 micrometers in diameter with single buds having a characteristic broad base

Colonies appear smooth
INFECTIONS/ PATHOGENESIS

Who is primarily infected by this organism?

How is it transmitted?

What are its symptoms?

What is the function of BAD1 gene?

What happens to the fungi in the host's lungs at 37 degrees?
Humans and other mammals are primarily infected by inhalation of spores from hyphae in soil where B. dermatitidis is believed to dwell as a saprophyte

The acute primary pulmonary infection with B. dermatitidis may be asymptomatic or may produce an influenza- like syndrome

An acute infection may resolve spontaneously, but progressive disease involved in the lungs/ other organs develops in many patients.

A surface protein, BAD 1 is require for virulence. It is homologous to invasion genes of gram -ve bacteria, and promotes uptake by macrophages

At 37 degrees, in the host, the conidial spores transform into pathogenic yeast- phase cells, which multiply in the lung and may disseminate in the bloodstream and lymphatics to visceral organs

The organism has a tropism for skin and bone.
EPIDEMIOLOGY/ DIAGNOSIS
The environmental distribution is difficult to define because of the lack of a specific, sensitive skin test.

The organism is antigenically cross reactive with H. capsulatum. Sporadic cases suggest endemic regions surround the Mississippi and Ohio river basins and in the Carolinas.

Recreational activity in the wooded areas along waterways is a major risk factor.

B. dermatitidis grows exclusively in the yeast form within hosts and may be detected with KOH mounts or fungal stains in infected tissue

Organisms can be cultured on special media; demonstration of dimorphism and the tissue form is necessary for identification

An immunodiffusion test for patient antibodies to the "A" antigen produced from culture filtrates of B. dermatitidis has been developed.
3) COCCIDIOIDES IMMITIS
*
What is the FREQUENCY/ CLINICAL SIGNIFICANCE of C. immitis?

What are the symptoms like? What do they sound like?

How long does the disease last?
40% of infected individuals have symptoms consistent with a lower respiratory infection and/ or systemic illness with some of the following symptoms:

- cough
- sputum
- chest pain
- malaise
- fever and chills
- night sweats, anorexia
- weakness
- arthralgia

The disease lasts 2-6 weeks and is called Valley fever.

A small number of cases progress to a chronic pulmonary form characterized by cavity formation

Disseminated disease occurs more commonly in those with immunosuppression, but can occur in immunocompetent adults as well
PROPERTIES/ CHARACTERISTICS OF C. IMMITIS

What are ARTHROCONIDIA and what is signifcant about it?

What are the SPHERULES?
The environmental mycelial phase of C. immitis contains barrel shaped ARTHROCONIDIA which are easily fragmented and highly infectious

These can be hazardous when cultured in the laboratory

Spherules, large (12- 100 micrometers), thick- walled structers containing numerous endospores, are formed in the host.
INFECTIONS/ PATHOGENESIS

What happens to the ARTHROCONIDIA in the lungs?

What results after the rupture of the spherules?

What does the initial host response consist of?
Inhaled ARTHROCONIDIA (2- 6 micrometers) lodge in the alveoli and develop into spherules in the tissue

Rupture of the spherules release large numbers of endospores into the tissue which develop into spherules

The initial host response consists of macrophage and neutrophils

Fungi are resistent to killing by neutrophils

THe onset of cell mediated immunity leads to protection
EPIDEMIOLOGY/ DIAGNOSIS OF C. IMMITIS

Where is C. immitis endemic?

Where does the fungus like to grow?

Who is most affected by this disease?
COCCIDIOMYCOSIS is endemic in certain areas of North, Central, and South America. Central Texas is situated in the Eastern edge of teh endemic areas in the US

100,000 people are infected anually

The fungus likes to grow in arid climates, hot summers, low altitude, and alkaline soil and sparse flora.. Positive culture have not been found in the soil.

Symptoms are more common in men of dark- skinned races, particularly Filipinos

Spherules may be detected with KOH mounts or fungal stains in infected tissue
How can you culture C. immitis

What does the skin test reveal?

Are the serologic tests useful?
Organisms can be cultured on special media; demonstration of dimorphism and tissue form is necessary for identification. The environmental form produces arthrospores that are hazardous to laboratory workers.

Skin tests become positive after 1- 4 weeks after the onset of primary symptoms and remians positive for life. However, disemminated infection can cause anergy.

Serologic tests are useful for monitoring the progress of the disease

IgM ppt ab becomes positive in th efirst three weeks of illness. Complement fixing IgG ab develop later; titers increase with disseminated disease.

Ab disappear with resolution of disease and persist with continuing infection.
PREVENTION/ TREATMENT
Avoid environmental exposure

ANTIFUNGAL treatment for disseminated disease