Histoplasma

capsulatum and
Histoplasmosis
1

Histoplasmosis
An
intracellular
mycotic
infection
of
the
reticuloendothelial system caused by the inhalation of the
fungus. Approximately 95% of cases of histoplasmosis are
inapparent, subclinical or benign. Five percent of the cases
have chronic progressive lung disease, chronic cutaneous
or systemic disease or an acute fulminating fatal systemic
disease. All stages of this disease may mimic tuberculosis.
Distribution: World-wide, especially U.S.A.
cases do occur in Australia.

Sporadic

Aetiological Agent: Histoplasma capsulatum, especially

from soil enriched with excreta from chicken, starlings and
bats.

Member of the phylum Ascomycota

Worldwide distribution
Naturally found in fecal-contaminated soils
Birds and bats appear to be reservoirs
Etiologic agent of histoplasmosis

 Dimorphic fungus
Sexual multi-cellular saprophytic
mycelia
Asexual single-celled parasitic
yeast

Mycelial form is most

commonly found in the
environment
Heterothallic species
Tightly coiled septate hyphae
(A)
Globose cleistothecia (C)
Pear-shaped asci (E)
Smooth, hyaline, spherical
ascospore (F)

 Infection begins with inhalation of microconidia or hyphal

fragments
Mycelial form transforms into yeast form
Triggered by elevated temperatures and increased cysteine levels

3-stage process
1. Heat shock
phenomenon
2. Restimulation of
cellular respiration
3. Increase of RNA
& protein synthesis

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The most common symptoms are:

Chest pain.
Chills.
Cough.
Fever.
Joint pain and stiffness.
Muscle aches and stiffness.
Rash (usually small sores on the lower
legs called erythema nodosum)
Shortness of breath.

Diagnosing histoplasmosis can be complicated,

depending on the area of the body being
affected. While testing is not usually necessary
for mild cases of histoplasmosis, it can be crucial
to help choose appropriate treatments in lifethreatening cases.
Each type of lab test for histoplasmosis has its
limitations. Your doctor may suggest a
combination approach to search for evidence of
the disease in samples of:
Lung secretions
Blood or urine
Biopsied lung tissue
Bone marrow

The diagnosis rests upon demonstrating the fungus or an immune

response to the fungus. Some of the many diagnostic laboratory
tests available include the following:

Cultures of body fluids or tissues to identify the fungus

Detection of surface markers ofHistoplasmain a urine test

Blood tests to measure antibody response toHistoplasma

Microscopic examination of samples of infected tissues

Chest X-rays in people with acute histoplasmosis are usually

normal. However, so-called coin lesions or histoplasmomas may be
seen in the chest X-rayof people with healed histoplasmosis.
These are round accumulations of scar tissue. Calcification of
lymph nodes around the bronchi may be evidence of prior healed
infections. Depending on the severity and stage of the disease,
infiltrates or other changes may be apparent on X-rays.

CT scans are useful to identify areas of spread in disseminated

Treatment for Histoplasmosis

Mild cases of histoplasmosis that are limited to the lungs will
resolve without specific treatment in about a month. Severe or
disseminated cases of histoplasmosis require treatment with
antifungal medications.
Itraconazole(Sporanox, Onmel),Fluconazole(Diflucan), and
amphotericin B(Ambisome, Amphotec; drug of choice for severe
disease) are antifungal drugs that are typically used to treat
histoplasmosis. Treatment may need to be continued for a
period of several months.

Amphotericin B
Amphotericin A & B are
antifungal antibiotics.
Amphotericin A is not used
clinically.
It is a natural polyene macrolide
(polyene = many double bonds )
(macrolide = containing a large
lactone ring )

Poorly absorbed orally , is

effective for fungal infection of
gastrointestinal tract.
For systemic infections given as
slow I.V.I.
Highly bound to plasma protein
.
Poorly crossing BBB.
Metabolized in liver
Excreted slowly in urine over a
period of several days.
Half-life 15 days.

ADVERSE EFFECT

1- Immediate reactions ( Infusion related toxicity ).

Fever, muscle spasm, vomiting ,headache, hypotension.
Can be avoided by :
A. Slowing the infusion
B. Decreasing the daily dose
C. Premedication with antipyretics, antihistamincs or
corticosteroids.
D. A test dose.

 NURSING CARE MANAGEMENT

Provide oxygen therapy if needed. Plan rest periods.
Obtain chest X-ray results to determine if the patient
has pulmonary or pleural effusion.
Assess the patient respiratory status every shift. Note
diminished breath sounds or pleural friction rub, and
evaluate for effusion.
Check the patients cardiovascular status every shift.
Monitor the patients neurologic status every shift and
report any changes in level of consciousness or nuchal
rigidity.

NURSING CARE MANAGEMENT

Observe forsigns and symptomsof
hypoglycemia and hyperglycemia, which
indicate adrenaldysfunction.
Test all stools for blood and report its
presence.
Teach the patient about drug therapy,
including adverse effects.
Inform the patient about the need for
follow-up care on a regular basis for at
least a year.
Tell the patient to report to the doctor
cardiac andpulmonarysigns that could
indicate effusions.