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APPENDIX B Answers to Case Studies: Under the Microscope
CHAPTER 3
Case Study 3-1: Under the Microscope
1. The most likely cause of the infection is the
atrial ameba Naegleria fowleri.
2. Patients who contract N. fowleri resulting in
colonization of the nasal passages are usually
asymptomatic. However, in this case, the
patient developed primary amebic meningoencephalitis
(PAM). This condition occurs when
the ameboid trophozoites of N. fowleri invade
the brain, causing rapid tissue destruction.
3. N. fowleri has three morphologic forms—
ameboid trophozoite, flagellate trophozoite,
and cyst. The ameboid trophozoites of N.
fowleri are the only form known to exist in
humans. Replication of the ameboid trophozoites
occurs by simple binary fission. The
ameboid trophozoites transform into flagellate
trophozoites in vitro after being transferred
to water from a tissue or culture. The
flagellate trophozoites do not divide but lose
their flagella and convert back into the
ameboid form, in which reproduction resumes.
The cyst form is known to exist only in
the external environment. It appears that the
entire life cycle of N. fowleri occurs in the
external environment; it is primarily found in
warm bodies of water, including lakes,
streams, ponds, and swimming pools. Humans
primarily contract this ameba by swimming
in contaminated water. The ameboid trophozoites
enter the human body through the
nasal mucosa and often migrate to the brain,
causing rapid tissue destruction. Some infections
may be caused by inhaling dust infected
with N. fowleri cysts. The mechanics of how,
when, and where the transition of the cysts to
ameboid trophozoites occurs after the cysts
have been inhaled by a human have not been
described. The ameboid trophozoite is the
diagnostic stage of the infection.
4. Unfortunately, medications used to treat meningitis
and amebic infections are ineffective
against N. fowleri. There is evidence, however,
that prompt and aggressive treatment with
amphotericin B may be of benefit to patients
suffering from infections with N. fowleri,
despite its known toxicity. In rare cases,
amphotericin B in combination with rifampin
or miconazole has also proved to be an effective
treatment. Amphotericin B and miconazole
damage the cell wall of N. fowleri,
inhibiting the biosynthesis of ergosterol and
resulting in an increased membrane permeability
that causes nutrients to leak out of the
cells. Rifampicin inhibits RNA synthesis in
the ameba by binding to beta subunits of
DNA-dependent RNA polymerase, which in
turn blocks RNA transcription. A person can
survive if signs are recognized early but, if
not, PAM almost always results in death. The
survival rate is low, so prevention and early
detection are important. However, because of
the numerous bodies of water that may potentially
be infected, total eradication of N.
fowleri is highly unlikely.
5. Microscopic examination of cerebrospinal
fluid (CSF) is the method of choice for recovery
of N. fowleri ameboid trophozoites (see
Chapter 2).
6. The diagnosis of PAM is difficult because the
infection is often confused with other bacterial
or viral infections because of similarities
in clinical manifestations and laboratory
results. The peripheral white blood cell (WBC)
count is elevated with a neutrophilia in
PAM. Analysis of the spinal fluid reveals an
increased pressure, resulting in a hemorrhagic
specimen. There is also a high white blood
cell count with a neutrophilic predominance
and high red blood cell (RBC) count, as well
as an elevated protein level and a low to
normal glucose level in the spinal fluid. The
Gram stain of the spinal fluid is negative for
bacteria. A basic metabolic panel may show
abnormalities such as hyponatremia associated
with acquired hyperglycemia. PAM is
obvious when the spinal fluid is purulent,
with no bacteria present. It is best diagnosed
with a wet mount examination of the spinal
fluid for N. fowleri along with standard laboratory
tests (e.g., WBC, RBC, glucose, protein,
bacterial and fungal cultures) of the spinal