LECTURE FIVE DR. Jabar Etaby
Pneumocystiscarinii
Pneumocystis carinii is an important cause of pneumonia in
immunocompromised individuals.The classification and life cycle of Pneumocystis
are unclear. Many aspects of its biochemistry indicate that it is yeast, but it also has
several attributes of a protozoan. An analysis of rRNA sequences and
mitochondrial DNA and of various enzymes supports the idea that it is afungus.
However, the findings that it does not grow on fungal media and that antifungal
drugs are ineffective have delayed acceptance of its classification as a fungus. Each
mammalian species is thought to have its own species of Pneumocystis.
Pathogenesis & Epidemiology
Transmission occurs by inhalation, and infection is predominantly in the
lungs. The presence of cysts in the alveoli induces an inflammatory response
consisting primarily of plasma cells, histiocytes, lymph resulting in a frothy
exudate that blocks oxygen exchange. (The presence of plasma cells has led to the
name "plasma cell pneumonia.") The organism does not invade the lung tissue.
P.carinii is distributed worldwide. It is estimated that 70% of people have
been infected.
Life cycle:
Trophic forms, sporocytes and mature cysts are the three main
morphological forms in the Pneumocystis life cycle. Trophic forms are the
most abundant stage: these vegetative forms appear as mononuclear, 2-8 µm
in diameter, with thin cell wall consisting of an electron-dense single layer.
ameboid in shape, trophic forms display cytoplasmic projections known as
filopodia, which allow them to attach closely to type I pneumocytes.
Ultra-structural studies as well as the recent discovery suggest the
existence of mating types and the probable conjugation of Pneumocystis
trophic forms in. Following the fusion of mating types, a round, thin-walled,
mononuclear and probably diploid early sporocyte is produced and shortly
thereafter enters a meiotic division process. Meiosis is followed by an
additional mitotic replication resulting in eight nuclei in the late sporocyte
stage.
An electron-lucent layer appears between the electron-dense layer
and the plasma membrane of the intermediate sporocyte. It further thickens
at the late sporocyte stage to finally produce a thick-walled mature cyst that
measures 4-7 µm in diameter. Its surface is rather smooth, with few
filopodia. In the mature cyst, eight individual spores are clearly delineated
and are protected by a cell wall that appears as thick as the cell wall of the
trophic form
Clinical Findings
The sudden onset of fever, nonproductive cough, dyspnea, and tachypnea is
typical of Pneumocystispneumonia.In infants, the disease usually has a more
gradual onset. The mortality rate of untreated Pneumocystis pneumonia approaches
100%.
Laboratory Diagnosis
Diagnosis is made by finding the typical cysts by microscopic examination
of lung tissue or fluids obtained by bronchoscopy, bronchial lavage, or open lung
biopsy. Sputum is usuallyless suitable. The cysts can be visualized with
methenamine-silver, Giemsa the cyste appear as a round masses of unstained
cytoplasm containing 2-8 purple stained nuclei. Fluorescent-antibody staining is
also commonly used for diagnosis. The organism stains poorly withGram stain.
There is no serologic test, and the organism has not been grown in culture. PCR-
based tests are being developed.
Treatment
The treatment of choice is a combination of trimethoprim and sulfamethoxazole
(Bactrim, Septra).
Sarcocystis
Causative agent of sarcocystosis
Sarcocystis hominis
Sarcocystis suihominis
Sarcocystis lindemani
Sarcocystis hominis and S. suihominisare known as human intestinal
parasites. Infection results from ingestion ofraw or insufficiently heated meat from
cattle (Sarcocystis hominis) or pigs (Sarcocystis suihominis), which frequently
contains muscle cysts of these species.The prevalence of intestinal sarcocystosis in
humans is low and is only rarely associated with illness, except in volunteers who
ingest large numbers of sarcocysts. Cases of infection of humans as intermediate
hosts, with intramuscular cysts, number less than 100 and are of unknown origin.
Life cycle:
Man gets infection by eating raw or undercooked meat that contained
sarcocyst, in the small intestine of definitive host (man) the brodyzoites are
released and they migrate to sub epithelial lining and develop to male and female
gametocyte. Fertilization occur to form thin-walled oocysts that sporulate in the
intestinalwall. Once the frail oocyst wall has burst, free sporocysts containing four
sporozoites each are excreted with stool in most cases. The sporozoites are
infectious for intermediate hosts.
When the intermediate host get these sporocysts it infect the endothelial cells
of blood vessels and schizogony cycle occurs. Those schizont rupture releases
merozoites in the blood vessels and go to striated muscles and develop into tissue
cyst ( sarcocyst). In case of sarcocytis lindemani similar man can act as
intermediate host and asexual cycle may occur in the striated muscle.
.
Clinical manifestations: Both speciescan cause short-lived (6 to 48 hours)
symptoms within 24 hours of eatingmeat containing cysts, for example nausea,
vomiting, and diarrhea as well as a mild fever. S. suihominis is more pathogenic
than S. hominis.
Diagnosis: An intestinal infection with Sarcocystis can be diagnosed by detection
of sporocysts (14 X 9 μm), or more rarely oocysts (approx. 20 X 13 μm) in stool
using the SAFC or the flotation method. The two Sarcocystis species cannot be
differentiated.
Treatment:An effective therapy hasnot yet been developed.
Prevention: consists in boiling or deep-freezing(–20 C for three days) of pork and
beef.