-
-
-
o Trophozoites: can be seen
in exodates or base of ulcer
o Asymptomatic
- Balantidial
dysentery/balantidiasis/ciliate dysentery
(cause by B. coli) vs. Amoebic dysentery
- Acute: 6-15 episodes of
diarrhea/day
- Chronic: Diarrhea alternate with
constipation
- Accompanied by Abdominal
Tenderness, anemia and cachexia
- Dysentery is an infective disease
of the large bowel which is characterize
by frequent passage of blood in mucous
with stool along with several abdominal
cramps
- Amoebic Dysentery or
amoebiasis is an infection of intestine or gut caused by an amoeba (E. hystolytica). Severe amoebic
dysentery is usually diarrhea with blood
Diagnosis
o DFS or concentration technique (trophozoite and cyst can be seen)
o Rectal biopsy
o Culture method (Barnet and Yarbrough’s medium, Balamuth’s medium)
Treatment
o Tetracycline (500 mg 4x daily for 10 days)
o Metronidazole 750 mg 3x daily for 5 days
Prevention
o Proper sanitation
o Safe water supply
o Protection of food from contamination
SYNTHESIS: Balantidium coli is the only pathogenic ciliate and is the largest protozoan parasitizing humans.
The most important key structure of identification of this protozoa is the presence of cilia. Some individuals
with B. coli infections are totally asymptomatic, whereas others have symptoms of severe dysentery similar in
amoebiasis caused by E. histolytica.
SECTION 5E: MORPHOLOGY, PATHOPHYSIOLOGY, LIFE CYCLE, SPECIMENS USED FOR
IDENTIFICATION, DIAGNOSTIC FEATURES, PREVENTION & CONTROL OF THE PHYLUM
APICOMPLEXA CLASS SPOROZOA
LESSON PROPER
The phylum Apicomplexa includes parasitic protozoa that live in the body fluids or tissues of the host.
It takes its name from the apical complex that is generally present at some stage. Most of the
Apicomplexa parasitizing humans belong to the class
Sporozoa, in which the life cycle is characterized by an alternation of generations, one sexual, and
one asexual, occurring in the same host, or requiring an alternation of hosts. In the asexual
reproductive life cycle of development, multiplication is by schizogony, while in the sexual cycle, it is
by sporogony, which involves fertilization or syngamy.
Locomotion of the mature organisms is by body flexion, gliding, or undulation of longitudinal ridges;
flagella are present only on the microgametes, of some groups; pseudopodia if present, are used for
feeding, not for locomotion.
GENERAL CHARACTERISTICS:
• Obligate intracellular parasites
• Life Cycle includes:
o Sexual reproduction (Sporogony): in arthropod vector
▪ The sexual cycle occurs within the intestinal lumen of the invertebrate host
▪ END PRODUCT: SPOROZOITE (infective stage to man)
o Asexual reproduction (Schizogony): in man
▪ Asexual cycle occurs in the epithelial cells of the intestinal mucosa
▪ END PRODUCT: SCHIZONTS (infective to mosquito)
MALARIAL PARASITES
PLASMODIUM
- Transmitted by the bite of infected plasmodium female mosquito
- Pigment producers (due to Hgb)
- Vertebrates: asexual cycle (Schizogony)
- Invertebrates: sexual cycle (Sporogony)
Module:
Phylum: Apicomplexa → Class: Sporozoa → Blood species: Plasmodium
• Pathogenic to man
• Causative agent of malaria
• Principal vector: Anopheles minismus var. flavirostris
• Characteristics:
o Obligate intracellular parasites of blood and tissues
o Alternation of generations (sexual and asexual development)
o Alternation of host:
▪ Sexual cycle – female mosquito (Anopheles minimus flavirostris)
▪ Asexual cycle – man
• Mode of Transmission:
o sporozoites liberated into the bloodstream via bite of an infected female mosquito;
o through blood transfusion
o vertical transmission
• Symptoms and Pathology:
o Anemia (due to massive red cell destruction), splenomegaly, joint pain
o Recurrent/Intermittent chills and fever (synchronized rupture of red blood cells)
▪ Every 36 hours: Malignant Tertian Malaria (P. falciparum)
▪ Every 48 hours: Ovale Malaria (P. ovale)
▪ Every 48 hours: Benign Tertian Malaria (P. vivax)
▪ Every 72 hours: Quartan Malaria (P. malariae)
Quotidian fever – is caused by the asynchronous release of merozoites in the
circulation
Stages of Development:
1. Trophozoite
o Feeding or growing stage in the asexual cycle
o Lives within the tissue cell
2. Schizont
o Sporozoan body during schizogony which includes the period of initial growth (the early
schizont or presegmenter) to complete splitting up of the nucleus with merozoite
production
3. Merozoites/late segmenters
o End product of schizogony in human reticuloendothelial cells
o Motile and escapes from the infected cells
o Released from the infected cell
o Some will infect other tissue cells going back to the trophozoite stage
o Others will be differentiated into male and female form (known as gametocytes)
o
Image 1: Picture of infected Red Blood Cells
4. Gametocyte- immature sexual form
a. macrogametocyte
o female gametocytes
o produce a macrogamete
o mature only to be fit for fertilization
b. microgametocytes
o male gametocytes
o produced a group of microgametes
5. Gametes – mature sexual forms
a. Macrogametes
o Female sex cells in sporozoa
b. Microgametes
o Male sex cell in sporozoa
6. Zygote
o Fertilized ovum/ova before cell division
o Union of macrogamete and microgamete
7. Oocyst
o Encysted zygote
8. Sporoblast
o One of a number of bodies into which zygote divide
o Developed into sporozoites
9. Sporocyst
o Membrane that surrounds a sporoblast
o the separated membrane that surrounds a sporoblast and subsequently the group of
sporozoites formed from this sphoroblast
o
10. Sporozoite
o End product of sexual multiplication of malarial parasite in mosquito
GLOSSARY:
• Bradyzoites – slowly multiplying trophozoite contained in the cyst of T. gondii
• Exflagellation – extrusion of rapidly waving flagellum-like mircogametes from
microgametocytes
• Gamete – mature sex cell of plasmodia
• Gametocyte – immature sexual form of plasmodia (male microgametocyteor female
microgametocyte) that is present in peripheral blood
• Gametogony – development phase in the life cycle of malaria and coccidian parasites in
humans in which male and female gametes are formed
• Hypnozoite – exoerythrocytic schizont of P. vivax and P. ovale in the human liver,
characterized by delayed primary development; responsible for true relapse in malaria
• Merogony – also known as schizogony; leading to the production of merozoites in some
intestinal coccidians
• Merozoite – product of schizogonic cycle in malaria; produced in the liver (pre-erythrocytic
cycle) and in the red blood cells (erythrocytic cycle); motile and infects the red blood cells
• Oocyst – encysted form of the ookinete that occurs in the stomach wall of Anopheles spp.
• Ookinete – motile zygote of Plasmodium spp; formed by microgamete fertilization of
macrogamete
• Paroxysm – fever, chills, sweats syndrome in malaria; spiking fever corresponds to the release
of merozoites and toxic material from the rupturing parasitized red blood cells, and shaking
chills occur during subsequent schizont development
• Recrudescence – increased severity of a disease after a remission or following treatment as a
result of an inadequate immune response by the host or inadequate response to treatment
• Relapse - a recurrence of illness/signs and symptoms of a disease after a period of
improvement; In malaria, it is caused by the reactivation of hypnozoites in the liver that begins
a new cycle in red blood cells; occurs only in Plasmodium vivax
and P. ovale infections
• Schizogony – (Asexual cycle) occurs on the epithelial cells of the intestinal mucosa producing
schizonts
• Schizont – developed stage of asexual division of the sporozoa; ruptures to produce
merozoites
• Sporogony – (Sexual cycle) occurs within the intestinal lumen of the invertebrate host. End
product → sporozoite
• Sporozoite – slender, spindle-shaped organism; infective stage of malaria parasites; inoculated
into humans by the bite of an infected female mosquito; It is the result of the sexual cycle in the
Anopheles mosquito
• Tachyzoites – rapidly multiplying stage in the development of the tissue phase of certain
organisms such as Toxoplasma gondii
• Trophozoite – feeding or growing stage in the asexual cycle
• Zygote – union of the macrogamete and microgamete; fertilized ovum/ova before cell division
Image 2: Life cycle of Plasmodium
SPECIES
Plasmodium vivax
-
Benign Tertian Malaria
Intermittent fever every 48 hours
Prepatent period: 11-15 days
Incubation Period: 12-20 days
Can lead to severe disease and death due to splenomegaly (enlargement of spleen)
Single large ring succeeded by amoeboid form in pale large red cell
Schuffner’s dot (condensed hemoglobin) in red cells
Only reticulocytes are invaded
Round gametocyte
Plasmodium ovale
Ovale Tertian Malaria
Intermittent fever every 48 hours
Prepatent period: 14-26 days
Incubation Period: 11-16 days
Recently shown by genetic method to consist of two sub-species. Plasmodium ovale curtisi
and Plasmodium ovale wallikeri
Single compact ring
Large pale red cells with Schuffner’s dots which may be oval
and fimbriated
Plasmodium malariae
Quartan Malaria
Intermittent fever every 72 hours
Prepatent period: 3-4 weeks
Incubation period: 18-40 days
Single large compact ring or band forms
Invades old RBCs
Schizont with merozoites arranges around central pigment
(resembles fruit pie)
Ovoid gametocytes
Plasmodium falciparum
Malignant Tertian Malaria
Intermittent fever every 36-48 hours
Prepatent period: 11-14 days
Note:
-
Incubation period: 8-15 days
Small ring forms (1/6 diameter red cell), applique forms, double nuclear dots
Organisms invades all ages of red blood cells (most severe)
Crescent/banana-shaped gametocytes
Plasmodium vivax infection is most widely distributed and most prevalent worldwide
Plasmodium falciparum infection is most likely fatal
o Cerebral malaria: red cells, organisms and pigment can block the brain vessels
o Blackwater fever: sudden massive intravascular hemolysis resulting to hemoglobinuria
Laboratory Diagnosis:
- Microscopic identification of the malarial parasites in thick and thin blood smears stained with
Giemsa or Wright’s stain is still important in making the definitive diagnosis and remains the
gold standard method.
- Collection of specimen must be prior to fever spike
- Bone marrow (through sternal puncture)
- Malaria RDTs (Rapid Diagnostic Tests):
o Plasmodium LDH – produced by both sexual and asexual stages and can distinguish
between P. falciparum and non-P. falciparum species
o Examples: Diamed Optimal IT
o Immunochromatography – detects Plasmodium-specific antigens; these target antigens
are called HRP II (Histidine-rich protein)
o Examples: Paracheck Pf test and ParaHIT f test
- Serological tests (to detect the presence of malarial antibodies)
MALARIAL PAROXYSM
3 stages:
1. Cold stage
o Sudden feeling of coldness
o Feeling of inappropriate comprehension
o Mild shivering, violent teeth chattering
o Vomitting and febrile convulsions
o Rigors last for 15-60 minutes
2. Hot Stage or Flush Phase
o Characterized by very high temperature
o Manifests with headache
o Palpitations, tachypnea, epigastric discomfort
o Temperature: 40-41 celsius
o Lasts for 2-6 hours
o Confusion and the patient can be delirious due to very high temperature
o Skin is flush and hot
3. Sweating Stage
o Profuse sweating
o Temperature lowers over the next 2 to 4 hours because of the sweating
o Symptoms diminish
o Total Duration: 8-12 hours
Asexual phase in man (SCHIZOGONY/MEROGONY)
Pre-erythrocytic/Exo-erythrocytic schizogony:
- Begins with the inoculation of the infective sporozoites to man during a mosquito blood meal
- Within ½ hour, they are carried through blood circulation into the liver parenchymal cells where
they undergo nuclear and cytoplasmic division and develop into pre/exo-erythrocytic schizonts
-
Schizonts rupture producing exoerythrocytic merozoites that reinvade liver cells, while other
invade the RBCs
- In the RBC, merozoite develops into trophozoite
- In P. vivax and P. ovale, sporozoites develop into hypnozoites which remain dormant for years
in the hepatocytes. At a predetermined time, the hypnozoites begin to grow and undergo exoerythrocytic schizogony releasing merozoites that invade RBCs causing a recurrence of the
malaria attack
Erythrocytic schizogony:
- The trophozoite further matures into schizont, then divide into erythrocytic merozoites
- RBC ruptures releasing merozoites into the bloodstream
Sexual phase in mosquito (SPOROGONY)
- The male and female gametocytes sucked in by the mosquito undergo maturation and
differentiate into micro- and macrogametes
- The microgamete exflagellates and fertilizes the macrogamete producing a zygote as a result
of fertilization
- Ookinete penetrates the stomach wall and forms an oocyst
- Within the oocyst, numerous sporozoites are formed
- Oocysts grows and ruptures releasing sporozoites
- Sporozoites migrate through tissues to the salivary glands
Plasmodium Species
Plasmodium Plasmodium
malariae
ovale
Quartan
Ovale malaria
malaria
72 hours
48 hours
Point of
Plasmodium
Differentiation falciparum
Disease
Malignant
malaria
Paroxysm
36- 48 hours
cycle
Appearance of Normal; multiply
RBC size
infected red blood
cells are common
Number of
merozoites
Schuffner’s
stippling
(precipitated
Hb)
Parasite
cytoplasm
Normal
Plasmodium
vivax
Tertian malaria
48 hours
Enrlaged; maximum
size may be 1 – 2
times normal RBC
diameter
6 – 32 (average is
20 – 24)
Enlarged;
approximately
20% or more
of infected
RBCs are
oval and/or
fimbriated
(border has
irregular
projections)
6 – 14;
average is 8
Positive:(Schuffner’s
dots; present with all
stages except in
early ring forms)
Young rings are
small, delicate,
often with double
Positive:
(James’ dots;
present in all
stages except
early ring
forms)
Rounded,
compact
trophozoites;
6 – 12
(average is
8); “rosette”
schizonts
Negative:(Maurer’s Negative:
dots occasionally
(Ziemann’s
seen)
dots rarely
seen)
Rounded,
compact
trophozoites
12 – 24; average is
16
Irregular, ameboid
trophozoites; has
“spread out”
chromatin dots;
gametocytes are
crescentshaped or
elongated
with dense
cytoplasm;
band-form
trophozoites
occasionally
slightly
amoeboid;
growing
trophozoites
have large
chromatin
mass
Red cell
containing
trophozoite
may have
fimbriated
edges
Dark brown,
conspicuous
appearance
Trophozoite
Accole or Applique
forms May have
multiple rings
Band
Appearance of
parasite
pigment
Shape of
gametocyte
Stages seen in
circulating
peripheral
blood
Black; coarse and
conspicuous in
gametocytes
Sausage or
crescentshaped
Rings and/or
gametocytes;
other stages
develop in blood
vessels of internal
organs but are not
seen in peripheral
blood EXCEPT in
severe infection
Dark brown,
coarse,
conspicuous
Round
Round
Round
All Stages
All stages; wide
range of stages may
be seen on any
given film
Yes
All stages;
wide variety
of stages
usually not
seen;
relatively few
rings or
gametocytes
generally
present
No
Multiple
infections
Others
No
Rare
High Mortality
Rarely Fatal
Least
common
Rarely fatal
May cause
relapses
Most common
Rarely fatal May
cause relapses
Amoeboid
Golden brown,
inconspicuous
ERYTHROCYTIC CYCLE:
- P. falciparum: 48 hours
- P. ovale and P. vivax: paroxysms occur on alternate days hence Tertian malaria
- P. malariae: paroxysmsn72 hours (on 1 and 4 days)
o Quartan malariae
Image 3: Disseminated intravascular coagulation in Falciparum malaria; thrombocytopenia
and prolong prothrombin time in Malariae; hyperfibrinogenemia
Image 4: Cerebral Malaria
Diagnosis
- Thick and thin blood examination
o Giemsa and Wright’s stain
o Specimen collection: anytime (every 6-8 hours is appropriate)
o In P. falciparum only the ring form can be found
▪ 10 days after symptoms begin gametocytes may be found
- Quantitative Buffy Coat (QBC)
o Malarial parasites: bright green and yellow under fluorescent microscope
o Only used for screening and needs traditional thick-thin films
o Special capillary tube coated with acridine orange
- ParaSight F test
o Antigen capture test
▪ Ag: trophozoite-derived histidine-rich protein II (HRP-II)
▪ High sensitivity and good specificity
▪ Deep stick test for simple and rapid diagnosis of P. falciparum
- Non-specific Test
o IHA
o Indirect Fluorescence Antibody Test (IFAT)
o ELISA
TREATMENT
- Causal Prophylactic Drugs
o Use to prevent establishment of parasite in the liver
- Blood Schizonticidal Drugs
o Attacks parasites in the RBC
- Gametocytocidal drugs
o Destroy sexual stage of parasite in blood
- Hypnozoiticidal or anti-relapse
o Prevent the occurrence of the disease
Sporonticidal Drugs
- Main uses of Anti-malarial drugs
o Protective (Prophylactic)
o Curative (Therapeutic)
o Prevention of transmission
- Inhibit the development of oocyst in the gut of mosquitos
Chloroquine
- Drug of choice
- 10 mg/kg once a day for 1st two days, then 5 mg/kg single dose on the 3rd day
- Pyrimethamine/sulfadoxine combination
- Quinine or quinidine: severe falciparum malaria
MALARIA LIFE CYCLE:
The life cycle of all species that infects human being is basically the same. There is an exogenous
asexual phase in the mosquito called the “Sporogony”, during this stage, the parasite multiplies.
There is also an endogenous asexual phase that takes place in the vertebrae or human host called
the “Schizogony”. This phase include the parasite development that takes place in the red blood
cells called erythrocytic cycle; and the phase that takes place in the parenchymal cells in the liver
called exoerythrocytic phase or also called the tissue phase. The Schozogony that takes place
here can occur without delay during the primary infection or it can be delayed during relapses in
malaria.
MALARIA TRANSMISSION CYCLE:
Babesia species
Phylum: Apicomplexa → Class: Sporozoa → Blood species: Babesia
• Pathogenic: Babesia microti
• Definitive host: Animals (Deer)
• Transmission: man infected by bite of a tick that belong to genus Ixodes (intermediate host);
can be transmitted through blood transfusion
• Infective stage: trophozoites liberated via the bite of deer tick
• Morphology:
o An obligate intracellular parasite (seen inside of an RBC measuring about 2 – 4 um)
o Pear-shaped
o Usually in pair or tetrads (resembling “maltese cross” appearance)
• Symptoms and Pathology: symptoms resemble Malaria
o Headache and fever
o Hemolytic anemia with hemoglobinuria in immunocompetent host
• Diagnostic stage: demonstration of characteristic ring forms in Giemsa-stained blood smears
(thick and thin smear)
•
•
•
Coccidians
Coccidian parasite are members of the Class Sporozoa in the Phylum Apicomplexa. The
subclass Coccidia includes species of Toxoplasma, Isospora, Sarcocystis, Cryptosporidium,
and Cyclospora
Life cycle:
o Schizogony (Asexual) in variety of nucleated cells
o Sporogony (Sexual) in intestinal mucosa of definitive host: infective oocyst are excreted
in the feces
Classification:
o Intestinal Coccidian:
▪ Prevalent in AIDS patient/immunocompromised persons
▪ Infective stage: oocysts
▪ Diagnostic stage: oocysts demonstrated in feces
o Tissue Coccidian
OPPORTUNISTIC SPOROZOANS:
1.
2.
3.
4.
Toxoplasma gondii
Cryptosporidium specie
Pneumocystis carinii
Isospora belli
Toxoplasma gondii
•
•
•
•
•
•
•
•
•
•
Tissue Coccidian
Disease: Toxoplasmosis
Morphology: Ovoidal, Pyriform or Cresentic
Mode of Reproduction: Longitudinal binary fission
MOT: Ingestion of uncooked, fecal contamination, nasal route, transplacental
Prevalent in AIDS patients/immunocompromised persons
Definitive host: Cat
Infective stage: OOCYST
Intermediate host: humans
Habitat: intracellular obligate parasite of endothelial cells, mononuclear leukocytes, body fluids,
and tissue of the host
• Transmission:
o Accidental ingestion/inhalation of oocysts from cat feces
o Ingestion of undercooked meat or oocysts from cat feces ➢ Transplacental
o Organ transplants
• Morphology:
o Crescent appearance in tissue fluids
• Tissue stages in man:
o Bradyzoites (Chronic Phase)
▪ slow proliferation during this
o Tachyzoites (Acute Phase)
▪ Rapid multiplication
• Pathogenesis:
o Associated with the RES or endothelium of the circulatory system
o Serous fluids in the body cavities
o Necrosis of the invaded area
• Disease: Toxoplasmosis o Major cause of encephalitis in AIDS patients
o Acquired toxoplasmosis:
▪ Appears after the infection and regional lymph node invasion
▪ Parasite is blood borne to many organs where intracellular multiplication takes
place o Major cause of congenital toxoplasmosis among the newborns:
▪ Congenital infection causes birth defects and mental retardation
PATHOLOGY AND SYMPTOMATOLOGY:
1. Congenital Toxoplasmosis
▪ Occurs in 1-2% per 100 pregnancies
▪ Severe and fatal
▪ Degree of severity varies with age of the fetus during the infection & antibody production
of the mother
▪ Hydrocephaly, chorioretinitis, microcephaly, psychomotor disturbances and convulsions.
2. Acquired Toxoplasmosis
▪ Regional lymph node invasion
▪ Intracellular multiplication in various organs
▪
▪
Acquired infection of toxoplasma in immunocompromised patients is generally
asymptomatic. However, 10-20% of patients with acute infection may develop
cervical lymphadenopathy or flue like illness.
Clinical course is usually benign and self-limited so symptoms usually resolve in
a few weeks to months.
DIAGNOSIS:
• Sabin-Feldman Dye Test
o Methylene blue staining of tachyzoites inhibited by prior addition of patient serum
containing antibodies of Toxoplasma
• Indirect Hemagglutination
o For circulating antibodies
• Serological diagnosis:
o EIA and IFA -for detecting neonatal toxoplasmosis
• ELISA test
• Xenogiagnosis
Note: T. gondii is a protozoan parasite that infects most species of a warm blooded animal including
man and can cause the disease called toxoplasmosis. Serologic prevalence data will indicate that
toxoplasmosis is one of the most common human infections throughout the world. High prevalence
infection in france has been related to a prevalence for eating raw or undercooked meat while high
prevalence in Central America has been related to frequency of stray cats in a climate favouring the
survival of oocyst and soil exposure.
_________________________________________________________
Cryptosporidium species
•
•
•
•
Diagnostic stage: Oocyst with 4 naked sporozoites
Infective Stage: Sporozoites
Important opportunistic infection in AIDS patients
Pathogenesis:
o Acute, self-limniting diarrhea of 1-2 weeks duration
o Intense abdominal pain and bloating, anorexia, weakness.
DIAGNOSIS:
• Biopsies of ileum and jejunum
• Cryptosporidium oocyst in stool:
o DFS
o Concentration Techniques
• Staining with Periodic Acid Schiff, Geimsa, Kinyoun or Ziehl-Neelsen Acid Fast
Intestinal Coccidia
Cryptosporidium parvum
• Intestinal Coccidian
• Important opportunistic infection in AIDS patients
• Mode of Transmission:
o Ingestion of oocysts from food or water contaminated with animal feces
o Oral-anal route
o Direct contact with infected individual or animal
• Method of infection:
o Upon ingestion, sporozoites released from oocyst
o Develop in brush border of intestinal epithelial cells
o Sporulated oocysts, containing 4 sporozoites each (no sporocysts), are passed in feces
o Infective oocysts are transmitted via fecal-oral route
•
Disease: Cryptosporidiosis
o Causes intestinal infection: associated with watery, frothy diarrhea with oocysts shed in
feces
o Causes chronic diarrhea in immunocompromised person
Cyclospora cayetanensis
• Intestinal Coccidian
• Method of infection:
o infective oocysts ingested in contaminated food and water
o outbreaks have been associated with contaminated berries
• Clinical disesase: indistinguishable from cryptosporidiosis
• Diagnosis:
o Modified AFS
▪ Oocysts stain from light pink to deep red (acid-fast variable)
▪ Average size: 8 – 10 um (larger than C. Parvum)
________________________________________________________
Pneumocystis jeroveci (carinii)
•
•
•
•
•
•
•
•
Disease: Interstitial plasmacellular pneumonia or pneumocystosis
Most common pneomocystic infection in patients with HIV
Rare cause of infection in the general population but it is a frequent cause of morbidity and
mortality in persons who are immunocompromise especially with patients with AIDS
Habitat: Lungs
MOT: airborne
Cyst: small, round with 8 uninucleated bodies
Trophozoites: crescent, sickle or pear-shaped with amoeboid movement
Pathogenesis:
o Alveolar septal infiltration with plasma cells
o In the lungs: Honeycombed masses of parasites within the alveoli
o Death due to Asphyxia or a condition where the body do not get enough oxygen. If left
untreated, it will cause coma or death.
TREATMENT:
• Trimethoprimsulfamethoxazole
o Drug of choice
DIAGNOSIS:
• Percutaneous needle biopsy of the lungs and the lung aspirates. The samples collected will be
stained with methenamine silver to demonstrate cyst and trophozoites.
_________________________________________________________
Isispora belli
•
•
Intestinal Coccidian
Infective Stage: Sporolated oocyst containing 2 sporocyst each with 4 sporozoites.
•
•
Mode of Transmission: ingestion of sporulated oocysts in fecally contaminated food or water
Definitive host: Humans
•
•
•
Recognized as opportunistic small bowel pathogen in patients with HIV
Disease: Human coccidiosis
Morphology:
o Immature oocyst
▪ Elongately ovoidal in shape with one end narrower than the other
▪ 20 – 33 um by 10 – 19 um
o Mature oocyst
▪ Contains 2 sporocyst, each containing 4 sporozoites
▪ 29 um by 14 um
Habitat: Small intestines of man
Pathogenecity: the organism is commonly found in tropicxal and sub-tropical climates
o Often asymptomatic and self-limiting
o Mild cases:
▪ Mild abdominal pain and mucoid diarrhea
o Severe Cases
▪ Severe abdominal cramps; milky, watery diarrhea.
Diagnosis: DFS
o DFS: Demonstration of oocysts in feces (transparent containing 1-2 sporoblast)
o Modified AFS
▪ Sporoblasts and/or sporocysts stain deep red
▪ Oocysts are ellipsoid with blunt ends
▪ Average size: 30 by 12 um
•
•
•
_________________________________________________________
D. Microsporidia
• Newest group of obligate intracellular parasite Enterocytozoon bieneusi (Encephalitozoon
intestinalis)
• The most common microsporidia causing enteritis among patients with AIDS
• The organism is very small measuring about 1.5 – 4 um
• Characteristic feature: spores containing a polar tubule, used to inject infective spore content
into the host cells
• Method of infection:
o Not certain; most likely by ingestion of spores
• Inhalation of spores, ocular exposure, and sexual intercourse may also be route of
transmission
• Clinical disease
o Similar with Cryptosporidiosis
•
o Spores are very resistant
Diagnosis:
o Electron Microscopy – necessary to speciate o Serological testing o Modified
Trichrome stain:
▪ Concentration must be 10x higher that traditional trichrome stain
▪ Performed on unconcentrated specimen
▪ Spore walls stains bright pink; background stains green or blue (depending on
the couterstain)
Synthesis/ Conclusion:
Plasmodium and Babesia spp. have morphologic forms that may look similar. However, because not
all species typically show all the morphologic forms in the peripheral blood, coupled with the fact that
other morphologic forms look different (e.g., mature schizonts, gametocytes) and whether pigment is
produced, allow accurate speciation of the malarial organism and differentiation of malaria from
babesiosis.
Synthesis (Module)
Most of the Apicomplexa parasitizing man has a life cycle that is characterized by an alteration of
generations, one sexual, and one asexual, occurring in the same host, or requiring an alternation of
hosts. As with all parasites, the proper identification of malaria and babesiosis is crucial to ensure that
the patient is adequately treated when necessary. Plasmodium and Babesia spp. have morphologic
forms that may look similar. However, because not all species typically show all the morphologic
forms in the peripheral blood, coupled with the fact that other morphologic forms look different (e.g.,
mature schizonts, gametocytes) and whether pigment is produced, allow accurate speciation of the
malarial organism and differentiation of malaria from babesiosis.
The miscellaneous protozoa (Coccidians) have morphologic similarities (e.g., the oocysts of Isospora
and Sarcocystis) and distinct differences. When screening suspected samples, attention to organism
size, shape, andstructural details is imperative to identify parasites correctly. Note that most of these
coccidians are opportunistic especially among immunocompetent individuals. Among all of the
coccidian parasites, T. gondii is the most clinically significant implicated in causing neonatal
toxoplasmosis.