MICROBIOLOGY AND - it is able to survive in cold water

PARASITOLOGY - Infective stage is the cyst ; while

pathogenic stage is the trophozoite

PROTOZOA (PART 2)
MICHAELA ARROFO BSN 1B
GOOD LUCK FIGHTING !!!!

Blood and Tissue Protozoa B. Epidemiology and Pathogenesis

1.Subphylum Sarcodina : - Parasite can be acquired :

Acanthamoeba (free-living Amoeba) (1) through aspiration or nasal

inhalation;

(2) through direct invasion in the eye

> Acquired usually while swimming in

contaminated water.

- Eye infection with

Acanthamoeba occurs primarily
in patients who wear contact
lenses. The parasite has been
recovered from contact lenses,
lens cases and contact lens
solutions.
A. Important Properties and Life Cycle
- Tap water contaminated with
- Acanthamoeba usually causes infection
parasites is the source of
in immunocompromised patients.
infection for contact lenses.
- it is a free-living amoeba that causes
> Inhalation of the cysts from dust
inflammation of the brain substance and
may also occur
its meningeal coverings
(meningoencephalitis)

- found widely in soil, contaminated

freshwater lakes, and other water
environment

1

C. Disease
1. Granulomatous amoebic
encephalitis
infections among
immunocompromised individuals.
> parasite produces granulomatous
amoebic encephalitis and brain
abscesses
> Symptoms develop slowly and may
include : headache, seizures, stiff
neck, nausea and vomiting.
> the brain lesions may contain both
the trophozoites and the cysts.
> In rare instances, granulomatous
lesions may spread in the kidneys,
pancreas, prostate, and uterus
2. Keratitis – infection of the cornea
of the eye.
> Symptoms include severe eye
pain, and vision problems. Loss
2
of vision may occur due to
perforation of the cornea.
D. Laboratory Diagnosis
- Finding both trophozoites and cysts
in the cerebrospinal fluid as well as
brain tissue and corneal scrapings.
- Calcofluor white, a stain usually used
to demonstrate fungi, may be used to
demonstrate the parasite in corneal
scraping specimens
Fluorescent microscopy of corneal
scrapings. Calcofluor white
fluorescent technique. Cysts and
trophozoite form of Acanthamoeba
E.TREATMENT
- Pentamidine, Ketoconazole or
Flucytosine may be effective in the
treatment of
infection, however, prognosis is poor
even with treatment.
- For eye and skin involvement, topical
miconazole, chlorhexidine,
itraconazole, rifampicin, or
propamidine may be used.
- Propamidine has been documented
to have best success record.
F. Prevention and Control ⬥ Flagellate form : pear-shaped ;
equipped with two flagella that is
- prevented through adequate boiling
responsible for the parasite’s jerky or
of water
spinning movement.
- regular disinfection of contact lenses
⬥ Cyst : non-motile form.
is also advised.
* The amoeboid trophozoite form is
- contact lens wearers are also advised
however the only form that is known
to avoid using homemade non-sterile
to exist in humans.
saline

solutions

2.SUBPHYLUM
SARCODINA:NAEGLERIA

A. Important Properties and Life

Cycle

- Classified as a free-living protozoan

Life Cycle of Naegleria fowleri
- found worldwide in soil and
contaminated water environment

- can survive in thermal spring water

- known pathogen worldwide is

Naegleria fowleri, which is the only
amoeba with three identified
morphologic forms – trophozoite,
flagellate, and cyst forms.

⬥ The trophozoite : exhibits

amoeboid motility, “slug-like”. B. Epidemiology and Pathogenesis

3
- usually acquired transnasally when
swimming in contaminated water.
- Parasite penetrates the nasal
mucosa and cribriform plate, enters
the central nervous system, and
produces a rapidly fatal meningitis
and encephalitis (primary amoebic
meningoencephalitis).
- Unlike Acanthamoeba, the parasite
produces infection in otherwise
healthy individuals, usually children.
- In some instances, the parasite may
be acquired through inhalation of dust
containing the parasite.
- The entire life cycle of the parasite
(amoeboid trophozoite > Flagellate
trophozoite > amoeboid trophozoite
> cyst form ) occurs entirely in the
external environment.
C. Disease
1. Asymptomatic infection – the
most common clinical presentation in
patients with colonization of the nasal
passages.
4
2. Primary Amoebic
Meningoencephalitis (PAM)
⬥ the result of colonization of the brain
by the amoeboid trophozoites leading
to rapid tissue destruction.
⬦ Symptoms : sore throat,
nausea, vomiting, fever and
headache. May eventually
develop meningeal irritation
(e.g. Kernig’s sign), as well as
alterations in their senses of
smell and taste.
⬦ if untreated, patients may die
within one week after onset of
symptoms.
D. Laboratory Diagnosis
- finding of the amoeboid trophozoites
in the cerebrospinal fluid
E. Treatment
- treatment is ineffective because of its
rapidly fatal course. However, some
patients
have been shown to recover from - Life cycle of the parasite involves a
infection due to early detection and vector, the female sandfly of the
initiation of Phlebotomus and Lutzomyia genera.

Treatment. ● Leishmania spp. are obligate

- Treatment of choice is
Amphotericin B in combination with
miconazole and
rifampicin (Murray, 2014).
F. Prevention and Control
intracellular parasites. It has
three morphologic forms
:amastigote, promastigote, and
epimastigote.
● The infective stage is
promastigote

- there is no known means of ● The pathogenic stage and

preventing Naegleria infection other diagnostic form is the
than the prevention of contamination amastigote
of water sources.

- adequate chlorination of swimming

pools and hot tubs is recommended.

3.Subphylum Mastigophora :
Hemoflagellates Leishmania spp.

> Leishmania donovani complex

> Leishmania braziliensis complex

> Leishmania tropica complex

Trypanosoma spp.

- Trypanosoma cruzi

- Trypanosoma brucei
gambiense and

Trypanosoma brucei
rhodesiense

A. Important Properties and Life

Cycle

5
 ⬥ Leishmania braziliensis
(mucocutaneous leishmaniasis).

Leishmania donovani
Complex

Leishmania donovani Complex

- Is the causative agent of visceral

leishmaniasis (also known as kala-azar
or dumdum fever).

- The complex consists of :

(1) L. donovani chagasi – which is

mainly seen in Central America
(mainly Mexico, West Indies,

and South America) and is transmitted

by the Lutzomyia sandfly ;

(2) L. donovani donovani found in

B. Epidemiology and Pathogenesis
parts of Africa and Asia (Thailand,
- has a worldwide distribution. Natural India, China, Burma, and
reservoirs include rodents, ant
East Pakistan) and is transmitted by
eaters, dogs, and cats.
the Phlebotomus sandfly.
- In endemic areas, the parasite may
3. . donovani infantum also
be transmitted in the
transmitted by the Phlebotomus
human-vector-human cycle.
sandfly and is found mainly in
- Three (3) major strains of Leishmania Mediterranean Europe, Near East and
: Africa.

⬥ Leishmania donovani (visceral (1) L. donovani chagasi – which is

leishmaniasis) mainly seen in Central America
(mainly Mexico, West Indies,
⬥ Leishmania tropica (cutaneous
leishmaniasis) ; and and South America) and is transmitted
by the Lutzomyia sandfly ;

6
(2) L. donovani donovani found in LIVER-Hepatomegaly or enlargement
parts of Africa and Asia (Thailand, of the liver also occurs
India, China, Burma, and
BONE MARROW-– anemia due to
East Pakistan) and is transmitted by destruction of red blood cells,
the Phlebotomus sandfly. bleeding tendencies due to reduction
of platelets (thrombocytopenia), and
3. L. donovani infantum also
increased risk for secondary infection
transmitted by Phlebotomus sandfly
because of reduction of white blood
and is found mainly in
cells (leukopenia).
Mediterranean Europe, Near East and
Note :
Africa.
● In light-skinned patients,
- The promastigote is injected into the
hyperpigmentation of the skin may be
human host through bite of the
seen (kala-azar means “black
sandfly. After entry into the host, it
sickness” or black fever”)
loses its flagella, is engulfed by
● Glomerulonephritis or
macrophages, and transforms into
inflammation of the glomeruli of the
amastigotes.
kidney may also occur
- The organs of the reticuloendothelial
● The disease may be fatal if
system (liver, spleen and bone
untreated.
marrow) are the most severely
affected)

C. Disease : Visceral Leishmania

(Kala-azar, Dumdum Fever)

After an incubation period of 2 weeks

to 18 months, the disease beings with
intermittent fever, weakness and
weight loss.
D. Laboratory Diagnosis
SPLEEN-Massive enlargement of the
- screening test is called Montenegro
spleen (splenomegaly) is
skin test. This test is similar to the
characteristic, leading to
tuberculin skin test for the diagnosis
hypersplenism and resulting anemia.
of tuberculosis.

7
> it is used as screening for large
population at risk but not used for
diagnosis.
⬥ Definitive diagnosis is done by
demonstration of the amastigote from
Giemsa stained slides of specimen
from blood, bone marrow, lymph
nodes, and biopsies of infected areas.
⬥ Culture of blood, bone marrow, and
other tissues may also be done, which
will show the promastigote forms.
⬥ Serologic tests are now available
such as indirect fluorescent
antibody (IFA), enzyme-linked
immunosorbent assay (ELISA), or
direct agglutination test (DAT).
E. Treatment
- drug of choice is liposomal
amphotericin B (Ambisome).
- Sodium stibogluconate has also
been found to be effective but the
development of resistance may occur.
8
- other patients have shown
favourable response to gamma
interferon in combination with
pentavalent antimony
F. Prevention and Control
- Control of the vector population is
important in the prevention of
infection.
- the use of repellents, protective
clothing, and installation of screens
may be helpful.
- prompt treatment of infected
humans is essential to help halt the
spread of the disease.
Leishmania braziliensis complex
Is the causative agent of
mucocutaneous leishmaniasis
which involves skin, cartilage, and
mucous membranes.
- Infection with L. braziliensis occurs
most commonly in Brazil and Central
America, primarily in construction
and forestry workers.
- The complex consists of L.
panamensis (Panama and
Colombia), L. peruviana (Peruvian
Andes), and L. guyanensis (The
Guianas, parts of Brazil and
Venezuela).
- Infection is transmitted by sandflies
(Lutzomyia and Psychodopigus)
through skin bite.
- the promastigotes invade the
reticuloendothelial cells where they
transform into amastigotes (diagnostic
stage).
- Reproduction of the amastigotes
result in tissue destruction. The
amastigotes are taken up by the
vector during a blood meal and are
transformed into promastigotes.
C. Disease : Mucocutaneous
Leishmaniasis
- also called espundia, begins with a
papule at the site of insect bite, then
forms metastatic lesions, usually at
the mucocutaneous junction of the
nose and mouth.
⬥ Disfiguring granulomatous,
ulcerating lesions destroy the nasal
cartilage (tapir nose) but not the
adjacent bone.
⬥ Death can occur from secondary
infections.
9
Clinical manifestations of
Mucocutaneous Leishmaniasis
D. Laboratory Diagnosis
- is confirmed by demonstration of
amastigotes in clinical specimens.
- Ulcer biopsy specimens are used
for the diagnosis of mucocutaneous
leishmaniasis.
- Microscopic examination of
Giemsa-stained ulcer biopsy
specimens reveals the diagnostic
amastigotes.
- Culture of infected materials may
show the promastigotes.
- Serologic testing may also be done.
E. Treatment
- most widely used is sodium
stibogluconate, although resistance
has been shown to develop.
- alternative drugs include liposomal
Amphotericin B, and oral antifungal
drugs (fluconazole, ketoconazole,
and itraconazole).
F. Prevention and Control
- the most important preventive
measure is the control of the insect
vector.
- measures should be undertaken to
protect individuals from sandfly bites
using netting, window screens,
protective clothing, and insect
repellents.
- prompt treatment can also help
prevent spread of the disease.
Leishmania tropica complex
A. Important Properties and Life
Cycle
- the complex consists of L. tropica, L.
aethiopica, and L. major. These are
the causative agents of what is
referred to as Old World cutaneous
leishmaniasis.
- the life cycle of L. tropica is similar to
what of L. braziliensis. All three
members of the complex are
transmitted by the Phlebotomus
sandfly and primarily attacks the
human lymphoid tissue of the skin.
B. Disease : Old World Cutaneous
Leishmaniasis
- is also known as Oriental sore, and
Baghdad or Delhi boil.r
- it is characterized by one or several
pus-containing ulcers that may heal
spontaneously.
10
- initial lesion : small, pruritic red
papule at the bite site.
- In patients with allergy and
hypersensitivity responses,
spontaneous healing does not occur.
> thick skin plaques with
multiple nodules may develop
especially on the limbs and
face.
C. Laboratory Diagnosis
- Microscopic examination of
Giemsa-stained slides of fluid
aspirated from beneath the ulcer bed
is the usual diagnostic procedure of
choice. Reveals the typical
amastigotes.
- Culture of specimens will show the
promastigote form.
- Serologic tests are also available
D. Treatment
- the drug of choice is sodium
stibogluconate.
- steroids with application of heat to
the infected lesions may be used.
- other alternative drugs are
meglumine antimonite, pentamidine,
and oral ketoconazole.
- paromomycin ointment may be
helpful in the healing of the ulcers.
E. Prevention and Control Trypanosoma cruzi
- preventive measures same with
B. Epidemiology and Pathogenesis
forms of leishmaniasis.
- primarily found in South and Central
- however, unlike the other
America
leishmania, a vaccine has been
developed against L. tropica which is - transmitted by the bite of the

currently undergoing clinical trials. reduviid or triatomid bud (Triatoma or

“cone- nose” bug or “kissing bug”)
Trypanosoma spp.
- It is transferred to a human host
- Trypanosoma cruzi when feces of the bug containing the
infective trypomastigotes is deposited
- Trypanosoma brucei gambiense
near the bite site.
and Trypanosoma brucei
rhodesiense - The feces are then introduced into
the bite site when the host scratches
A. Important Properties and Life
the bite area.
Cycle
- Other routes of transmission include
- are also hemoflagellates like
blood transfusion, sexual intercourse,
Leishmania. The major difference
transplacental transmission, and
between the two lies in their
through the mucous membranes,
diagnostic stages, which is the
when the bites is near the eye or
amastigote for Leishmania and the
mouth.
trypomastigote for the trypanosomes.
- Humans and animals (domestic cats
- the trypomastigotes are curved,
and dogs, and wild species such as
assuming the shape of letters C, S, or
armadillo, raccoon, and rat) serve as
U.
reservoir hosts.
- the trypomastigotes are visible in the
peripheral blood

11

C. Disease : Chagas Disease
(American Trypanosomiasis
⬥ The acute phase begins with a
nodule (chagoma) near the bite site ;
also with unilateral swelling of the
eyelid with conjunctivitis (Romana’s
sign)
⬦ The eyelid swelling may be due to
the bug feces being accidentally
rubbed into the eye.
⬦ This is accompanied by fever, chills,
malaise, myalgia, and fatigue.
⬦ Patients may recover or may enter
the chronic phase.
● Chronic Phase :
Hepatosplenomegaly, enlargement of
lymph nodes (lymphadenopathy) , and
myocarditis with cardiac arrhythmia
12
characterize the chronic phase of
Chagas disease.
> cardiac muscle is the most
frequently and most severely affected
tissue
> Loss of tone of the colon and
esophagus due to destruction of the
Auerbach’s plexus may lead to
abnormal dilatation of these organs,
called megacolon and
megaesophagus, respectively.
> CNS involvement may also be seen
in the form of meningoencephalitis
and cysts
> Death may occur due to cardiac
failure and arrhythmias.
D. Laboratory
● Acute disease diagnosed by the
finding of trypomastigotes in thick or
thin films of the patient’s blood.
● Other diagnostic methods can be
used include : bone marrow
aspiration, muscle biopsy, culture on
special medium, and xenodiagnosis.
● Xenodiagnosis entails allowing an
uninfected laboratory – raised
reduviid bug to feed on an infected
patient.
> after several weeks the intestinal
content of the bug
are examined for the presence of the Trypanosoma brucei gambiense
parasite. and Trypanosoma brucei

● Serologic test is also helpful. rhodesiense

● Both Xenodiagnosis and serologic A. Epidemiology and Pathogenesis

tests are useful in the chronic form of - two species are similar in
the disease morphology and life cycle

- involve the tsetse fly (Glossina) as the

vector

⬥ Reservoir

⬦ Humans : for T. brucei

E. Treatment
gambiense ;
- Drug of choice are benznidazole and
⬦ Domestic animals (especially
nifurtimox but these are less effective
cattle) and wild animals serve as
during the chronic phase of the
the reservoir for T. brucei
disease.
rhodesiense
- Alternative agents are allopurinol
⬥ The infective and pathogenic stage is
and ketoconazole
the trypomastigote

- T. gambiense infection : (West

E. Prevention and Control African or Gambian Sleeping Sickness)

is chronic while ;
- protection from the bite of the
reduviid bug, improvement of housing - T. rhodesiense infection : (East

conditions, and insect control. African or Rhodesian Sleeping

Sickness) is more rapidly fatal
- Education regarding the disease and
its transmission is also helpful

13
- The disease is endemic in
sub-Saharan African is the natural
habitat of the tsetse fly.
T. gambiense causes disease along the
water courses in West Africa while T.
rhodesiense causes disease mostly in
the arid regions of East Africa.
B. Disease : African Sleeping
Sickness
⬥ The initial lesion is an indurated
ulcer called chancre at the site o f the
inset bite.
⬥ Intermittent weekly fever and
lymphadenopathy then develop.
⬦ Enlargement of the posterior
cervical lymph nodes
(Winterbottom’s sign) is
commonly seen.
⬦ Other manifestations : red
rash accompanied by pruritus,
localized edema, and a delayed
pain sensation (Kerandel sign).
⬥ The encephalitis is characterized by
headache, insomnia, and mood
changes.
> muscle tremors, slurred
speech, and apathy follow,
progressing to somnolence
(sleeping sickness) and coma.
⬥ Untreated disease is fatal.
14
C. Laboratory Diagnosis
● microscopic examination of
Giemsa-stained slides of the blood,
lymph node aspirations and CSF will
reveal the trypomastigotes during the
early stages of the disease.
● Aspiration of the chancre or
enlarged lymph nodes may also reveal
the parasites.
● Parasites are isolated from the CSF
of patients with CNS involvement.
● Serologic tests can also be helpful as
well as detection of the presence of
IgM in the CSF of patients.
● the presence in the serum and/or
CSF of IgM is considered diagnostic.
D. Treatment
- this include melarsoprol, suramin,
pentamidine and eflornithine (Zeibig,
2013).
- The choice of drug will depend on
whether the patient is pregnant or
not, the age of the patient, and the
stage of the disease.
E. Prevention and Control
- involve protection against bite of the
fly.
- Use netting and protective clothing
are recommended.
- Use of fly traps and insecticides may
be helpful.
- Clearing forests around the villages
are also helpful measures.
Subphylum Apicomplexa :
Plasmodium spp.
A. Epidemiology and Pathogenesis
- Malaria is the caused by five
plasmodia species : Plasmodium vivax,
Plasmodium malariae, Plasmodium
ovale, Plasmodium knowlesi, and
Plasmodium falciparum.
- The vector and definitive host is the
female Anopheles mosquito.
- The sexual cycle (sporogony) occurs
primarily in mosquitoes ; and the
asexual cycle (schizogony) occurs in
humans (intermediate hosts).
15
EXOERYTHROCYTIC PHASE
- The infective stage is the sporozoite
from the saliva of the biting mosquito,
which is taken up by the liver cells –
this is called the exoerythrocytic
phase.
- Multiplication of sporozoites into
merozoites occur during this stage.
- P. vivax and P. ovale produce a latent
form (called hypnozoite or sleeping form)
in the liver which is the cause of the
relapse or recrudescence seen in vivax
and ovale malaria.
ERYTHROCYTIC PHASE
⬥ Merozoites (pathogenic stage) are
released from liver cells and infect the red
blood cells.
⬦ the parasites life cycle now enters the
erythrocytic phase. These merozoites
multiply and are eventually released to
infect other red blood cells.
⬦ the periodic release of merozoites
causes the typical recurrent symptoms
seen in malaria patients
⬦ some merozoites then develop into
microgametophytes (male gametocytes)
and macrogametocytes (female
gametocytes).
⬦ the gametocyte-containing red blood
cells are ingested by the mosquito during
feeding.
⬦ Sexual reproduction then ensues.
 - The primary vector is Anopheles
flavirostris, which breeds in clear, slow-
flowing streams near foothills and forests.

● Main mode of transmission of malaria is

the bite of the female mosquito vector.

○ however, the parasite can also be

transferred through blood transfusion
(transfusion malaria), intravenous drug
abuse with sharing of IV needles
(“main-line malaria”) and

transplancetal transmission (congenital

malaria).

● Most of the pathologic findings result

from the destruction of red blood cells.

● P. falciparum and P. knowlesi can

infect both young and old red blood cells
leading to high levels of parasitemia.

● P. vivax and P. ovale mainly infects

young red blood cells, while P. malariae
infects old red blood cells.

- Plasmodium knowlesi is a natural

parasite of macaque monkeys

throughout the Southwest Asia region.

Cases of infection have been noted

in Thailand, Singapore, Brunei and

Indonesia, Myanmar, Vietnam and the
- occurs worldwide. Primarily in tropical
and subtropical areas, especially in Asia, Philippines (Murray, 2014).
Africa, and Central and South America.
- The red blood cells infected by P.
- 69% of cases : Philippines : knowlesi have normal morphology. All
Plasmodium falciparum while the
developmental stages of the parasite may
remaining 31 % are due to Plasmodium
be seen in the peripheral blood.
vivax (World Malaria Report 2013).

16
B. Disease ■ The dark color of the patient’s urine is
due to kidney damage giving rise to the
● Paroxysms of malaria are divided into
term “black water fever”.
three stages : cold stage, hot stage and
the sweating stage. ● P. vivax and P. ovale cause benign
tertian malaria that is characterized by
○ these paroxysms are considered
relapses that can occur up to several
partially as allergic responses to the
years after the initial illness and is due to
schizonts and to the antigens released
the latent hypnozoites in the liver.
following the release of the merozoites
- Most cases, P. knowlesi infection
○ the malarial paroxysm presents with resembles infection in patients by other
abrupt onset of chills (rigors) malarial Parasites.
accompanied by headache, muscle pain
- a small number of cases of patients
(myalgia), and joint pains (arthralgia). This
develops severe infection.
stage lasts for approx 10-15 mins or
longer. - the severity of the infection is due to the
high parasitemia levels produced due to
○ spiking fever lasting 2-6 hours follows,
its ability to infect all stages of red blood
reaching up to 41 degree C, accompanied
cells and its 24-hour erythrocyte cycle
by shaking, chills, nausea, vomiting, and
(quotidian malaria)
abdominal pain. This is then followed by
drenching sweats.

○ Splenomegaly is often present and

anemia is prominent.

● The timing of the fever cycle is 72 hours

for P. malariae, in which symptoms recur
every 4th day

(quartan malaria) C. Laboratory Diagnosis

● Malaria caused by P. vivax, P. ovale and ● Is based on the examination of

P. falciparum recur every 3rd day (tertian Giemsa-stained or Wright-stained thick
malaria). and thin smears of the blood.

○ P. falciparum causes malignant tertian
malaria since it causes severe infection
which is potentially life-threatening due to
extensive brain (cerebral malaria) and
kidney damage.
○ the thick smears are used for screening
purposes while the thin blood smears are
used to differentiate the various
Plasmodium species.

17
● The best time to take blood films is
midway between paroxysms of chills and
fevers or before the onset of fever
○ this is the time when the greatest
number of intracellular organisms are
present.
⬥ Characteristic trophozoites will be seen
within the infected red blood cells.
⬥ P. falciparum will show characteristic
crescent-shaped or banana-shaped
gametocytes. Infection is highly
considered if there are > 10 infected red
blood cell consisting only of ring forms.
⬦ P. malariae and P. knowlesi,
demonstration of the characteristic
rosette schizont is diagnostic.
⬦ As to the merozoite count :
⬩ P. knowlesi – 16/red blood cell
hypnozoites.
🞂 For chloroquine-resistant strains of P.
falciparum other agents may be used
including mefloquine + artesunate,
artemether-lumefantrine, atovaquone-
proguanil, quinine, quinidine,
pyrimethamine-sulfadoxine (Fansidar),
and doxycycline (Murray, 2014).
🞂 Artemisinin-based combination
therapies (ACTs) are now recommended
for uncomplicated malaria and for
chloroquine-resistant vivax malaria.
🞂 Artesunate is the drug of choice for
severe malaria, in combination with either
amodiaquine, mefloquine, or
sulfadoxine-pyrimethamine.
🞂 P. knowlesi infection is managed similar
to P. falciparum due to its potential to
produce severe infection.

⬩ P. malariae – 10-12/ red blood cell 🞂 Chemoprophylaxis of malaria for

travelers to endemic areas consists of
⬥ The presence of early trophozoite forms
mefloquine or doxycycline.
and two to three parasites per blood cell
(similar to P. - travelers where the other plasmodia are
found should take chloroquine starting
falciparum) is more suggestive of P.
two weeks before arrival and continued
knowlesi infection.
for 6 weeks after departure, followed by a
D. Treatment 2 week course of primaquine if exposure
was high.
🞂 Drug of choice for malarial infection are
chloroquine or parenteral quinine. 🞂 Other preventive measures :avoidance
of the bite of the vector through the use
🞂 However, chloroquine does not affect
of mosquito netting, window screens,
the hypnozoites of P. vivax and P.
protecting clothing and insect repellants.
ovale.
- protection is important during the night.
- for vivax and ovale malaria, primaquine
is given to destroy the

18

🞂 Include also insecticide sprays, as well
as drainage of stagnant water in swamps
and ditches.
Phylum Apicomplexia :Toxoplasma
gondii
A. Epidemiology and Pathogenesis
Host:
⬥ definitive host : domestic cat or other
felines
⬥ intermediate host : humans and other
mammals
B. Epidemiology and Pathogenesis
🞂 Infection by T. gondii occurs worldwide.
🞂 Infection is usually sporadic but
outbreaks associated with ingestion of
raw meat or contaminated water can
occur. Individualswho are severely
immunocompromised are more likely to
develop severe disease.
🞂 The parasite can be transmitted in two
ways : (1) ingestion of improperly cooked
meat of animals that serve as
intermediate hosts,and (2) ingestion of
oocyst from contaminated water.
🞂 Transplacental transmission may occur.
🞂 Sharing of needles by IV drug users as
well as blood transfusion are less
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common modes of transmission of the
parasite.
C. Disease : Toxoplasmosis
1. Infection in immunocompetent
individuals – usually asymptomatic.
- acute infection may manifest
non-specific symptoms such as chills,
fever, headache and fatigue.
- this may be accompanied by
inflammation of lymph nodes
(lymphadenitis).
- chronic infection may manifest with
lymphadenitis, hepatitis, myocarditis, and
encephalomyelitis.
- Chorioretinitis leading to blindness may
also occur.
C. Disease : Toxoplasmosis
2. Congenital Infection
● occurs in infants born to mothers who
were infected during pregnancy.
○ Infection during the first trimester of
pregnancy may result to miscarriage,
stillbirth, or severe infection (encephalitis,
microcephaly, hydrocephalus, mental
retardation, pneumonia).
○ If the infant acquires during the last
trimester, symptoms may not develop
until months to years after delivery.
○ The most common manifestation is
chorioretinitis with or without blindness.
C. Disease : Toxoplasmosis
3. Infection in immunocompromised - For pregnant women, clindamycin or
hosts spiramycin may be given.

– usually manifest with neurologic F. Prevention and Control

symptoms similar to patients with
- The most effective preventive measure
encephalopathy, meningoencephalitis, or
is through adequate cooking of meat.
brain tumors.
- Pregnant women should refrain from
- Reactivation of latent toxoplasma
eating undercooked meat and
infection is common. Other sites of
infection include the lungs, eye, and should avoid contact with cats and refrain
testes. from handling litter boxes.

D. Laboratory Diagnosis - Cats should not be fed raw meat.

⬥ Demonstration of high antibody titers

through immunofluoroscence assay is
essential for the diagnosis of toxoplasma
infection.

⬥ Microscopic examination of
Giemsa-stained preparations will show
the crescent- shaped trophozoites during
the acute infection.

- Cysts may be seen in the tissues.

⬥ Prenatal diagnosis can be done through

ultrasonography and amniocentesis
with PCR analysis of the amniotic fluid
(method of choice)

E. Treatment

- The regimen of choice for

immunocompromised patients, especially
those with AIDS, is initial high-dose
pyrimethamine plus sulfadiazine given for
an indefinite period.

- Alternative regimen for those who

develop symptoms of drug toxicity is
clindamycin plus pyrimethamine.

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