Parasitology 1

TERMS
HOST
• Intermediate host; in which larval or asexual
stages develop.
• Definitive host; in which the adult or sexual stages
occur.
VECTORS
 Vectors are living transmitters (e.g., a fly) of
disease and may be
 Mechanical, which transport the parasite but there
is no development of the parasite in the vector.
 Biologic, in which some stages of the life cycle
occur.
2OYEKAN SEUN M.D MB;BS (LASUCOM)

GENERAL CHARACTERISTICS
 Protozoa are free-living,
 Single celled, eucaryotic cells
 They come in many sizes, from 5 micrometers
to 2 millimeters.
 They have an outer layer of cytoplasm
(ectoplasm) and an inner layer (endoplasm)
 The protozoa ingest solid pieces of food
through a small mouth called the cytostome.
 They reproduce both sexually and asexually
 They can occur in two form the cyst(infective
form) and the trophozoite

THE INTESTINAL PROTOZOA
 There are 6 intestinal protozoa that cause
diarrhea.
 Entamoeba histolytica causes a bloody
diarrhea
 Giardia lamblia and Cyclospora
cayetanensis cause a non-bloody diarrhea.
Both occur in normal individuals.
 Cryptosporidium, Isospora belli ,Cyclospora
and Microsporidia cause severe diarrhea in
individuals with defective immune systems
(such as patients with AIDS).

Entamoeba histolytica
 It is the only pathogenic Entamoeba specie
 Moves and feed with the aid of a pseudopodia
 About 10% of the world population are infected
though most of these infections are asymptomatic.
 These carriers pass the infective form, the cyst, to
other individuals by the fecal-oral route.
 It is noteworthy that homosexual men commonly
are asymptomatic carriers(veneral transfer).
 The motile feeding form of the amoeba is the
trophozoite, which cruises along the intestinal wall
eating bacteria, other protozoa, and even human
intestinal and red blood cells.

 This trophozoite can convert to a precyst
form, with two nuclei, that matures into a
tetranucleated cyst as it travels down and out
the colon
 The precyst contains aggregates of ribosomes,
called chromotoid bodies, as well as food
vacuoles that are extruded as the cell shrinks to
the mature cyst;
 Mature cyst is passed out, eaten therefore
infecting others.

 Sometimes (10% of infected individuals) the
trophozoites invade the intestinal mucosa
causing abdominal pain, a couple of loose
stools a day, and flecks of blood and mucus in
the stool.
 The infection may become severe, with bloody,
voluminous diarrhea.
 The trophozoites may penetrate the portal blood
circulation, forming abscesses in the liver,
followed by spread through the diaphragm into
the lung. Here the trophozoite infection causes
pulmonary abscesses and often death

Diagnosis, prevention and
treatment The stool is examined for the presence of cysts or
trophozoites.(iodine and trichrome stain)
 Trophozoites with red blood cells in the
cytoplasm(endoplasm) suggest active disease, while cysts
or trophozoites without internalized red cells suggest
asymptomatic carriage.
 Entamoeba histolytica must be differentiated from other
intestinal protozoa including: E. coli, E. hartmanni, E.
dispar
 differentiation may therefore be based on isoenzymatic or
immunologic analysis or molecular studies
 CAT scan or ultrasound imaging of the liver will reveal
abscesses if present.
 Prevention rests on good sanitation: proper disposal of
sewage and purification (boiling) of water.
 Metronidazole is the drug of choice
9
OYEKAN SEUN M.D MB;BS (LASUCOM)

Giardia lamblia
 It exists in 2 forms: as a cyst and as a mature motile
trophozoite.
 It occurs mostly as an asymptomatic infection.
 Outbreaks occur when sewage contaminates drinking
water.
 The organism is also harbored by many rodents and
beavers; campers frequently develop Giardia lamblia
infection after drinking from "clear" mountain streams.
 After ingestion of the cyst, Giardia lamblia converts to the
trophozoite form and cruises down and adheres to the
small intestinal wall.

Giardia lamblia
 They cause decrease expression of brush border
enzymes and morphological changes of the microvilli
 Attachment of the trophozoite causes villus flattening
 The organism coats the small intestine, interfering
with intestinal fat absorption. The stools are therefore
packed with fat, which has a horrific odor!
 The patient will have a greasy, frothy diarrhea, along
with abdominal gassy distension and cramps.
 Since Giardia do NOT invade the intestinal wall, there
is NO blood in the stool!!
 It can also cause lactose intolerance

treatment
 Examination of stool for cysts or
trophozoites(falling leaf motility).
 Commercial immunoassay kit to detect
Giardia lamblia antigens in aqueous extracts
of stool specimens.
 Sanitation measures.
 Treat these patients with metronidazole

Cryptosporidium
 It is now apparent that this critter is everywhere!
 Animals and humans are equally infected
 A good percentage of humans show serologic evidence of past
infection.
 It can cause outbreaks of diarrhoea from contaminated municipal
water sources and in infants in day care centers.
 Sporadic cases can occur in travelers.
 Cryptosporidium is ingested as a round oocyst that contains 4
motile sporozoites.
 Its life cycle occurs within the intestinal epithelial cells, and it causes
diarrhea and abdominal pain.
 These symptoms are self limiting in immunocompetent individuals.
However, in immunocompromised patients, this organism causes a
severe, protracted diarrhea that is life threatening.
 These patients may have 3-17 liters of stool per day.

Development of Cryptosporidium in human body
Meront with
merozoites
♂
♀
Zygote
Thick-walled oocysts
External autoinfection
Thin-walled oocysts
Internal autoinfection
Sporozoite attack brush
border of epithelial cells
Merogony
(asexual reproduction)
Gametogony
(sexual reproduction)
gametocyte
OYEKANSEUNM.DMB;BS(LASUCOM)
16

Ingestion of thick-walled oocysts:
In contaminated food or drink (called heteroinfection).
By faeco-oral route (hand to mouth) in already infected
patient ( called external autoinfection).
Thin-walled oocysts in intestinal lumen of already
infected patient causes internal autoinfection.
Thick-walled
Thin-walled

Cryptosporidium
20%
80%
OYEKAN SEUN M.D MB;BS (LASUCOM) 18

Isospora and Cyclospora
 These organisms cause a severe diarrhea in
immunocompromised individuals and may lead to
dissemination of the parasite to the
oesophagus, gall bladder, respiratory tract and
urinary bladder
 They are transmitted via the fecal-oral route.
 Autoinfection may occur in isospora but never in
cyclospora
 Trimethoprim with sulfamethoxazole is effective
against Isospora and cyclospora
 CRYPTOSPORIDIUM AND ISOSPORA ARE
IDENTIFIED USING MODIFIED ZIEHL NEELSEN
STAIN

Development of Cyclospora in human body
merozoites
♂
♀
Zygote
Sporozoite attack brush
border of epithelial cells
gametocyte
Unsporulated oocyst
Pass in stool
of the patient
Sporulated oocyst
Infective stage
Autoinfection DOES NOT occur
20

Development of Isospora in human body
merozoites
♂
♀
Zygote
Sporozoite enters
epithelial cells
gametocyte
Unsporulated oocyst
Pass in
stool of
the
patient
Sporulated oocyst
Infective stage
Autoinfection MAY OCCUR
21

Mode of Infection of
Ingestion of sporulated oocysts in contaminated
food or drink.
Cyclospora cayetanensis Isospora belli
Autoinfection DOES NOT occur
Unsporulated
oocyst
Pass out in
patient’s stool
Sporulation
occurs on the
ground
Autoinfection MAY occur
Patient passes both
unsporulated and
sporulated oocysts in stool
22

State True Or False
 Cryptosporidium parvum produces severe watery diarrhoea
in the immunocompetent patient.
 Cryptosporidium parvum can be detected in stool
only after staining stool smear by MZN stain.
 Autoinfection may occur in isosporiasis.
 Both unsporulated and sporulated Cyclospora
oocysts are infective to man.
 Cryptosporidiosis is a pure human disease.
 Cryptosporidium sporozoites invade the brush border of
epithelial cells lining the rectum.
False
True
True
False
False
False

Case
An AIDS patient developed severe watery diarrhoea with
no mucus or blood. Stool examination showed no
eggs of helminths. Diagnosis was confirmed by
microscopic examination of stained stool smear by
special stain.
a- What is (are) the revealed causative parasite (s)?
C.parvum, C.cyaetenensis, I.belli, Microsporidia.
b- Name the type of stain used to reveal the causative parasite
(s)?
Modified Ziehl-Neelsen stain.
c- If the parasite could be transmitted by autoinfection, what
would be your diagnosis?
C.parvum infection and may be I.belli infection.

FREE LIVING MENINGITIS
CAUSING AMEOBAE
 Naegleria fowleri and Acanthamoeba
 Live in fresh water and moist soils.
 Infection often occurs during the summer
months when people swim in freshwater lakes
and swimming pools that harbor these
organisms.
 Occur in contact lens saline solutions
(Acanthamoeba): cysts from dust contaminate
 Although large numbers of persons are
exposed, actual infection rarely occurs.

 When it does, the organisms penetrate the
nasal mucosa, through the cribriform plate,
into the brain and spinal fluid.
 Both amoeba can cause an infection of the
meninges and brain (meningoencephalitis).
 Naegleria fowleri will cause a sudden
deadly infection in immunocompetent
persons, while
 Acanthamoeba will cause a slow
granulomatous infection, usually in
immunocompromised persons.

Naegleria fowleri
 95% of patients will die within 1 week.
 Infected persons will present with a fever, headache,
stiff neck, nausea, and vomiting, which is very similar
to a bacterial meningitis.
 If asked, they will give a history of swimming a week
earlier.
 Examination of cerebrospinal fluid (CSF) reveals a
high neutrophil count, low glucose, and high protein,
exactly like a bacterial meningitis!!!
 The Gram stain and culture will reveal NO bacteria,
and microscopic examination may show the motile
amoeba.
 Patients who survived were treated with intrathecal
amphotericin B, an antifungal agent.

Acanthamoeba
 It is responsible for a chronic, granulomatous, brain
infection in immunocompromised patients.
 Over a period of weeks, they will develop headache,
fever, seizures, and focal neurologic signs.
 Examination of the CSF and brain tissue will reveal
Acanthamoeba in both the cyst stage and trophozoite
stage.
 Treatment is difficult and involves multiple antifungal
drugs with pentamidine.
 This organism may also infect the cornea (in
immunocompetent persons), often when contact
lenses are not properly cleaned. This corneal infection
(keratitis) can lead to blindness. Treatment is with
antimicrobial eye drops.

Balantidium Coli
 Largest and only pathogenic ciliate
 B. coli cysts are found in food or water contaminated
by pig feces
 These cysts mature into ciliated trophozoites, and
travel to the intestinal tract.
 The trophozoites dig into the intestinal wall, where
they consume the native bacteria.
 Most infected individuals are asymptomatic, while
some will develop diarrhea.
 B. Coli trophozoites are notable for being the largest
parasitic protozoans found in the intestine.
 Diagnosis is made by identifying the ciliated
trophozoites or cysts in stool specimens.
 Tetracycline is effective at treating this infection.

THE SEXUALLY TRANSMITTED
PROTOZOAN
Trichomonas vaginalis
 It exists only in one morphologic statge(trophozoite) and
cannot encyst
 Trichomonas vaginalis is transmitted sexually(direct, skin to
skin contact) and hangs out in the female vagina and male
urethra.
 The trophozoite of Trichomonas vaginalis is a flagellated
protozoon.
 A female patient with this infection may complain of itching
(pruritus), burning on urination, and copious vaginal
secretions.
 On speculum examination you will find a thin, watery, frothy,
greenish musty malodorous discharge in the vaginal vault.
 Males are usually asymptomatic.

treatment
 Microscopic examination of vaginal discharge
on a wet mount preparation will reveal this
highly motile parasite(trophozoite).
 Examination of urine may also reveal
Trichomonas vaginalis(trophozoite).
 Treat your patient with metronidazole , locate
and treat sexual partners.
 Even though males are usually asymptomatic,
they must be treated or the female partner will
be reinfected (since this organism is not
invasive, no immunity is acquired.

35
•Hemoflagellates infect blood and tissues
•Transmitted by the bite of a blood-sucking
insect.
•They can exist as rounded cells without flagella,
called amastigotes, or as flagellated motile
forms called promastigotes, epimastigotes,
and trypomastigotes.
•They cause an initial skin ulcer at the site of
the insect bite, followed by systemic invasion.
•They are transmitted via blood product
transfusion.
OYEKAN SEUN M.D MB;BS (LASUCOM)

Leishmania
 Always as amastigotes in macrophages, blood or organs
 Promastigote is seen in the sand flies intestinal tract and
often migrate to its salivary gland
Trypanosoma brucei gambiense and rhodesiense
 In human blood, lymphatic tissue and CNS as trypomastigotes with
flagellum and undulating membrane
 Trypomastigote in tsetse fly moves and is converted to epimastigotes
in the midgut and back to trypomastigote in the salivary gland
Trypanosoma Cruzi
 In macrophages and tissues(lymph node,heart and other organs) as
amastigotes (oval cells having neither the flagellum nor undulating
membrane)
 Reduvic bug ingests trypomastigots, changes to
epimastigotes in the midgut and back to
trypomastigotes in the faeces

Leishmaniasis
(Leishmania tropica, Leishmania chagasi,
Leishmania major, Leishmania braziliensis,
Leishmania donovani)
 Leishmania is zoonotic, carried by rodents, dogs, and foxes,
with the exception of the visceral form of L. tropica and L. donovani,
where no animal host/reservoir has been found to date.
 Transmitted to humans by the bite of the sandfly.
(Phlebotomus, Lutzomyia)
 Following transmission from the sandfly, the promastigote
invades phagocytic cells (neutrophils, macrophages) and
transforms into the non-motile amastigote.(digenetic life cycle)
 The amastigote multiplies within the phagocytic cells in the
reticuloendothelial system (lymph nodes, spleen, liver, and
bone marrow) and also burst to affect other cells
 The different diseases caused by Leishmania depend on the
invasiveness of the species as well as the host's Cell
mediated immune response.

 It appears that some patients have
genetically deficient defenses against
Leishmania and will be afflicted with more
severe disease.
 Leishmaniasis presents in a spectrum of
disease severity: from a single ulcer that
will heal without treatment; to widely
disseminated ulcerations of the skin and
mucous membranes; to the very severe
infection striking deep into the
reticuloendothelial organs, the spleen and
liver.

3 clinical forms of this disease
Cutaneous leishmaniasis
Simple cutaneous lesions
Diffuse cutaneous lesions
Mucocutaneous
leishmaniasis
Visceral leishmaniasis

Cutaneous Leishmaniasis
 A sandfly injects Leishmania into the skin, where they migrate
to reticuloendothelial cells (fixed phagocytic cells in lymph
nodes).
 At the site of the sandfly bite, a skin ulcer(painless or painful)
develops, called an "oriental sore“ “Baghdad boil” “Delhi boil”
 If Cell-mediated immunity is intact they attack and clear the
organism, this ulcer heals in about a year, leaving a
depigmented (pale) scar.
 Because of the intact cell-mediated immunity, this organism
invokes a delayed hypersensitivity reaction i.e Diagnosis can be
made by injecting killed Leishmania intradermally (Leishmania
skin test).
 Just like the PPD test of tuberculosis, a raised indurated papule
48 hours later supports the presence of a Leishmania infection.
 Diagnosis is made by observing Leishmania in stained skin-
scrapings from the ulcer base.

Diffuse Cutaneous
Leishmaniasis
 A chronic form of cutaneous leishmaniasis occurs in patients
with deficient immune systems.
 A nodular skin lesion arises but does not ulcerate. With time,
numerous nodular lesions arise diffusely across the body.
 There is often a concentration of lesions near the nose.
 The untreated infection can last more than 20 years.
 The disease is diffuse because the host's immune system
does not respond to the invasion by Leishmania, due to a
defect in cell-mediated immunity.
 Therefore, the promastigotes are able to spread and infect the
skin, causing the diffuse nodular lesions.
 Due to the defect in cell-mediated immunity, the Leishmania
skin test is negative

Mucocutaneous Leishmaniasis
(Espundia, Uta)
 Initially, a dermal ulcer, similar to cutaneous
leishmaniasis, arises at the site of the sandfly
bite and soon heals.
 However, months to years later, ulcers in the
mucous membranes of the nose and mouth
arise. If untreated, the infection is chronic, with
erosion of the nasal septum, soft palate, and
lips, over a course of 20-40 years.
 Death by bacterial secondary infection may
occur.
 Diagnosis is made via skin scrapings.

Visceral Leishmaniasis
(Kala-azar,dum dum fever)
 The sandfly transmits Leishmania donovani or
Leishmania chagasi to an individual (mostly
malnourished children)
 Months later will complain of abdominal discomfort
and distension, low-grade fevers, anorexia, and
weight loss.
 This abdominal enlargement is due to Leishmania
donovani's invasion of the reticuloendothelial cells
of the spleen and liver, causing hepatomegaly and
massive splenomegaly. (even bone marrow)
 Patients also develop a severe anemia and the
white blood-cell count can also be very low.
 Most cases (over 90%) are fatal if untreated.

Diagnosis, prevention and treatment
 Diagnosis is made by liver and spleen biopsies (Giemsa-stain
smear) demonstrating these protozoa
 Serological tests by :
 high IgG level .
 fluorescent antibody (FA) test.
 Enzyme-linked immunosorbent assay (ELISA).
 The Leishmania skin test is negative during active disease as cell-
mediated immunity is deficient.
 Prevention :
 Treatment of infected persons
 Elimination of diseased dogs by destroying them .
 Control of sand flies by using of insecticides and applications
 vaccination.
 All forms of leishmaniasis can be treated with the pentavalent
antimonial stibogluconate.

Trypanosoma brucei rhodesiense Trypanosoma brucei
gambiense(salivarian Trypanosoma )

 Transmitted by blood-sucking tsetse fly
 Mother to child infection: the trypanosome can
sometimes cross the placenta and infect the fetus.
 Also transmitted by blood transfusion and in blood
laboratories
 Following this bite, the motile flagellated form of these
2 organisms, called a trypomastigote, spreads via the
person's bloodstream to the lymph nodes and central
nervous system
 The entire life cycle of the fly takes approximately 3
weeks.
 The entire life cycle of African trypanosomes is
represented by extracellular stages(i.e donot enter any
cell)

Life cycle of Trypanosome

 Definitive host : Mostly cattle and human
 Intermediate host: Tsetse flies(Glossina palpalis)
 Winterbottom's sign, the tell-tale swollen lymph nodes
along the back of the neck, may appear.
 First manifestation is a hard, red, painful skin
ulcer that heals within 2 weeks
 With systemic spread, the
 Patient then experiences fever, headache,
dizziness, and lymph node swelling.

 These symptoms can last a week, and then the fever
subsides for a few weeks followed by renewed fevers.
 This pattern of fevers with fever-free intervals can
occur for months.
 Untreated diseases can cause anemia, endocrine, cardiac, and kidney
dysfunctions.
 Finally, CNS symptoms develop, with drowsiness in
the daytime (thus sleeping sickness), behavioral
changes, difficulty with walking, slurred speech, and
finally coma and death
 Damage caused in the neurological phase is irreversible.
 Tryptophol is a chemical compound that induces sleep in
humans. It is produced by the trypanosomal parasite in
sleeping sickness.

2 forms of African sleeping
sickness West African sleeping sickness, caused by
Trypanosoma brucei gambiense, is notable for slowly
progressing(chronic) fevers, wasting, and late
neurologic symptoms.
 Also found in central africa
 Humans are the main reservoir though can be found in pigs
 East African sleeping sickness, caused by
Trypanosoma brucei rhodesiense, is similar to the
West African variety but more severe(acute), with
death occurring within weeks to months. There is
rapid progression from recurrent fevers to early
neurologic disease (drowsiness, mental deterioration,
coma, and death).
 Wild game animals and cattle are the main reservoir of T. b.
rhodesiense.

Why the intermittent fevers???
 Variable surface glycoproteins (VSG).
 The trypanosomes are covered with about 10 million
molecules of a repeating single glycoprotein called the
VSG.
 They possess genes that can make thousands of
different VSGs.
 They will make and express, on their surface, a new
VSG in a cyclical nature
 Every time the human host develops antibodies
directed against the VSG , the trypanosomes
produce progeny with a new VSG coat.
 Thus, there are waves of new antigens,
producing recurrent fevers and protection from
our immune defenses.

Diagnosis ,Prevention and
treatment
 Gold standard; Visualization of trypomastigotes
in peripheral blood, lymph nodes aspirate, or
spinal fluid others include chancre fluid, bone
marrow and during the neurological stage,
cerebrospinal fluid.
 Detection of trypanosome-specific antibodies can be
used for diagnosis, but the sensitivity and specificity of
these methods are too variable to be used alone for
clinical diagnosis.
 Seroconversion occurs after the onset of clinical
symptoms during a T. b. rhodesiense infection, and
therefore is of limited diagnostic use[

Diagnosis ,Prevention and
treatment
 Prevention by eradication of the tsetse fly and use of the
sterile insect technique.
 Medical or veterinary means to reduce spread of the
parasite by monitoring, prophylaxis, treatment, and
surveillance to reduce the number of people/animals that
carry the disease.
 Patients are treated with suramin if the central
nervous system (CNS) is not involved
 Suramin does not penetrate into the CNS.
 With CNS involvement, the arsenical
melarsoprol, which is extremely toxic, is used.

Trypanosoma cruzi
The American Trypanosome
stercorarian Trypanosoma

 A disease of the Americas, ranging from the
southern U. S. (Texas), Mexico, Central
America, and down into South America.
 An estimated half a million Americans are
infected, creating some risk of transfusion
transmission in U.S.
 Pathogenesis and epidemiology differ greatly
from the African trypanosomes
 T. cruzi survives in wild animal reservoirs
such as rodents, opossums, and armadillos
 Vector is the reduviid bug (kissing bug or
Triatoma infestans)

AMERICAN TRYPANOSOMIASIS

 Feeds on humans while they sleep and defecate while
it sucks, Scratching implants T.cruzi trypomastigotes
present in the feces into the breached mucosa
 The trypomastigote loses its undulating membrane and
flagellum and rounds up to form the amastigote, which
rapidly multiplies.
 Organisms invade the local skin, macrophages, lymph
nodes, and spread in the blood to distant organs
 Amastigote net, usually present in muscles and neural
tissue
 Definitive Hosts::-Humans, dogs, armadillos, raccoons, and
others
 Intermediate Hosts:-Reduviid bugs

Acute Chagas' Disease
 It is an immediate reaction to infection
 It occurs only in 1% of infected individuals
 At the skin site of parasite entry, a hardened, itchy red area
develops, called a CHAGOMA.
 Romana sign; red, swollen, pus filled sore on the eye caused from rubbing
fecal into the eye
 This is followed by systemic spread with fever, malaise, and
swollen lymph nodes.
 Organs that can be infected include the heart and central
nervous system (CNS). Heart inflammation results in
tachycardia and electrocardiographic changes, while the CNS
involvement can result in a severe meningoencephalitis (usually
in young patients and immunocompromised)
 Other symptoms includes Anemia, nervous disorders, muscle and bone pain,
heart failure and death after 3-4 weeks of infection.

 This acute illness resolves in about a month
and patients then enter the intermediate
phase(8 to 10weeks after infection) . In this
phase there are NO SYMPTOMS, but there
are persistently low levels of parasite in the
blood as well as antibodies against T. cruzi.
 Most persons will remain in the intermediate
phase for life. For reasons that are poorly
understood, some persons will develop
chronic Chagas' disease years to decades
later.

Chronic Chagas' Disease
 Occurs 10 to 20/30 years after infection
 The organs primarily affected are the heart and some hollow
organs such as the colon and esophagus.
 Intracellular T. cruzi amastigotes cannot usually be found, and it
is unclear why disease develops in these organs.
1. Heart: Arrhythmias are the earliest manifestation (heart block
and ventricular tachycardia). Later there is an increase in heart
size and heart failure (dilated cardiomyopathy and heart failure)
.
2. Megadisease of colon and esophagus: A big, dilated, poorly
functioning esophagus develops with symptoms of difficulty and
pain in swallowing, and regurgitation of food. A dilated colon
(megacolon) results in constipation and abdominal pain.
Patients can go weeks without bowel movements.
It is often postulated that toxins released cause denervation and the
muscle parasite penetration causes lose of elasticity resulting in
megacolon, and megaesophagus.

Diagnosis
 Acute Chagas' disease:
 Direct examination of the blood for the motile
trypomastigotes(thick blood smear).
 Xenodiagnosis(sensitive test)
○ Forty laboratory-grown reduviid bugs are allowed to
feed on the patient, and one month later the bugs'
intestinal contents are examined for the parasite.
 Chronic Chagas' disease:
 Classic clinical findings (cardiac and
megadisease) along with serologic evidence of
past T. cruzi infection allows for presumptive
diagnosis.

Prevention and Treatment
 Control:
 Protect yourself while sleeping by raise sleeping area off ground, or
sleep in netting.
 DDT- poison
 Keep village clean of dogs, raccoons and other possible
hosts with the parasite.
 Although nifurtimox and benznidazole can be used
for acute cases, there is currently no effective therapy
for the chronic manifestations of this infection.
 Therefore individuals should take precautions to
prevent kisses by the kissing bug (insect repellent,
bednets)

MALARIA

MALARIA
 Malaria is a febrile disease
 They infect about 300-500 million persons
worldwide each year, resulting in 20-40 million
deaths.
 The anopheles mosquito carries the organisms
within its salivary glands and injects them into
humans while it feeds.
 The organisms then grow in the liver and spread to
the human red blood cells, where they reproduce.
 Plasmodium vivax : Most predominant and
extends to temperate regions(50%)
 Plasmodium falciparum : Most pathogenic
species(43%)

 The red cells fill with protozoa and burst. The red
cells all burst at the same time, releasing the
protozoa into the bloodstream and exposing them
to the immune system, which results in fever
 Different species of Plasmodium burst the red
cells at different time intervals.
 Erythrocytic schizogony is the time taken for
trophozoites to mature into merozoites before
release when the cell ruptures.
 P. Vivax and P. Ovale burst loose every 48 hours,
So they both produce chills and fever followed by
drenching sweats every 48 hours, which is called
Tertian malaria

 P. malariae bursts loose every 72 hours,
causing a regular 3-day cycle of fevers and
chills, followed by sweats. This is called
Quartan malaria
 P. falciparum, the most common and deadly of
the Plasmodia, bursts red cells more
irregularly, between 36--48 hours. Thus the
chills and fevers tend to either fall within this
period or be continuous, with less pronounced
chills and sweats(quotidian or malignant tertian
or subtertian or irregular)

Endemicity
 Endemicity refers to the amount or severity of malaria in an area or
community. Malaria is said to be endemic when there is a constant
incidence of cases over a period of many successive years.
Endemic malaria may be present in various degrees. Recognised
categories of endemicity include :
A. Hypoendemicity - little transmission and the disease has little effect on the
population.
B. Mesoendemicity - varying intensity of transmission; typically found in the
small, rural communities of the sub-tropics.
C. Hyperendemicity - intense but seasonal transmission; immunity is insufficient
to prevent the effects of malaria on all age groups.
D. Holoendemicity - intense transmission occurs throughout the year. As people
are continuously exposed to malaria parasites, they gradually develop immunity
to the disease. In these areas, severe malaria is mainly a disease of children from
the first few months of life to age 5 years. Pregnant women are also highly
susceptible because the natural immune defence mechanisms are impaired
during pregnancy.

Plasmodia Life Cycle
Each Plasmodium has two distinct hosts.
 A vertebrate such as the human where asexual phase
(schizogony) takes place in the liver and red blood
cells.
 An arthropod host (Female Anopheles mosquito)
where gametogony (sexual phase) and sporogony
take place.
 Thin, motile, spindle-shaped forms of the Plasmodia,
called sporozoites, swim out of the mosquito's sucker
and into the human bloodstream.
 They wiggle their way to the liver and burrow into a
liver cell. This marks the beginning of the pre-
erythrocytic cycle in the liver,
 So-named because this cycle occurs before the red
blood cells (erythrocytes) are invaded.

 The sporozoite rounds up to form a ball within the
liver cell. This ball, now called a trophozoite
 Trophozoite undergoes nuclear division, forming
thousands of new nuclei called a schizont.
 A cytoplasmic membrane then forms around each
nucleus, creating thousands of small bodies called
merozoites
 The new overloaded liver cell(hepatocyte) bursts
open, releasing the merozoites into the liver and
bloodstream. Some will reinfect other liver cells as
the sporozoite did initially, repeating the same
cycle discussed above, which is now called the
exo-erythrocytic cycle.

 Other merozoites will enter the bloodstream and
enter red blood cells, starting the erythrocytic
cycle
 The merozoite rounds up to form a trophozoite. In
the red cells the trophozoite is shaped like a ring
with the nuclear material looking like the diamond
on the ring.
 Nuclear division then occurs with formation of a
large multinucleated schizont. Cytoplasm surrounds
each nucleus to form new merozoites within the late
schizont.
 Red cell lysis occurs with release of merozoites.
 The released merozoites stimulate an immune
response, manifested as fevers, chills, and sweats.

 The merozoites can continue to invade other
red cells and then grow for another 2-3 day
cycle followed by rupture and release again.
 Some merozoites will change into male and
female gametocytes.
 These cells circulate and will be taken up by a
biting anopheles mosquito.If they are not, they
will shortly die.
 Two of the species, P. vivax and P. ovale,
produce dormant forms in the liver
(hypnozoites) which can grow years later,
causing relapsing malaria.

 In the mosquito, the gametocytes are sucked
into the stomach where the male and female
gametocytes fuse to form an ookinete
 DNA is mixed and the fused gametocytes
become an oocyst. The oocyst divides into
many spindle-shaped wiggling sporozoites,
which disseminate within the mosquito.
 They may find their way into the mosquito
salivary gland and will be injected into the
human for asexual reproduction.

Severe malaria
 Severe malaria is defined as symptomatic malaria in a patient
with P. falciparum asexual parasitaemia with one or more of the
following complications:
 Cerebral malaria (unrousable coma not attributable to other
causes).
 Generalised convulsions (> 2 episodes within 24 hours)
 Severe normocytic anaemia (Ht<15% or Hb < 5 g/dl)
 Hypoglycaemia (glood glucose < 2.2 mmol/l or 40 mg/dl )
 Metabolic acidosis with respiratory distress (arterial pH < 7.35 or
bicarbonate < 15 mmol/l)
 Fluid and electrolyte disturbances
 Acute renal failure (urine <400 ml/24 h in adults; 12 ml/kg/24 h in
children)
 Acute pulmonary oedema and adult respiratory distress syndrome
 Abnormal bleeding
 Jaundice
 Haemoglobinuria
 Circulatory collapse, shock, septicaema (algid malaria)
 Hyperparasitaemia (>10% in non-immune; >20% in semi-immune)

Diagnosis and Control of Malaria
 Examination of thin and thick smears (1000x) of blood, under
oil-immersion magnification, reveals the trophozoites and
schizonts within the erythrocytes.
 Field stain and Giemsa stain can be used.
 Sometimes the gametocytes can be visualized.
 Fluorescently labeled antibodies may be used to identify the
responsible species.
 Prevent mosquito bite:
 Eliminate vector with pesticides (pyrethins) at dusk in living and
sleeping areas.
 Use insect repellants (containing DEFT) and
 mosquito nets, and wear long-sleeved shirts and long pants.
 Chemical Prophylaxis for travelers: When traveling to an area
without chloroquine resistance, chloroquine is used.
 If in a chloroquine resistant area, mefloquine or doxycycline may be
used for prophylaxis.
 It is wise to carry a pyrimethamine/sulfadoxine (fansidar)

Many animals are infected with Toxoplasma, and humans are
infected by the ingestion of cysts in undercooked meats (raw
pork) or food contaminated with household cat feces.

Toxoplasma gondii
 Obligate intracellular parasitic protozoan
 80% of cats are infected in the United States
 Cats are the only hosts within which T.gondii can sexually reproduce to
complete and begins its lifecycle, though it can affect any warm blooded
animal
 It is excreted in the feces of cats as the infectious cyst.
 It causes disease by reactivation of a latent infection in an
immunocompromised person or as a primary infection in a pregnant
woman leading to transplacental infection of the fetus.
In healthy individuals
 Toxoplasma acquired after birth is most commonly asymptomatic or a
mild, non-specific flu-like illness with lymphadenopathy and fever;
heterophile negative mononucleosis
 Once infected, as immunity develops, bradyzoites encyst, but
generally remain viable as evidenced by a positive antibody titer.

Toxoplasmosis
 Immunocompromised patients
 They are susceptible to growth of the latent Toxoplasma gondii.
 Infact Unless prophylactic drugs are given, AIDS patients who
are seropositive for Toxoplasma will have reactivational
infections.
 The infection can present in many ways-with fever; lymph node,
liver, and spleen enlargement; pneumonia; or frequently with
infection of the meninges or brain.
 Infact, Toxoplasma encephalitis is the most common central
nervous system infection in AIDS patients.
 Brain scan will describe ring-enhancing lesions (growing mass,
much like a tumor) with symptoms of headache and focal
neurologic signs (seizures, gait instability, weakness, or sensory
losses).
 Infection of the retina, chorioretinitis, is also common, resulting
in visual loss.
 Examination of the retina reveals yellow white, fluffy (like cotton)
patches that stand out from the surrounding red retina.

Toxoplasmosis
 Pregnant patients
 Toxoplasma is one of the transplacentally acquired TORCHES organisms
that can cross the blood-placenta barrier.
 Transplacental fetal infection can occur if a pregnant woman who has never
been previously exposed to Toxoplasma gondii is infected.
 Congenital toxoplasmosis does not occur in pregnant women who have
serologic evidence of previous exposure, most likely because of a protective
immune response.
 Women who acquire Toxoplasma as a primary infection during pregnancy
present with flu-like illness/heterophile-negative mononucleosis.
 If primary maternal infection occurs during pregnancy, the fetus may be
infected.
 If Toxoplasma crosses the placenta early, severe congenital infections
(intracerebral calcifications, chorioretinitis, hydro- or microcephaly or
convulsions, mental retardation, encephalitis) may occur.
 If Toxoplasma crosses the placenta later, infection may be inapparent,
but may lead to progressive blindness in the child later in life (teens).
 Maternal antibodies (secondary infection) protect the fetus
during pregnancy, even if the mother is re-exposed during
pregnancy.

Diagnosis and Treatment
 CAT scan of brain will show a contrast-
enhancing mass.
 Examination of the retina of the eye will
reveal retinal inflammation.
 Serology: Elevated immunoglobulin titers
suggest that the patient has at some time
been exposed to this organism.
 Sulfadiazine plus pyrimethamine can be
used to treat patients with acute
toxoplasmosis.

BABESIOSIS aka Piroplasmosis
Babesia microti, Babesia divergens
 Babesiosis(red water fever) is an infection very much like
malaria.
 Primarily a disease of cattle, transmitted to humans by tick.
 Humans strain include Babesia microti, WA1 , & M01 strains
 It invades red blood cells causing fever and hemolysis (anemia)
 May occur as a Co-infections with Borrelia
 In some part of USA Babesia Microti is spread by the bite of
the same tick that spreads lyme disease, Ixodes scapularis.
 After biting the white-footed mouse, the reservoir for B.
microti, the tick will leap to the next carefree golfer who walks
into the rough.

 Like Plasmodium, Babesia sporozoites slither out of
tick salivary glands into the blood of the hapless
golfer. The sporozoites invade erythrocytes and
differentiate into pear or ring-shaped trophozoites.
 Trophozoites asexually bud and divide into 4
merozoites that stick together, forming a cross or x-
shaped tetrad ("Maltese cross").
 Trophozoite and merozoite growth ruptures the host
erythrocyte
 Red cell infection results in only mild hemolysis, so
infection is usually asymptomatic and sub-clinical.
 Asplenic patients are unable to clear the organisms
as well and may have severe infection similar to
falciparum malaria

Diagnosis and Treatment
 Giemsa or wright-stained thin and thick
blood smears reveal ring-shaped
trophozoites that look like Plasmodium
and the distinctive cross or x-shaped
tetrad of merozoites (Maltese cross).
 Treat infected patients with quinine and
clindamycin.

References
 Clinical microbiology made ridiculously
simple. Edition 3 by Mark Gladwin M.D
and Bill Trattler M.D
 USMLE step 1 on immunology and
microbiology lecture notes

Parasitology 1

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