2017

Part 2:

[PARASITOLOGY]
Parasitology 2017

 Entamoeba histolytica
The Forms of E.histolytica: E. histolytica can exist in two forms, both forms are
present in contaminated food and drinks.
1. Trophozoites (free amoeba) :
-Morphology : ectoplasm with ectoplasmic pseudopodia and endoplasm .
-Histolytica type nucleus: single spherical nucleus surrounded by nuclear membrane. The
chromatin materials found on inner surface of nuclear membrane with regularly distributed
granule and in the center of the nucleus there is a karyosome.
-The trophozoite ingests RBCs which may be seen in fresh specimen or stained smear (a
diagnostic feature for E.histolytica)
-Ingesting the trophozoite form is not harmful (not infective).
2. Cyst of E.histolytica:
-Morphology : early cysts have rounded ends chromatid bodies.
-Mature cysts have four nucleus. Mature cyst are infective.
-When ingested they form trophozoites(excystation).

Mode of transmission:
1- feco – oral route(water, fresh fruits, and vegetables) 2- Cyst passing carrier 3- Sexual
transmission among homosexuals.
Pathology of E.histolytica:
-They inhabit the cecum mainly and sigmoidorectal area less often.
-The amoeba can actually 'bore' into the intestinal wall and typical flask-like primary ulcers
due to large necrotic areas are produced.
-It may reach the blood stream. From there, it can reach different vital organs of the human
body, usually the liver(liver abscess), but sometimes the lungs, brain……etc.

o Medicine
-Infections range from asymptomatic colonization to amebic colitis and life-threatening
abscesses.
 Invasive intestinal disease:
-May occur days to years after initial infection , characterized classically by abdominal pain
and bloody diarrhea and (rarely) fever, The right side of the colon is commonly involved.
-Patients at increased risk of severe disease include those who are very young, very old,
malnourished, or pregnant and those who are receiving corticosteroids.
-Complications: Extensive fulminant necrotizing colitis, formation of an annular intraluminal
mass (ameboma), bowel obstruction, perforation, peritonitis.
 Amebic liver abscess
-Most patients present with a single abscess, tender hepatomegaly and pain in the right
upper quadrant. ALA is commonly accompanied by fever, as well as by rigors, chills, and
profuse sweating. Jaundice is not typically present, elevated bilirubin levels,ALP.
-Most patients with ALA do not have concurrent colitis and cysts, and trophozoites are not
always seen on fecal smears.
-Complications: perforation into peritoneal, pleural, and pericardial cavities; septic shock;
and death.
 Pulmonary Amebiasis
-Rarely primary, rupture of liver abscess through diaphragm, 2nd bacterial infections
common, fever, cough, dyspnea, pain, vomica
 Secondary menigoecephalitis(cerebral amoebiasis)
-The clinical symptoms of cerebral amoebiasis are usually preceded by gastrointestinal,
hepatic or respiratory symptoms. History of headache or sensorial disturbances are the most

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Parasitology 2017
common initial presentations of cerebral amebiasis history of convulsions and tendency to
sleep. Amebic brain abscesses may be single or multiple.
Diagnosis
-Clinical presentation , exposure history and radiologic findings are helpful.
- Should be confirmed with microbiological laboratory results.
 In invasive intestinal disease :
- 3 stool specimens on different days during a period of 10 days,
-Light microscopy to find the characteristic trophozoites containing RBC and cysts.
-Microscopy alone cannot differentiate E histolytica from E dispar unless trophozoites
containing ingested red blood cells are identified.
-Differentiating E histolytica from E dispar requires otherwise molecular techniques.
 Amebic liver abscess
-Stool specimens from patients with disseminated disease may not contain cysts and
trophozoites, despite repeated examinations.
-Serologic tests are tests of choice. sensitivities and specificities exceed 95%.
-Cannot distinguish between past and current infection unless IgM is detected.
 Other tests include fecal antigen tests and DNA based tests (highest sensitivity and
specificity).
Treatment:
-Treating all cases of proven E histolytica, regardless of symptoms.
-Asymptomatic intestinal infection with E histolytica should be treated with luminal
amebicides, such as paromomycin.
-Intestinal and extraintestinal invasive disease treated tissue amebicides such as (eg,
metronidazole) followed by a luminal agent to eradicate any potential intestinal reservoirs.
-ALA typically responds well to a 5- to 10-day course of metronidazole, which should also be
followed with a luminal amebicide
-Surgical or percutaneous drainage of ALAs is generally not recommended

o Pharma
Drugs for Amebiasis
1.Mixed amebicides
a)Metronidazole:
-Clinical uses : effective against both the luminal& systemic forms of the disease.
-Mechanism: Formation of reduced cytotoxic compounds that bind to proteins &DNA
resulting in cell death.
-Side effects: GIT effects , unpleasant metallic taste, Pancreatitis& CNS toxicity, Disulfiram-
like effect occurs if taken with alcohol.
b)Tinidazole
2.Luminal Amebicides
a)Iodoquinol b)Paromomycin.
Effective against the luminal trophozoite&cyst forms but not against trophozoites in
the intestinal wall or extraintestinal tissues
3.Systemic amebicides
a)Chloroquine b)Emetine& dehydroemetin.

Prepared by :
Haitham N.Khalid
Baghdad medical school

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Parasitology 2017

 Giardia lamblia
The life cycle consists of two stages: the trophozoite and the cyst
1-the trophozoite: pear-shaped with two nuclei, four pairs of flagella, and a suction disk with
which it attaches to the intestinal wall.
2-the cyst: oval cyst is thick-walled with four nuclei(infective stage).
-Each cyst gives rise to two trophozoites during excystation.
Mode of transmission :
Ingestion of cysts, usually in contaminated water.
Pathogenesis:
Trophozoites inhabits the small intestine , ventral disk embeds the parasite into the
epithelial microvillus layer→ malabsorption. (this is proposed but not definite mechanism).
o Medicine
Signs and symptoms:
-Most people are asymptomatic; only about a third of those infected exhibit symptoms.
-Symptoms typically develop 1-3 weeks after exposure and include dirrhoea,abdominal
cramps, weakness,anoraxiea,nausea and vomiting, bloating, tendereness.
-Symptomatic infections are well recognized as causing lactose intolerance.
-blood in the stool and fever are infrequent.
Diagnosis:
-Detection of antigens in stool specimens is the current test of choice.
-Microscopic examination of the stool for motile trophozoites or for the distinctive oval
G.lamblia cysts.
-Note: cysts are found in formed stools while trophozoites in loose ones.
Treatment:
-When symptoms are present treatment is typically with either tinidazole or metronidazole,
nitazoxanide.
-Milk avoidance due to possible lactose intolerance.

 Pneumocystis jiroveci
-Pneumocystis jiroveci is an important cause of pneumonia in immunocompromised
individuals. Molecular analysis supports the idea that it is a fungus.
Life cycle:
Trophic forms(1N) →fusion →sporocyte(2N)→meiosis+mitosis→mature cysts which contain
eight spores.
Pathogenesis
-Transmission occurs by inhalation. The presence of cysts in the alveoli induces an
inflammatory response consisting primarily of plasma cells "plasma cell pneumonia.",
histiocytes, lymphocytes resulting in a frothy exudate that blocks oxygen exchange. The
organism does not invade the lung tissue. 70% of people have been infected with it.
Clinical Findings
-The sudden onset of fever, nonproductive cough, dyspnea, and tachypnea in an
immunocmpromised patient is typical of Pneumocystis pneumonia.
-Mortality approaches 100% if untreated.
Laboratory Diagnosis
Finding the typical cysts by microscopic examination of lung tissue or fluids. Sputum is
usually less suitable.
Treatment
-Trimethoprim+sulfamethoxsazole.
-Note: Cryptosporidium hominis causes watery,nonbloody diarrhea that persist for long
periods in immunocompromised individuals.

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 Trichomonas vaginalis
-Exists in trophozoite stage only, which reproduced by binary fission
Morphology:
-pear shaped, consist of 4 anterior flagella and one back posteriorly
-undulating membrane run to the half of the body
-in a wet mount the trophozoite has characteristic jerky motility.
-T.vaginalis is an obligate parasite, the organism cannot survive long outside the host; The
normal habitat of the parasite is the vagina and urethra of women. In male the organism
inhibits urethra, seminal vesicles, and prostate.
Mode of infection: 1-sexual contact 2-New born may get infection from infected
mother through birth canal 3-Fomites have been implicated in transmission.
The essential factors for T.vaginalis growth are: 1-presence of glycogen in vaginal
cell 2-PH of vagina [optimal PH for growth of T.vaginalis is 5.5]

*Why the incidence of T.vaginalis infection is high among mature females?

 In mature female [15-40], because of the high glycogen content, the normal vaginal
PH will be acidic [PH 4-4.5] maintained by lacto-bacilli.
1- seminal fluid can elevate the acidity of vagina to PH 5.5 [optimal PH]
2- they need less than 10 to the power 4 to be infected (whereas the male needs 10
to the power 6 to be infected).
-both T.vaginalis and bacterial flora [lactobacilli] lives on glycogen and acidic PH, therefore
during trichomoniasis no chance for bacteria to live and the PH of vagina rises to PH 5.5
 in other groups: no glycogen →no lacto bacilli growth →ph rises →trichomonas
cannot grow.
 The glycogen content of epithelium is high and increases during pregnancy, so
pregnant female is more liable for infection.
-T.vaginalis loses its viability below PH 3.8 and above PH 7.5
-they have been implicated as factor in transmission of HIV.
-2-7%of female babies acquire trichomoniasis by directed vulvovaginal contamination
-Use of antibiotics and presence of other infection increase the risk.

Clinical findings:
 In females: asymptomatic infections have been observed in 50% of female patients
[asymptomatic carrier ].
-vaginitis ,cervicitis and urethritis: intense vaginal and vulvar pruritis and discharge(has a foul
smell and is frothy , creamy or yellowish –greenish exudates), occurring during or after
menstruation. in moderate and sever cases, there may be complaints of local irritation or
burning and itching sensation in the vulva.
 In males : often mild or asymptomatic, although at sometimes associated with
urethritis which represents the most common symptomatic presentation(non
gonococcal urethritis).

Laboratory diagnosis:
Examination of vaginal and urethral discharge → direct wet preparation examined by
microscope, search for actively motile trophozoite with jerky motilities.
Treatement :
- Metronidazole is the drug of choice. Treat the patient and the partner.

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Parasitology 2017

 Toxoplasma gondii
-Toxoplasma is an obligate intracellular parasite. Its life cycle includes two phases called the
intestinal and extraintestinal phases. The intestinal phase occurs in cats only and produces
"oocysts.".
-The extraintestinal phase occurs in all infected animals and produces "tachyzoites" and,
eventually, "bradyzoites" or "zoitocysts.“.

Pathogenesis:
-In first contact →tachyzoites in blood →engulf by monocytes→ repliaction within the
macrophages to form the pseudocyst(acute stage).
-The parasites invade organs(muscle,eye,brain) to escape the immune system→replication
slows down in those organs ,bradyzoites, to form the true cysts ,zoitocysts. (chronic stage).
-The chronic stage doesn’t change to acute stage (tachyzoites) unless the Immunity is Low.
-Immunity : Cell Mediated Immunity is protective and humoral response is of diagnostic
value.

Community:
-The definitive hosts of T. gondii are cats and other felines. The intermediate hosts of T.
gondii include sheep, goats, rodents, swine, cattle, chickens and birds all may carry an
infective stage of T. gondii encysted in tissue, especially muscle and brain. Tissue cysts
remain viable for long periods, perhaps lifelong.
Mode of transmission :
1- Infections arise from eating raw or undercooked infected meat containing tissue
cysts
2- Ingestion of infective oocysts in food or water contaminated with feline
feces(chidren from dirt in sandboxes, playgrounds and yards in which cats have
defecated)
3- Transplacental infection occurs in humans when a pregnant woman has rapidly
dividing cells (tachyzoites) circulating in the bloodstream, usually during primary
infection.
4- Inhalation of sporulated oocysts (rare)
5- Infection may occur through blood transfusion or organ transplantation from an
infected donor.

o Medicine
Up to half of the world's population are infected by toxoplasmosis but have no symptoms.
Acute toxoplasmosis:
-Often asymptomatic in healthy adults, caused by tachyzoites.
-Symptoms may manifest and are often influenza-like , swollen lymph nodes , headaches,
fever, and fatigue or muscle aches and pains that last for a month or more.
-In immuncompromised people(Young children, HIV/AIDS, on chenmotherapy, received a
transplant) severe toxoplasmosis may develop. This can cause damage to the brain
(encephalitis) or the eyes (necrotizing retinochoroditis), , lung problems that may resemble
tuberculosis or Pneumocystitis.
Latent toxoplasmosis:
-In most immuncompetent people, the infection enters a latent phase, during which only
bradyzoites (tissue cysts) are present. Latent stage can change into acute stage if cell
mediated immunity is weakened.

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o Pediatrics
Congenital Toxoplasmosis:
-First trimester > Severe disease, Second trimester > intermediate severity, Third trimester >
mild or asymptomatic.
-Transmission is most commonly in third trimester.
-Key Features:
-Chorioretinitis, Intracranial calcifications, Hydrocephalus.
-Note: Initially asymptomatic infants are still at high risk of developing abnormalities,
especially chorioretinitis.

Diagnosis
1-Serological tests are the tests of choice.
-Acute infection : IgM (persist for six months after recovery) or 4x rise in IgG .
-Chronic (past) infection: IgG to detect past infection (pesists for life).
2-PCR : this is indicated in two situations,
a-in prenatal diagnosis →PCR for amniotic fluid.
b-in immunodeficient (AIDS) patients.
3-newborn diagnosis : IgM in newborn serum.

Treatment
- Indicated only for people with serious health problems, such as people with HIV whose CD4
counts are under 200 cells/mm.
 Acute infection : Sulfadiazine used in combination with pyrimethamine.
 Latent infection: Clindamycin in combination with atovaquone→kill cysts.
Prophylaxis:
1- In AIDS: Trimethoprim/sulfamethoxazole
2- In pregnancy: spiramycin.

Prepared by :
Haitham N.Khalid
Baghdad medical school

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Parasitology 2017

 Test yourself …. Part 1

Case scenario for question 1-2
A 4 yr old child presents with colicky abdominal pain, blood-stained diarrhea, and tenesmus,
all of acute onset. There is no fever. Trophozoites are seen in the stool. The family has
recently returned from a trip to Mexico.
1-Regarding the causative agent :
A. have eccentric karyosome within the nucleus
B. usually inhabits the large intestine
C. exists in one form
D. the cause of primary menigoecephalitis
E. trophozoites are usually found in formed stools.
2-All of the following statements concerning the treatment of Entamoeba histolytica
amebiasis are true EXCEPT:
A.Asymptomatic cyst excreters usually do not need to be treated
B. metronidazole can cause nausea and vomiting
C.A nitroimidazole, such as metronidazole or tinidazole, is recommended for initial
treatment of invasive intestinal amebiasis
D. Surgical drainage of amoebic liver abscess is generally not recommended
E.Metronidazole therapy should always be followed by paromomycin
Case scenario for question 3
A 7 yr old girl presents with fever, abdominal pain and distention, and hepatic tenderness.
CT reveals a single, 7 cm, fluid filled cavitary lesion in the right hepatic lobe. The test most
likely to confirm the diagnosis is:
A.Upper gastrointestinal endoscopy and duodenal biopsy
B.Stool culture
C.Mesenteric lymph node biopsy and culture
D.Stool ova and parasites
E.Serologic testing
Case scenario for question4-5
A 19-year-old college student presents to the emergency department with crampy
abdominal pain and watery diarrhea that has worsened over 3 days. Stool examination
shows yellow, greasy, and foul smelling stools with small cysts containing four nuclei, and
stool antigen immunoassay is positive for Giardia
4-What attribute of this parasite imparts its pathogenicity?
(A) Lytic enzymes
(B) Flagella
(C) Ventral sucking disc
(D) Encystment
(E) Toxic metabolites
5-All of the following statements concerning the treatment of Giardia lamblia infections
are true EXCEPT:
A.Asymptomatic cyst excreters usually do not need to be treated
B.patients with acute diarrhea require treatment
C.patients with chronic diarrhea require treatment
D.Tinidazole or nitazoxanide are the treatments of choice
E.Metronidazole therapy should always be followed by iodoquinol
Case scenario for question6
An HIV-positive patient with a CD4+ count of 47 presents with diarrhea. Acid fast
structures are found in the stool. From this finding, which of the following is true?
(A) Infection is short lasting and self-resolving and requires no treatment

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(B) If treated with antibiotics, the infection should resolve in 3–6 days
(C) Infection will resolve only with a combination of antituberculous drugs,
and then it may take weeks
(D) Infection could have been prevented by avoiding cat feces and undercooked
or raw meat
(E) Even with the best treatment, the infection may be unrelenting
Case scenario for question 7
A 17-year-old woman presents to the clinic complaining of vaginal itchiness and malodorous
discharge. She is sexually active with multiple partners, and she is interested in getting
tested for sexually transmitted diseases. A wet-mount microscopic examination is
performed, and trichomonal parasites are identifed.
Which of the following statements regarding trichomoniasis is true?
A. No treatment is necessary as disease is self-limited.
B. Trichomoniasis can only be spread sexually.
C. The patient’s sexual partner need to be treated only if symptomatic.
D. pregnant women are more liable for infection.
E. cyst passing asmpytomatic carriers are the usual source of infection.
Case scenario for question 8
A 24-year-old primiparous woman in her eighth month of gestation develops a
positive IgM titer to Toxoplasma gondii for the first time. She should be advised
by her physician that
(A) this child and all future fetuses are likely to be infected
(B) a newborn with a positive anti-Toxoplasma IgG response should be treated
with anti-parasitics
(C) future infections can be avoided by proper vaccination and worming of
cats
(D) retinochoroiditis can be prevented by drug treatment of an infant with a
positive IgM response
(E) major organ damage can be reversed by prompt treatment of the newborn
9-Which is the most common result of primary Toxoplasma gondii infection in children?
A.Cellulitis
B.Lymphadenitis
C.Meningitis
D.Pneumonia
E.No specific symptoms
10-Toxoplasmosis causes all of the following patterns of disease EXCEPT:
A.Congenital infection manifested in neonates by chorioretinitis, cerebral calcifications, and
hydrocephalus due to 1st-trimester infection
B.Congenital malformations, such as cleft palate or patent ductus arteriosus
C.Localized or generalized lymphadenopathy in previously healthy persons
D.Encephalitis in patients with acquired immunodeficiency syndrome (AIDS)
E.Retinal lesions involving the macula and leading to blindness
11-A 29-year-old HIV positive man is admitted with right-sided hemiplegia. For the past four
days he has been complaining of headache and flu-like symptoms. CT scan shows multiple
ring enhancing lesions. A diagnosis of cerebral toxoplasmosis is suspected. What is the most
suitable management?
A.Artemether and lumefantrine
B.Co-trimoxazole
C.Supportive treatment
D .Pyrimethamine and sulphadiazine
E.Metronidazole and gentamicin

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 Genus leishmania
General features:
1-Two hosts : final (human,dog,rodent) and intermediate (female of sand fly)→vector.
2- Amastigote in the final host(human) and promastigote in the intermediate(infective
stage).
3-multiplies by binary fission.
4- infects RES of skin and viscera(liver,BM,spleen) of final host.
Life cycle : sand fly bites and injects promastigotes → engulf by macrophages
→amastigotes inside macrophages →multiplication → sand fly bites →amastigotes
into promastigotes in midgut.
 L. tropica complex: 3 serologically and biochemically distinct species.

1-Leishmania tropica minor 2- Leishmania tropica major

dry sore or urban cutaneous leishmaniasis
2month – 3year incubation period
chronic disease, lasts for year or longer.
dry lesions that ulcerate only after several
months
Single lesions and occur primarily on the face
wet sore or rural cutaneous leishmaniasis
2 weeks incubation period
acute infection with duration of 3-6 months.
The lesions are moist and tend to ulcerate
very early.
primarily on the lower limb, there may be
secondary or satellite lesions.

3- L. aethiopica(causes diffuse cutaneous leishmaniasis): Produces a chronic disease similar

to that caused by L. tropica.

Pathogenesis:
-Amastigotes in the macrophages and other endothelial cells of the capillaries and small
blood vessels→ lysis of amastigotes caused by T-cell mediated activation of macrophages→
granulomatous reaction →nodule formation→Ulceration of the area.
-Cell mediated immune response is crucial for disease resolution (Th1 over Th2).
-The sores can change in size and appearance over time. They often end up looking
somewhat like a volcano, with a raised edge and central crater. The sores can be painless or
painful.
Findings:
-The first sign of the infection is a small red papule The papules are dry (dry lesions) and
ulcerate only after several months in L. tropica and L. aethiopica infection. In L. major
infection, the papule is covered with serous exudates (moist lesion) and ulcerates early.
-Ulcer may associate with local disfiguration, pyogenic complication, pain and some time
septicemia. dry lesion usually (& also moist)heal spontaneously.
Diagnosis:
-Tissue sample (scraping, aspirate or punch biopsy) for smear and culture.
-Smear: Giemsa stain – microscopy for LD bodies (amastigotes).
-Note: 1-Scraping is usually from the periphery of the lesion(active borders)
2-There are other diagnostic modalities like PCR( for researches),culture on NNN medium
and leishmanin skin test.
3- Serology is not useful→ most patients do not develop a significant antibody response.

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 Leishmania donovani
-Reservior host: involving canine such as Dog, Jackal and other wild carnivorouses.
-Mode of transmission: By insect bite , Phlebotomus(Sand fly).
-Infects RES of liver , spleen and bone marrow, with prominent reticuloendothelial cell
hyperplasia .Infected macrophages have a diminished capacity to initiate and respond to an
inflammatory response, thus providing a safe haven for the parasite.
-Amstigotes can be seen inside macrophages in tissue biopsy.
-Melanocyte stimulation → hyperpigmentation so called black fever(kala azar).

Visceral Leishmaniasis VL (Kala-azar)

-Subclinical infection occurs considerably more frequently than does active cutaneous or
visceral disease, which can be identified by a positive delayed type hypersensitivity response
to leishmanial antigens.
 Clinical manifestations and spectrum:
-kala-azar typically affects children less than 5 yr of age. After inoculation the child may have
one of the following destinies:
1- Asymptomatic infection : show no clinical evidence of disease.
2- Oligosymptomatic illness: either resolve or goes into active form.
Presents with mild constitutional symptoms (malaise, intermittent diarrhea, poor activity
tolerance) and intermittent fever. In most of these children the illness will resolve without
therapy, but in approximately 25% it will evolve to active kala-azar within 2-8 months.
3-Active Kala-azar
-classic clinical features of High fever, marked splenomegaly, hepatomegaly, and severe
cachexia. Typically develop approximately 6 months after the onset of the illness, but a rapid
clinical course over 1 month has been noted in up to 20% of patients.
-At the terminal stages: hepatosplenomegaly is massive, gross wasting, the pancytopenia is
profound, and jaundice, edema, and ascites may be present. Bleeding episodes, especially
epistaxis, are frequent.
- often complicated by secondary bacterial infections, which frequently are the causes of
death. Without treatment mortality rate>90%.

 Diagnosis
1- Non specific: Anemia, thrombocytopenia, leucopenia , elevated hepatic transaminase
levels, and hyperglobulinemia.
2- Specific: serological tests are the tests of choice(high Ab titers).
-An enzvme-linked immunosorbent assay using a recombinant antigen (K39) has a
sensitivity and specificity for VL that is close to 100%.
3- Definitive diagnosis: demonstration of amastigotes in tissue specimens(splenic, bone
marrow, or lymph node aspirations) or isolation of the organism by culture.

 Treatment
-All patients with VL should receive therapy.
-The pentavalent antimony compounds (sodium stibogluconate also called Pentostam)is the
mainstay of antileishmanial chemotherapy. Duration :28 days. Clinical resistance to
antimony therapy has become common.
-Relapses are common in patients who do not have an effective antileishmanial cellular
immune response(usually evident within 2 mo after completion of therapy) →multiple
courses of therapy or a chronic suppressive regimen.
-Other options for therapy include : Amphotericin B , Recombinant human interferon ,
Miltefosine as the 1st oral treatment for VL, Paromomycin and Pentamidine.

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-Note: Adverse effects of antimony therapy are dose and duration dependant: Fatigue,
arthralgia and myalgias, Abdominal discomfort, elevated hepatic transaminase level,
elevated amylase and lipase levels, mild hematologic changes. Sudden death due to cardiac
toxicity is extremely rare and associated with very high doses of antimony Rx.

 Follow up
1- Clinical : 1)General condition (1 st week) 2)Body temperature (1 st week)
3)Liver and spleen size (weeks to months)
2- Hematological: CBC (weeks to months).
3- Serological : 1)K39 assay 2)PCR

 Plasmodium species
General characteristics:
1-parasities of tissue & blood of their host
2-life cycle include sexual (gametogony & sporogony)→occurs in mosquito & asexual
(schizogony)→vertebrate host like human.
3-No organil of locomotion but at certain stages can move by body flexible or flagella as
microgamete.
4-requires intermediate host (human) and final host(female anophele mosquito) which is
also the vector.
-Species that cause Malaria in man are : Plasmodium vivax, Plasmodium falciparum,
Plasmodium malariae, Plasmodium ovale.

Notes about plasmodium LIFE CYCLE:

 Infective stage : sporozoite.
 Within less than an hour they enter the paranchyma of the liver, this is called Tissue
phase “liver”. In this phase the Primary Exo-erythrocytic cycle, Pre-erythocytic cycle
takes place.
 Primary E.E.C.: Sporozoite inside liver cell →trophozoites→nuclear division→
immature schizont→cytoplasmic division→ mature schizont →contian 1000s of
merozoites. no clinical manifestation produced , it takes 8 days in P. Vivax ,6 days in
P. falciparum.
 Fate of merozoites: 1-Phagocytized by kupffer cell. 2-Secondary exo-erythro. cycle
“para-erythro. Cycle: this is a 2nd E.E.C that happens for one more time only.
3-Dormant for indifinite time “hypnozoite” in P. vivax & oval only relapse.
4-Blood erythocytic cycle.
 Erythrocytic Cycle: Merozoite enter RBC ,cytoplasm of RBC ingested by the
parasite→Ring stage, As the trophozoite grows the ring enlarges with pseudopodia
in all direction →Amoeboid stage, After 24 hour vacuole disappears & nuclear
division started (12- 24nuclei) →Immature schizont, Then cytoplasmic division
→mature schizont with specific number of merozoites in each type.
 Hemozoin: end product of parasite´s digestion of the host’s Hb, is an insoluble
polymer of heme also called malaria pigment. appears from the ring stage and has a
toxic effect on the body & macrophage ,depressing their phagocytes activity
(responsible for symptoms of malaria).
 Then RBC rupture releazing merozoites+metabolic wastes including hemozoin.
Merozoites enter new RBC & repeat eryth. Cycle.

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 some merozoites when enter RBC become microgametocyte( male) or
macrogametocyte (female). Those gametocytes develop in internal organs(Spleen ,
BM) and appears in peripheralblood only when mature.
 Carrier: individual who harbor gametocytes in his peripheral blood.
 When female anopheline mosq. takes erythrocytes containing gametocytes the
sexual cycle begin : gametogony + sporogony.
 Gametogony: gametocytes develops into gametes.
Macro gametocyte→ one macrogamete, Microgametocyte→ 6-8 microgamete by
process called exflagellation. One micro gametes fertilize macrogamete →zygote
(mobile ookinete)in the gut of mosq.
 Sporogony : Ookinete penetrates the gut mucosa to outer side of the gut.
sporoblast divides rapidly to form thousands of sporozoites break out of oocyte
→salivary gland →next patient.

P.species P. Vivax (43%) P.Falciparum 50% P. Malariae P. Oval

7%
Benign tertian Malignant tertian, Quartan Mild tertian
Irregular fever spikes; 72-hour fever 48-hour fever
Disease malaria, 48-hour causes cerebral spikes; spikes
fever spikes malaria recrudescence
Persistent No persistent Persistent
hypnozoites No persistent stage stage; hypnozoites
Liver stage Relapse* Recrudescence Relapse
only young RBC Invade any RBC Only old Oval, jagged,
Cause multiple RBCs,low infected
Blood (reticulocyte) , infection with parasitemia. RBCs
smears infected RBC hyperparasitemia.
enlarge ,pale Bar and band
,with Peripheral blood forms;
Multiple ring forms rosette schizonts
schuffner’s And crescent-
dots . mature shaped gametes
schizont usually
contain 16
merozoits
Treatement Chloroquine Chloroquine Chloroquine Chloroquine
then primaquine resistance a problem then
primaquine

Notes about Plasmodium species:

 In P.vivax merozoite enter RBC through receptor which is the duffy blood group
protein Ag fy a ,fy b.Black people usually with no such Ag fy0 →resistant to
P.vivax.
 Multiple infection means more than one merozoite infect the same RBC.
Hyperparasitemia(heavy infection) means that large fraction (25%)of RBCs are
infected. Both are seen in P.falciparum.
 In P.falciparum trophozoite produce protein that are deposite in the eryth.
surface membrane in the deformation called knobs, these protein bind to
certain glyco-protein on the post capillary venular endothelium this binding
cause sequestration of the infected RBCs so stick to venular endothelium ,also
those RBCs stick to normal RBC →thrombosis.

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Parasitology 2017
 In P.falciparum amoeboid & schizont (8-32merozoites) ,not seen in the
peripheral blood but in the capillaries of the internal organ (spleen , B.M.)so only
ring stage and gametocyte are seen in blood smears.
 P.malaria can live in blood up to 50 years so important in blood transfusion
transmission.
Malaria pathogenesis :
-Due to two factors :
1-host response which produce chills & fever. 2-anemia.
-Severity depends on species of malaria ,most serious one is P. falciparum.
-RBC lyses→ hemozoin in circulation→ TNF →fever.
Causes of anemia in malaria :
1-RBCs destruction
2-Hemozoin cannot be utilized as an iron source → hypochromic microcytic anemia
3-Bone marrow suppression due to TNF toxcicity.
4- Hypersplenism causing destruction of normal and infected RBCs.
-Anemia may produce jaundice.
Febrile paroxysms :-
-Each paroxysm shows 3 stages
1-Cold stages: (last usually 1/2hr) Chill , felling of intense cold ,although temp. 40˚C
,shivering
2-Hot stages: (last 2-4hr) Fever , 40 -41˚C ,headache ,mild delirium
3-sweating stages: (last 2- 3 hr) Perspiration
-The total duration of febrile cycle ≈ 6-8 hr ,these paroxysms synchronies with the
eryth. Shizogony. so in tertian fever the paroxysms recurs every 48 hr ,while in
quarter malaria (P. malaria )recurs every 72hr.
in P. falciparum ,acute Massive lyses of RBCs ,high level of Hb & its products
→renal insufficiently & renal failure. Hb & it’s products in urine→ dark (black)
urine.
-This is called black water fever.
-Usually occur in patient who is taking inadequate or irregular treatment with
quinine drug→ autoimmune hemolytic anemia. Treated with steroids.
Relapse and Recrudescence:-
-Relapse is a return of clinical symptoms from liver stages (hypnozoites).it occurs in
p.vivax and p.ovale only. May occur at irregular intervals for up to 5 years.
Recrudescence is a reoccurrence of symptoms from low levels of organisms
remaining in red cells. Occurs in P. malariae.
-In P. falciparum, the patient is either cured from acute attack or death.
Immunity to malaria is specific ,strain & variant specific.
Genetic resistance to malaria:
1-Black people (Duffy blood group) natural resistance to P. vivax
2-Sickle cell anemia
favism abnormal Hb.
Thalassemia

Community
 Notes :
 High Risk population are Pregnant women and young children. when infected are
highly susceptible to development of severe and complicated malaria.
 Malaria in a pregnant woman increases the risk of maternal death, miscarriage,
stillbirth and neonatal death.

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Parasitology 2017
 Case-fatality Among untreated children and adults can reach 10%–40% or higher.
 The disease causes over 1 million deaths per year in the world, most of these in
young children in Africa.
 Mode of transmission:
1- Bite of an infective female Anopheles mosquito., sporozoite induced.
2- Injection or transfusion of infected blood, trophozoite induced.
3- Use of contaminated needles and syringes (e.g. injecting drug users).
4- Congenital transmission occurs rarely.
 Incubation period:
-The period between an infective bite and detection of the parasite in a thick blood
smear is the “prepatent period ”. it ranges from 8–12 days for P. vivax. and 6– 12 days
for P. falciparum.
 Period of communicability:
-Humans : infect mosquitoes as long as infective gametocytes are present in the blood;
this varies with parasite species and with response to therapy.
-Mosquitoes : remains infective for life.

 Insecticide-treated mosquito nets (ITNs) are the most universally useful measure for
the prevention of malaria.
 The most important factors that determine the survival of patients with falciparum
malaria are early diagnosis and immediate treatment.
 Malaria prophylaxis agent of choice is chloroquine +\- primaquine except in areas
where chloroquine resistant falciparum malaria is present( Mefloquine is used).

o Medicine
Signs and symptoms:
-The classic symptom of malaria is paroxysm: a cyclical occurrence of sudden coldness
followed by shivering and then fever and sweating, occurring every two days (tertian
fever) in P. vivax and P. ovale infections, and every three days (quartan fever) for P.
malariae.
-P. falciparum infection can cause recurrent fever every 36–48 hours, or a less
pronounced and almost continuous fever.
-The presentation may include headache, fever, shivering, joint pain, vomiting,
hemolytic anemia, jaundice, hemoglobin in the urine, retinal damage, and convulsions.
Complications:
 Renal failure is a feature of blackwater fever.
 Cerebral malaria in falciparum malaria.
 Enlarged spleen, enlarged liver.
 Respiratory distress(metabolic acidosis, noncardiogenic pulmonary oedema,
concomitant pneumonia, and severe anaemia)
 Spontaneous bleeding, coagulopathy, and shock
 Low blood sugar
 Malaria in pregnant women is an important cause of stillbirths, infant mortality,
abortion and low birth weight
Diagnosis:
-The blood film is the gold standard for malaria diagnosis.
-Blood film is of two types :
1-Thin: for species identification and degree of parasitemia.
2-Thick: quick diagnosis.
-Timing : Just before or at beginning of paroxysms.

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Parasitology 2017
-Other methods: PCR (most sensitive) ,Dip-stick method for detection of malarial Ag.

-Degree of suspicion might be elicited by any of the following:

recent travel history, splenomegaly, fever, anemia,thrombocytopenia, ↑bilirubin in
the blood combined with a normal level of white blood cells.
Treatment:
 Simple or uncomplicated malaria may be treated with oral medications.
 Recommended treatment for severe malaria is the intravenous use of
antimalarial drugs.
 The most effective treatment for P. falciparum infection is the use of
artemisinins in combination with other antimalarials (known as artemisinin-
combination therapy, or ACT)
 Other forms of malaria are treated with chloroquine with or without primaquine
(review the table).
 Severe and complicated malaria are medical emergencies since mortality rates
are high (10% to 50%)
 For severe malaria, parenteral artesunate was superior to quinine.

o Pharma
1- Chloroquine:
-Interfere with Formation of hemozin.
-Uses: P.vivax,P.ovale and P.malariae(blood form only)…drug of choice for prophylaxis in
malaria regions.
2- Primaquine:
-Uses: agent of choice in treating liver stage( hypnozoites).
-Side effects: Drug induced hemolytic Anemia in G6pd, Occasional methemoglobinemia.
-Contraindications: G6PDdeficiency, pregnancy.
3- Quinine:
-P.vivax and P. ovale, p.falciparum→ blood form (parentral and oral).
-Side effects: Hemolysis with G6PD deficiency, Positive Coombs test for hemolytic anemia,
-Cinchonism(A syndrome causing nausea, vomiting, tinnitus and vertigo is the major adverse
effect).
4-Pyrimethamine:
-Inhibitors of Folate synthesis.
-Blood-all forms, Chloroquine-resistant p.falciparum.
5- Mefloquine:
-Suppressing and curing infections caused by multi-drug resistant forms of P.falciparum.
6- Artemisinin:
-severe, multi-drug resistant P.falciparum malaria.It's the only drug reliably effective against
quinine resistant.

Prepared by :
Haitham N.Khalid
Baghdad medical school

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Parasitology 2017

Test yourself…..part2
A 44-year-old woman returns home to New York after a 2-week camera safari to East
Africa. She started chloroquine antimalarial prophylaxis 2 weeks prior to her
departure for Kenya and continued throughout her foreign travel. She stopped
taking the pills on her arrival home because they made her nauseated.
Two weeks after her return, she develops paroxysmal fever and diaphoresis and
is quickly hospitalized with febrile convulsions, jaundice, and anemia. Blood smears
reveal red blood cells multiply infected with delicate ring-like trophozoites
and rare sausage-shaped gametocytes.
1)Which of the following organisms is the most likely cause?
(A) Leishmania species
(B) Plasmodium falciparum
(C) Plasmodium malariae
(D) Plasmodium ovale
(E) Plasmodium vivax
2)The stage of the parasite life cycle that is responsible for the appearance of the
parasites 2 weeks after departure from the malarious area is the:
(A) hypnozoite
(B) sporozoite
(C) exoerythrocytic schizont
(D) erythrocytic schizont
(E) merozoite
3)The fever of malaria:
(a) can be tertian (occurring every 48 hours).
(b) can be quartan (occurring every 72 hours).
(c) occur with no pattern at all.
(d) a&b are correct.
(e) all of the above.
4) All of the following are recognized complications of her infection except:
(a) non cardiogenic pulmonary edema
(b)cerebral malaria
(c)black fever
(d)hypoglycemia
(e)spontaneous bleeding

Case scenario for question 5&6

A patient who has recently returned from the Ivory Coast presents with cyclical fever and
headache. He is found to have splenomegaly on examination. Following a blood film he is
diagnosed as having Plasmodium vivax malaria.
5.All of the following could be seen in a peripheral blood film from a p.vivax infected
patient except:
(a) infected RBCs are enlarged
(b)shcuffners dots
(c)fraction of infected RBCs is almost 5%
(d)mature schizont containing 16 merozoites
(e) gametocytes oval in shape

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Parasitology 2017
6.What is the benefit of the primaquine in vivax infection?
(a) Cover Plasmodium ovale in case of co-infection
(b)Reduce the risk of chloroquine-related retinopathy
(c)Reduce the incidence of chloroquine resistance
(d) Destroy liver hypnozoites and prevent relapse
(e)Prevent immature trophozoites forming gamatocytes
(7)All of the following statements is accurate in reference to diagnosis of malaria EXCEPT:
A. A thick smear is performed to increase sensitivity in comparison to a thin smear.
B. Careful analysis of the thin blood film allows for prognostication based on estimation of
parasitemia and morphology of the erythrocytes.
C. In the absence of rapid diagnostic information, empirical treatment for malaria should be
strongly considered.
D. Morphology on blood smear is the current criterion used to diferentiate the four species
of Plasmodium that infect humans.
E. the best timing for a blood smear sample is immediately after the end of a paroxysm.
(8)Recognized presentations of leishmaniasis include:
A. A papular lesion on the face
B. Large nonulcerating papules that resemble leprosy
C. Nasal mucosal involvement with recurrent epistaxis
D. Fever, marked splenomegaly, hepatomegaly, and cachexia
E. All of the above

A 3-year-old child from India is seen for evaluation of several weeks of fever that has
decreased in intensity, but he now has developed abdominal swelling.. Physical examination
shows palpable splenomegaly and hepatomegaly and difuse lymphadenopathy. Diffuse
hyperpigmentation is present in his skin. Visceral leishmaniasis is suspected.
(9)Which of the following diagnostic techniques is most commonly employed?
(A) Culture of peripheral blood for Leishmania
(B) PCR for Leishmania donovani nucleic acid in peripheral blood
(C) Rapid ELISA test for recombinant antigen rK39 from L. donovani
(D) Smear of stool for amastigotes
(E) Splenic aspiration to demonstrate amastigotes

Case scenario for question 10&11

A 35-year-old captain in the army reserves has been plagued by a painful, erosive lesion near
his ear lobe since his return from Operation Desert Storm several years ago. Punch biopsy of
lesion reveals macrophages distended with oval amastigotes.
(10)Regarding his illness :
(A) serological tests are recommended before biopsy
(B) only presents with painful lesions.
(C) since the lesion is present for several years, L.major is more likely than L.minor.
(D) biopsy speciemen is taken from periphery rather than center of lesion.
(E) high antibody titers develop but not protective.
(11)How was this infection acquired?
(A) Contact with contaminated drinking water
(B) Bite of Anopheles mosquito
(C) Bite of reduviid bug
(D) Fecal contamination of food
(E) Direct human contact in barracks
(F) Bite of sandfly
(G) Bite of tsetse fly

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Parasitology 2017
A 24-year-old man is admitted to the Emergency Department with breathing difficulties and
confusion three weeks after returning from a holiday in Cambodia. His partner says he has
had 'the flu' for the past two weeks. A blood film is positive for malarial parasites and a chest
x-ray and arterial blood gases suggest acute respiratory distress syndrome. A diagnosis of
severe falciparum malaria is suspected
13How would you treat him?
(A) Oral artesunate combination therapy
(B) Oral chloroquine
(C) IV artesunate
(D) IV mefloquine
(E) IV quinine

Prepared by :
Haitham N.Khalid
Baghdad medical school

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Parasitology 2017

 Cestodes
General characters:
 Are the tapeworms.
 Consist of 3 basic portions: the head or scolex; a “neck” section, which produces the
proglottids; and the segments or proglottids, which mature as they move away from
the scolex. (The combination of the neck and proglottids is called the strobila.)
 Are hermaphroditic, with each proglottid developing both male and female
reproductive organs, and mature eggs developing in the most distal proglottids.
 Adhere to the mucosa via the scolex, which has either suckers or a sucking groove.
 Have no gastrointestinal (GI) tract; they absorb nutrients from the host’s GI tract.
 Have for the most part complex life cycles involving an intermediate and final host
except H.nana.
 Extraintestinal larva mature in intermediate host and adults mature in final host
intestine.
Note : When humans are the intermediate host (with extraintestinal larva), these infections
are generally more serious than the intestinal infections with adult tapeworms.

 Taenia saginata

Final host Human

Intermediate host Cattle
Infective stage cysticercus bovis (larva form) in raw or
undercooked meat.
Habitat upper jejunum
Dx Eggs or proglottids in feces.
Rx praziquantel
Other notes -Also called beef tapeworm
- Has an unarmed scolex.
-Gravid segments with Median uterus with
15-30 lateral uterine branches

Disease:
-Taenia saginata (beef tapeworm), cause only intestinal infection.
-Mostly asymptomatic and usually produces little or no intestinal upset in human beings, but
knowledge of its presence, by noting segments in the faeces or on underclothing, may
distress the patient.
 Taenia solium

Final host Human

Intermediate host Swine, rarely: human.
Infective stage cysticercus cellulosae in undercooked pork,
rarely:egg is the infective stage
Habitat Upper jejunum
Dx Eggs or proglottids in feces.
Rx Praziquantel
Other notes -Also called pork tapeworm.
-Have an armed scolex.
- Gravid segments with Median uterus with
7-13 lateral uterine branches

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Parasitology 2017

Diseases:
-If human ingest the larva form then infection is intestinal and human is final host.
-Symptoms are like those in tenia saginata.
-If human ingest the egg by contamination of food or water or by autoinfection then
infection is systemic (Cysticercosis ) and man is an intermediate host.
-Cysticercosis : eggs → larva develop in brain,eye, heart, lung, etc.
-severity depend on •Location •Size •Number of larvae •Host immune response.
-Neurocysticercosis: larva in brain causing epilepsy,lesion in the brain,blindness ,tumor like
growths.

 Hymenolepis nana

Final host Human, Mice,Rats

Intermediate host Optional(can parasatize without an intermediate host), Fleas,
Beetles.
Infective stage 1- Eggs (if it eaten directly by Definitive host). 2-Cysticercoid larvae
from insects(I.H)
habitat Small intestine
Dx Eggs in feces.
Other notes -also called The Dwarf-Tape-Worm
- armed scolex
-eggs have polar filaments that lie between the eggshell and the
oncosphere.

Disease :
Most cases are asymptomatic, but with heavy infection there may be:
1- Abdominal pain, nausea, vomiting, diarrhea.
2- Nervous symptoms, including dizziness and irritability, can occur in children.

 Hymenolepis diminuta

Final host Rats & mice, human is an accidental

host.
Intermediate host fleas, beetles, cockroaches
Infective stage Cysticercoid larvae in body cavity of insect.
habitat In ileum of rats and mice, occasionally in
human.
Dx Eggs in stool.
Other notes - Rat tape worm
- eggs are yellowish brown in color

Differences between H.nana and H.diminuta eggs:

1- Eggs of H.diminuta are larger.
2- Eggs of H.diminuta have 2 polar thickening but no polar filaments.

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 Dipylidium caninum

Final host Dogs, Cats, Humans

Intermediate larva of dog fleas
host
Infective stage cysticercoid for F.H
Habitat Small intestine
Dx Examination of stool for characteristic segments and eggs capsule (less
common)
Other notes - Dog or cat tapeworm; double- pored dog tapeworm
-armed scolex
-segments diagnostic feature (pumpkin-seed shape) or vas shaped .
- demonstrate two genital pores(double- pored)
Disease :
-Dipylidiasis ,rare and normally restricted to young children. Light infections are
asymptomatic but can still cause abdominal pain, diarrhea, and anal itch in some individuals.

 Diphyllobothrium latum

Final host Man, Dog, cat, Fox

Intermediate host 1st I.H. : Fresh water crustacean
2nd I.H.: Fresh water fish
Infective stage 3rd stage larva→ Plerocercoid
larvae(Sparganum)in fish
habitat Small intestine
Dx Demonstation of egg (oprecululated egg )
Other notes - Fish tapeworm
- Scolex with a pair of suctorial grooves,
known as bothria
-proglottids: rosette shaped uterus; the
uterine pore is centrally located
- Eggs exhibit an operculum

Disease:
-Diphyllobothriasis: vague abdominal discomfort and loss of appetite, leading to weight loss.
Among some groups a vitamin B12 deficiency leading to various levels of pernicious anemia
may rarely develop.
-Sparganosis: is a parasitic infection happens when human harbors the plerocercoid larva.
-The infection is transmitted by ingestion of contaminated water, ingestion of a second
intermediate host such as a frog or snake.
-The plerocercoid larvae migrate to a subcuteneous location, where they typically develop
into a painful nodule . Migration to the brain results in cerebral sparganosis, while migration
to the eyes results in ocular sparganosis.

Prepared by :
Haitham N.Khalid
Baghdad medical school

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Parasitology 2017

 Echinococcus granulosus

-Definitive Hosts: dogs ,wolves.

-Intermediate Hosts: sheep, goats & Man(dead end host)
-Infective stage: eggs in the dog feces.
Life Cycle:
-Adult is in the small bowel of the definitive host(dog)→eggs in feces→ ingested by an
intermediate host (sheep,human)→ egg hatches in the small bowel and releases an
oncosphere→ penetrates the intestinal wall→ into circulation and into various
organs→cysts with protoscolices(the larva)→eaten by a definitive host →adult in intestine
again.
-Organs affected are : liver 70% ,lung 20%, others 10%.
Morphology:
 Small in length(one of smallest tapeworms).
 Has an armed scolex.
 The eggs of E. granulosus and Teania spp. are indistinguishable(spherical with
hexacanth embryo).

Primary hydatid cyst Secondary hydatid cyst

Developed from the ova Developed from protoscolex
Most common organs are liver and lungs Any anatomic site
Mostly (but not always) fertile Mostly afertile

Layers of hydatid cyst:

1- An outer pericyst(adventitia) derived from compressed host organ
tissues(defense Mech. From the body)
2- An intermediate hyaline ectocyst(laminated layer) which contain Dead cells→ is
non-infective.
3- An inner endocyst that is the germinal membrane (unicellular layer).
Contents of unilocular hydatid cyst:
-Cystic fluid, brood capsules, protoscolex, daughter cysts (hydatid sands)→Fertile cyst.
Note:
1-Non fertile cysts don’t have hydatid sands(daughter cysts and protoscolex)
2-Evaginated protoscolex are more infectious than invaginated.
Pathogenesis:
1-Localization with mechanical effects→ local and systemic effects.
2-Allergic reactions : due to absorption of parasitic antigens or rupture of cyst →may
cause anaphylaxis and shock.
Note: cyst rupture has two complications 1-immunological reactions 2-secondary
hydatid cysts.

o Surgery
Classification:
-Standardised ultrasound classification→ Three groups :
Group 1: Active group – cysts larger than 2 cm and often fertile.
Group 2: Transition group – cysts starting to degenerate and entering a transitional stage
because of host resistance or treatment, but may contain viable protoscolices.
Group 3: Inactive group – degenerated, partially or totally calcified cysts; unlikely to contain
viable protoscolices.

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Parasitology 2017
Spectrum of clinical presentation
1-Asymptomatic and discovered coincidentally.
2. Symptomatic disease presents with a swelling causing pressure effects.
a) A hepatic lesion causes dull pain from stretching of the liver capsule,
b) A pulmonary lesion, if large enough, causes dyspnoea.
c) Daughter cysts may communicate with the biliary tree causing obstructive jaundice
d) Features of raised intracranial pressure or unexplained headaches in a patient from a
sheep-rearing community should raise the suspicion of a cerebral hydatid cyst.
e) Present as an emergency with severe abdominal pain following minor trauma when the
CT scan may be diagnostic.
f) Present as an emergency with features of anaphylactic shock without any obvious cause
such patient may cough up white material that contains scolices.
Diagnosis
-There should be a high index of suspicion
 Investigations :
-Ultrasound and CT scan are the investigations of choice. X-ray can be used to visualize
calcified cysts.
-Raised eosinophil count; serological tests(Antigen B & Ag 5) such as ELISA are useful in
follow up after surgical or pharmacological treatment.
-Note: biopsies are forbidden.
Treatment
-Whether the patient is treated only medically or in combination with surgery will depend
upon a) The clinical group (which gives an idea as to its activity), b)The number of cysts and
their anatomical position.
1-An asymptomatic cyst which is inactive (group 3) may just be observed.
2-Albendazole (400 mg twice daily for 3 months) is the drug of choice.
3-After pharmacological therapy →Surgical treatment by minimal access therapy (PAIR –
puncture, aspiration, injection and reaspiration)
4-Radical total or partial pericystectomy with omentoplasty or hepatic segmentectomy
(especially if the lesion is in a peripheral part of the liver)
5-A laparoscopic approach to these procedures is being tried.

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 Trematodes
General Characteristics:
 Are commonly called flukes.
 Are leaf-shaped worms, which are generally flat and fleshy(unsegmented).
 Are hermaphroditic except for Schistosoma, which has separate male and female.
 Have complicated life cycles occurring in two or more hosts.
 Have operculated eggs (except for Schistosoma), which contaminate water,
perpetuating the life cycle, and which are also used to diagnose infections.
 The first intermediate hosts are snails.
 Head with out hook but with oral and ventral suckers.
 Body cavity is absent and Alimentery canal is incomplete.

 Fasciola hepatica

Final host Sheep,goat,cattle, and humans.

Intermediate host Snails(species of Lymnaea).
Infective stage Encysted metacercariae on raw aquatic vegetation
Habitat Bile duct of liver.
Dx Eggs in stool specimen
Other notes -The sheep liver fluke
-Oral and ventral sucker
-At the anterior end, distinct conical projection is observed

Life cycle:
-Eggs in stool→ embryonated in fresh water→hatch as miracidia →Lymnaeidae snail
→sporocysts →rediae→cercariae→encysted metacercariae on aquatic vegetation→ingested
by final host→penetrate intestine into peritoneal cavity→migrate to bile ducts→in 3-4
months develop into adults.
Disease :
-The triad of fever, hepatomegaly, and eosinophilia in endemic area suggests fascioliasis.
-Biliary obstruction→Acute epigastric pain, pruritus, and jaundice are common.
Fasciola hepatica Egg:
-Unembyonated. Thin egg shell. operculated. .Yellowish-brown in color. Oval in shape.
Diagnostic stage.

 Fasciolopsis buski

Final host Mainly human

Intermediate host Fresh water snails(genus Segmentina)
Infective stage Encysted metacercariae on vegetations
Habitat Lumen of small intestine(especially
duodenum of man and pig).
Dx Eggs in stool specimen
Other notes - Giant intestinal fluke of man.
- lack of cephalic cone or "shoulders" and the
unbranched ceca
- pigs are the reservoir host.

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Parasitology 2017

Clinical features:
-In Fasciolopiasis ,most infections are light and asymptomatic. In heavier infections,
symptoms include diarrhea, abdominal pain, fever, ascites, and intestinal obstruction.
-The eggs are indistinguishable from those of Fasciola hepatica.

 Paragonimus westermani

Final host Human, also other mammals.

Intermediate host 1st I.H. Water snail(Oncomelana)
2nd I.H. Crustaceans ,Crabs
Infective stage Encysted metacercariae
Habitat Encapsulated in Lungs
Dx Eggs in sputum or feces
Other notes - The oriental Lung Fluke
- The oral and ventral suckers are similar in
size

Life cycle:
-Eggs in sputum → Two weeks later, miracidia develop in the egg and hatches→penetrate
the 1st I.H. Water snail(Oncomelana)→sporocyst→rediae→cercariae →penetrate fresh
water crabs and encyst in its muscles becoming metacercaria→ingested→the metacercaria
excysts and penetrates the gut, diaphragm and lung where it becomes an adult worm in
pairs.
Disease:
-Paragonimiasis is associated with granuloma formation. Chronic cough , difficulties
breathing , sputum with blood.
-When moves to brain, can cause blindness, paralysis , disequilibrium , epilepsy.
-Dx: eggs and serology.
-Eggs: Large, thick, dark shell. Prominent operculum at the broad end. Thick posterior
end.Unembryonated. Yellowish in color.

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 Schistosomes

Features of schistosomes that differ from other trematodes:

-Have separated sexes
-Adults live in blood vascular system, so called blood flukes.
-non-operculated eggs (eggs with spine)
-Have forked tailed cercariae
-Infect human by penetration of skin by cercariae.
-No redia formation

Life cycle :
Cercariae penetrates the skin→ schistosomulae→ travel to the lungs and stay 3-8 days→
Migrate to liver portal system where maturation into adult males and females occurs→
male and female pair up in liver→ migrate into favoured sites→ Females release eggs which
are 50% trapped in tissues and 50% excreted.

S. haematobium S. mansoni S. japonicum

Habitat vesical plexus of inferior mesenteric superior mesenteric
urinary bladder vein vein
Spine of ova terminal spine lateral spine short lateral spine
(rudimentary)
Disease Bilharziasis (urinary Intestinal Intestinal
schistosomiasis) schistosomiasis schistosomiasis
Ova excretion in urine, less in stool, rarely in in stool
frequenitly in stool urine
Geographical Africa and portion of in Africa esp. Egypt limited to the Far
location Middle East, East
including Iraq

Pathogenesis:
The pathogenesis is mainly related to egg deposition and liberation of antigens of adult
worms and eggs. enzyme elaborated by eggs helps to digest the overlying tissue and
together with necrosis of the tissue caused by pressure and the effect of the spine, works to
liberate the egg from the tissues into the lumen of the intestine or bladder.
The major pathogenic lesion is the granulomatous response observed around eggs trapped
in the tissue, this may complete heal or may progress to fibrosis and scar formation.
During late stage of chronic infection, fibroblasts replace the granulomas leading to fibrosis.

Medicine
Clinical manifestations:
1-swimmer’s itch: itching lasting 1–2 days at the site of cercarial penetration caused by a
hypersensitivity reaction to schistosomal antigens.
Note: swimmer’s itch is caused by species of schistosoma that ordinary infects birds,
semiaquatics mammals but not the human species.
2-acute Infection (Katayama syndrome): allergic manifestations such as urticaria, fever,
muscle aches, abdominal pain, headaches, cough and sweating. These are caused by
hypersensitivity reaction toward antigens released from eggs.
O/E: hepatomegaly, splenomegaly, lymphadenopathy and pneumonia may be present.

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Acute infection manifests After a symptom-free period of 3–5 weeks.
Rx: resolve without any treatment within 4-6 weeks.

3- Chronic Infection:
 In Schistosoma haematobium
The severity of S. haematobium infection varies greatly, and many with a light infection are
asymptomatic. Painless terminal haematuria is usually the first and most common
symptom. Frequency then follows due to bladder neck obstruction.
Complications : frequent urinary tract infections, bladder or ureteric stone formation,
hydronephrosis, and ultimately renal failure with a contracted calcified bladder.
squamous cell carcinoma of bladderis associated with long-term urinary schistosomiasis.
 In Schistosoma mansoni
Characteristic symptoms begin 2 months or more after infection. They may be slight, no
more than malaise, or consist of abdominal pain and frequent stools which contain blood-
stained mucus(dysenteric type of manifestation).
Complications: fibrosis with thickening of bowel wall, Intestinal Polyps, portal hypertension
which leads to massive splenomegaly, fatal haematemesis from oesophageal varices, or
progressive ascites.
Diagnosis :
In S.hematobium, the eggs can be found by microscopic examination of the centrifuged
deposit of terminal stream urine.
In S. mansoni or S. japonicum, the characteristic egg with its lateral spine can usually be
found in the stool.
Other investigations:
Eosinophilia, ELISA as screening tests, dipstick urine testing shows blood and albumin in
S.hematobium, Ultrasound is useful for assessing the urinary tract, rectal biopsy can be
examined in light S. mansoni infection.
Management:
Praziquantel is the drug of choice for all forms of schistosomiasis.
Praziquantel therapy in early infection reverses pathologies such as hepatomegaly and
bladder wall thickening and granulomas.

Prepared by :
Haitham N.Khalid
Baghdad medical school

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 Nematodes
 Are the roundworms
 Have round unsegmented bodies
 Are transmitted by:
– Ingestion of eggs (Enterobius, Ascaris, or Trichuris);
– Direct invasion of skin by larval forms (Necator, Ancylostoma)
 Separated sexes.
 Tubular digestive systems with openings at both ends.

 Ascaris lumbricoides

Life cycle:
-Begins by ingesting worm eggs in food or water contaminated with human feces→ hatch in
small intestine →larva migrate through gut wall into bloodstream→lungs →bronchi
→swallowed again into the GI tract→Within the small intestine, they become adults→eggs
into feces→become embryonated in warm,moist conditions.

-Note: Adults are the largest intestinal nematodes and derive their sustenance from
ingested food.
Pathogenesis
-The major damage occurs during larval migration rather than from the presence of the
adult worm in the intestine.
-Larva: in lungs inflammation with an eosinophilic exudate occurs in response to larval
antigens.
-Adults: a heavy worm burden may contribute to malnutrition, sometimes also bowel
obstruction.
o Medicine
Clinical findings :
 Tissue migration can provoke both local and general hypersensitivity reactions,
with pneumonitis, eosinophilic granulomas, bronchial asthma and urticaria.
 Intestinal ascariasis causes symptoms ranging from occasional vague abdominal
pain through to malnutrition
 It causes up to 35% of all intestinal obstructions in tropical and subtropical
areas,most commonly in the terminal ileum.
 Obstruction can be complicated further by intussusception, volvulus,
haemorrhagic infarction and perforation.
Diagnosis :
 The diagnosis is made microscopically by finding ova in the feces(oval with an
irregular surface).
 Adult worms are frequently expelled rectally or orally
 There is eosinophilia
Management
-A single dose of albendazole (mebendazole,ivermectin,pyrantel pamoate are also effective).
-Patients should be warned that they might expel numerous whole, large worms.
-Obstruction should be treated with nasogastric suction, piperazine and intravenous fluids.

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 Ancylostoma duodenale&Necator americanus
Life cycle:
Filariform larvae in moist soil penetrate the skin→bloodstream and into lungs→bronchi and
trachea then swallowed→adults in the small intestine→eggs in feces→ rhabditiform
(feeding, non infectious) larva→ third stage filariform infectious larva.
Pathogenesis
 Adults attach to the wall with either cutting plates (Necator) or teeth
(Ancylostoma),they feed on blood from the capillaries of the intestinal villi→loss of
blood.
 Ground itch: a pruritic papule or vesicle, can occur at the site of entry of the larvae
into the skin.
 Pneumonia with eosinophilia can be seen during larval migration through the lungs.
o Medicine
Clinical features (hookworm infection)
 Adults: vomiting and epigastric pain resembling peptic ulcer disease may occur.
Sometimes, frequent loose stools are passed. Anaemia with high-output cardiac
failure may result. The mental and physical development of children may be
retarded in severe infection
 An allergic dermatitis, usually on the feet (ground itch).
 Paroxysmal cough with bloodstained sputum, associated with patchy pulmonary
consolidation and eosinophilia
Diagnosis
 By finding eggs in the stools
 Occult blood is positive, blood eosiophilia.
Management
 Single dose of albendazole is the treatment of choice.
 Oral iron for anaemia and associated heart failure.

 Enterobius vermicularis
Life cycle:
-Eggs are ingested (via person-to-person or autoinfection) →larva in small intestine→adults
in colon→mating→females migrate nocturnally to perianal area to lay eggs .
-Note: all of those are methods for infection.
-Cross infection: person to person infection(clothes,baths…etc)
-Autoinfection: the person infects himself (finger to mouth)
-Retroinfection: Newly hatched larvae migrate back into the anus.
Pathogenesis
-Migration of female pinworms to the anus to lay eggs with insertion of the tail pin into the
mucosa →perianal itching.
-Scratching →excoriate the skin and lead to secondary bacterial infections.
o Medicine
Clinical features
-Pinworm infection affects mainly children,1/3 of those infected are asymptomatic, most
commonly presents with intense itching, especially at night. In females, the genitalia may be
involved. The adult worms may be seen moving on the buttocks or in the stool.
Diagnosis
-Via “Scotch tape” test, where a clear adhesive cellulose tape is applied to the anal area
early in the morning before bathing or defecation for detection of ova.
-Eggs are oval and flattened on one side .Colorless and transparent, thick and asymmetric
shell, content is a larva.

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Management
-A single dose of mebendazole.
-If infection recurs in a family, each member should be treated. During this period all
nightclothes and bed linen are laundered. Fingernails must be kept short and hands washed
carefully before meals.

 Trichuris trichura
Life cycle:
-Infective eggs are ingested and hatch in the human small intestine→larvae penetrate the
villi and continue to develop in the small intestine→young worms move to the cecum and
penetrate the mucosa and there they complete development→eggs in stools into soil
→within two to three weeks they become embryonated(infective).
Morphology
Narrow anterior esophageal end and shorter and thicker posterior anus→it looks like a
whip.
Pathogenesis
They attach to the host through their slender anterior end and feed on tissue secretions
instead of blood. Mechanical damage to the mucosa may occur as well as toxic or
inflammatory damage to the intestines of the host.
Clinical features (whipworm infection)
-Light infestations are frequently asymptomatic. Heavy infestations may have :
 Bloody diarrhea→ iron-deficiency anemia.
 Rectal prolapsed
 Vitamin A deficiency
Diagnosis
Eggs are detected in stool examination(barrel-shaped and unembryonated, having bipolar
plugs and a smooth shell)
Treatment
Mebendazole or albendazole. Iron and vitamin A if there is deficiency in any of them.
Surgical treatment of rectal prolapse.

Prepared by :
Haitham N.Khalid
Baghdad medical school

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Parasitology 2017

Test yourself…..part 3
A 3-year-old girl presents to her pediatrician with intense perianal itching. Her mother
explains that the child has also been extremely irritable during the day and has not been
sleeping well at night. Eggs with a flattened side were identified by the laboratory
technician.
1-Infection with which of the following organisms is most likely?
A. Ascaris lumbricoides
B.Echinococcus granulosus
C.Entamoeba histolytica
D. Enterobius vermicularis
E. Trichuris trichiura
2-Regarding her clinical condition, all of the following are true except:
A. can be treated with a single dose of mebendazole.
B. diagnosed by finding eggs in stools.
C. genitalia can be involved.
D. caused by a nematode
E. can be complicated by secondary bacterial infection.
3-A 12-year-old girl from Guatemala was brought to the emergency room with a
prolapsed rectum. Examination of the rectum reveals small worms that resemble
whips attached to the mucosa. A stool sample reveals eggs that are barrel
shaped, with bipolar plugs. Which of the following is the most likely cause?
A. Ascaris lumbricoides
B. Echinococcus granulosus
C. Entamoeba histolytica
D. Enterobius vermicularis
E. Trichuris trichiura
4-All of the following are clinical manifestations of Ascaris lumbricoides infection EXCEPT:
A. Asymptomatic carriage
B. Fever, headache, photophobia, nuchal rigidity, and eosinophilia
C. Nonproductive cough and pleurisy with eosinophilia
D. Right lower quadrant pain
E. Small bowel obstruction

A 44-year-old woman presents to the emergency department with recurrent episodes of

right upper quadrant pain, On examination, she is jaundiced and in obvious discomfort due
to right upper quadrant pain. She is afebrile and tachycardic. Her physical examination is
notable for an enlarged liver. Ultrasound examination confirms the large liver and
demonstrates a complex 14-cm cyst with daughter cysts extending to the liver edge with
associated biliary tract dilation.
5-Which of the following is the most appropriate management
approach to this patient?
A. Albendazole medical therapy
B. Albendazole followed by surgical resection
C. Needle biopsy of the cystic lesion
D. PAIR (percutaneous aspiration, infusion of scolicidal agent, and reaspiration)
E. Serologic testing for Echinococcus granulosus
Case scenario for questions 6-9
A 24-year-old student returns from a gap year in Malawi complaining of visible haematuria,
dysuria and urinary frequency. She says she felt well throughout her trip but experienced an
itchy rash on her legs a few hours after swimming in Lake Malawi which has now resolved.

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6- What was the most likely means by which this girl was infected ‫؟‬
A) Ingestion of ova
B) Ingestion of larvae
C) Ingestion of cysts in muscle
D) Skin penetration by larvae
E) Mosquito transmission of sporozoites
7-the pathology of her disease is mainly due :
A)worms multiplying in the host
B)worms migrating in the mesenteric venules
C)dying worms eliciting host immune responses
D)egg deposition
E)immune mediated attack to the adult worms
8-How would you treat her?
A) Albendazole
B) Trimethoprim
C) Prednisolone
D) Doxycycline
E) Praziquantel
9-her Infection is most strongly associated with:
A)Transitional cell bladder cancer
B)Lung cancer
C)esophageal varices
D)Vulval carcinoma
E) Squamous cell bladder cancer

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