CHAPTER SIX

HEMOPARASITES
 MALARIA
Definition:
• Malaria is an acute infection of the blood caused
by protozoa of the genus plasmodium.

Infectious agent:
• Plasmodium falciparum

• Plasmodium vivax

• Plasmodium ovalae

• Plasmodium malarial
 Cont…

• Plasmodium falciparum:
– Malignant tertian: invades all ages of RBC.
– RBC cycle is 48 hrs.
• Plasmodium vivax:
– Benign tertian: invades reticulocytes only.
– RBC cycle is 48 hrs
• Plasmodium ovalae:
– Tertian: invades reticulocytes only.
– RBC cycle is 48hrs
• Plasmodium malariae:
– Quartan malaria: invades reticulocytes only.
– RBC cycle is 72 hrs.
 Occurrence:
• Endemic in tropical and subtropical countries of
the world. Affects 40% of the word population.

• Children less than 5 years of age, pregnant women

and travellers to endemic areas are risk groups.

• P. falciparum 60% and p. vivax 40% are common

in Ethiopia.

• Socio-economic factors like immigration, war,

poverty, ignorance, agricultural irrigation farms
are among the predisposing factors.
 Co..nt
Reservoir:
• Humans

Mode of transmission
• By the bite of an infective female anopheles
mosquito which sucks blood for egg maturation.
• Blood transfusion.
• Hypodermic needles.
• Organ transplantation and
• Mother to fetus transmission is possible.
 Life cycle
• Asexual phase in humans and sexual phase in mosquito.
• Bite of infected mosquito introduces asexual forms of the
parasite called sporozoites  enter the liver cells and form
the schizonts  undergo maturation and multiplication.
• Rupture liver cells and release merozoites into the blood 
enter and multiply in the erythrocytes /RBCs/  ring forms
and then develop into trophoizoites and rupture of
erythrocytes releases the merozoites and antigenic +
pyrogenic substances.
• Again infect new RBCs resulting in repeated cycle of RBC
hemolysis & paroxysms of malarial fever
 Life cycle
• Some Sporozoites convert to dormant forms
called hypnozoites which can cause relapse
months or years later (p. vivax and p. ovale).

• Some merozoites in the RBCs differentiate into

the sexual forms called male and female
gametocytes.
• Taken by the mosquito and completes the
sexual phase of the life cycle and develops to
Sporozoites (the infective stages).
 Pathogenesis
1. Fever due to the release of pyrogenic substances during rupture of
RBCs.
2. Anemia due to:
 Hemolysis
 Dyserythropoiesis
 Sequestration of erythrocytes in the microvasculature of the
spleen &
 Bone marrow suppression
3. Immune-pathologic events
 Hyper-gamma-globulinemia
 Immune complex formation
 Release of cytokines
4. Tissue anoxia due to cyto-adherence of infected RBCs.
 Incubation period
Varies with species:
• P. falciparum:-7-14days
• P. vivax: -8-14 days
• P. Ovalae:-8-14 days
• P. Malariae: -7 -30 days
 Period of communicability

• Mosquitoes are infective as long as

infective gametocytes are present in the
blood of patients.

• Once infected, mosquito remains

infective for life
 Susceptibility and resistance
• Susceptibility is universal except in some host –resistance factors.
Non specific factors
• Increased splenic clearance reaction.
• Hyperpyrexia-which is said to be schizonticidal.
• Sickle cell traits are resistant to P. falciparum.
• Duffy blood group deficiency (Duffy antigen negative RBC) lack
receptor for P.vivax.
• Because of passive immunity infants are resistant in early life.
Specific factors:
• This is a humoral and cell mediated immunity that is species and
strain specific, and hard-won after repeated infection.
 Clinical Manifestations:
• Chills and rigor

• Fever and headache

• Abdominal pain and diarrhoea

• Hallucinations

• Renal or respiratory symptoms and jaundice.

 Diagnosis:
• Based clinical manifestations and epidemiological
grounds.

• Blood film for hemo-parasites.

• White blood cell count.

• Blood culture to rule out species.

• Chest x-ray to rule out pneumonia.

• RDT (Rapid Diagnostic Test)

 Treatment:

Management of uncomplicated P.
falciparum malaria:
• For non-pregnant mothers, Adults, and
children >5kg:
– Artemether-Lumefantrine 4 tabs PO BID for 3
days.

• For pregnant mothers and children <5kg

– Quinine 600mg PO TID for 7 days.
 Treatment:
Management of severe (Complicated) P.
falciparum malaria:
• Quinine loading dose 20mg/kg in 500cc DNS or
DW to run over 4hrs, 5hrs interval of rest then
maintenance dose 10mg/kg in 500cc DW to run
over 4hrly until the patient can take orally i.e. at
least for the 1st 48 hrs.
• Give IV glucose 40% (IV push or in the bag)
simultaneously with quinine.
• Then quinine PO or Coartem for the remaining
period of treatment.
 Treatment..
Management of other forms of
malaria:
• Chloroquine 4,4,2 po daily for 3 days
followed by Primaquine 15mg daily for
14 days for P. vivax.
 Complications:
• Cerebral malaria- un-arousable coma caused with
falciparum malaria.
• Anaemia: - Hg<5g/dl due to acute destruction of RBC
and spontaneous bleeding.
• Renal failure due to:
– Low blood pressure or shock
– Parasite sequestration to micro circulation of the kidney
– Acute tubular necrosis
• Hypoglycemia (BGL<40g/de)
• Fluid, electrolyte and acid- base disturbances – due to
– Dehydration and
– Oxygen shortage in tissues-leads to metabolic
acidosis.
 Complications:
• Pulmonary edema - due to
– Cardiac problem (CHF)
– Excess fluid replacement especially when there is renal failure.
• Management Pulmonary edema:
– M - Morphine /pet dine)
– O - Oxygen
– I - Infusion
– S - Sitting position
– T - Tourniquet
– D - Digoxin
– A – Aminophiline
– M – Manitol /lasix
– P – phlebotomy
 Complications:
• Circulatory collapse leading to shock (algid
malaria): - When systolic BP<80 mmHg due to
dehydration and systemic infection.
• Spontaneous bleeding and disseminated intra-
vascular coagulopathy due to thrombocytopenia.
• Hyper pyrexia (Temperature axillary >40oC Rectal
>42 oC)
• Hyper parasitemia: - Parasite load or density above
5% or >5+
• Malarial haemoglobinuria
 Prevention and control
• Chemo prophylaxis for travellers to
endemic areas.

• Vector control.
– Avoiding mosquito breeding sites.
– DDT spray or other chemicals.
– Personal protection against mosquito bite (use
of bed net)

• Chemo therapy of cases.

 QUIZ
1. Clearly describe the life cycle of Ascariasis??

2. Describe the Functions of `HIV Enzymes??

3. Discuss the similarities and differences of

Amebiasis and Gardiasis??

4. The Hallmark of Trichriasis and Enterobiasis??

 TRYPANOSOMIASIS (sleeping sickness)
Definition:
• It is a disease caused by protozoan hemo-
flagelletes.
• Transmitted to human, cattle and wild animals by
the Glossina fly or Tsetse fly.
Characterized by:
– Chronic fever

– Generalized weakness

– Cerebral involvement and death

 Epidemiology:
Two trypanosome species infect human:
1. Trypanosoma brucei gambience (Tbg):
– Cause chronic slowly progressing sleeping sickness.

– Reservoir: Pigs, dogs and antelopes.

– Found in western and central Africa.

– Transmission occur at river crossings and water

holes

– Vector: Glossina palpilis

 Epidemiology:
2. Trypanosoma brucei rhodesience (Tbr):
– Cause acute rapidly progressing sleeping
sickness.
– Reservoir: Antelope and pigs.
– Found in Eastern Africa, especially
Uganda.
– Transmission occur by crossings the bush
lands
– Vector: Glossina mortalis
 Cont…

MOT:
• Bite of Tsetse fly or Glossina fly:
– That is infected with trypanosomes when they
take blood meal from an infected persons or
animals.

– Transmit it to others when it bites another

susceptible host.
 Clinical pictures:
• Both species have similar clinical features except
their IP:
• Has three stages:
1. Primary (chancre) Stage:
– Commonly seen in Tbr.

– Painful indurated erythematous nodes at the

site of bite.

– Occur in 70% of cases in Europe.

 Clinical pictures:
2. Systemic Illness (Blood) stage: trypanosome
disseminates to blood, lymph nodes and lymph
– Intermittent fever for days or weeks.
– Debilitation (weakness)
– Anemia
– Lymphadenopathy [supraclavicular and posterior cervical]
which is called Winter-bottom’s sign
– Splenomegaly
– Pruritic rash
– Anorexia and weight loss
– Pitting edema of face and lower legs
– Impotence and menstrual irregularity
 Clinical pictures:
3. Cerebral (Sleeping sickness) stage:
• Terminal stage of invasion of the brain.
• Lasts 2 years for Tbg and few months for Tbr.
– Mental deterioration
– Convulsion
– Hemiplegia and facial palsy
– Weakness
– Sleeping during the day and restless at night
– Coma and death
 Diagnosis:
• Microscopic exam of chancre fluid for live organism.
• Wet blood smear and visualize
• Thick blood smears to visualized large population of
organism.
• CBCs reveals:
– Anemia
– Thrombocytopenia
– Raised ESR
– Increased monocytes
• Serologic test: - increased IgM both in blood and CSF
• Lymph node aspiration
• CSF analysis
 Differential Diagnosis:
1. Due to fever:
• Malaria
• Relapsing fever
• Typhoid fever

2. Due to debilitation and weakness:

• Meninigitis
• Leukemia
• Psychosis
• Hook worm infection
 Treatment:
Strict observation is important due to drug
toxicity:
• In Tbg:
– If CSF is normal = Suramin
– If CSF is abnormal = Suramin + Melarsoprol

• In Tbr:
– If CSF is normal = Suramin
– If CSF is altered = Suramin + Melarsoprol
 Prevention and control:

• Early detection and treatment of cases.

• Vector control:
– Bush clearing
– Use of insecticide
– Baited flytraps
– Establishment of settlements by turning bush
lands to agricultural lands.
 LYMPHATIC FILARIASIS
(elephentiasis)
Definition:
• A disease caused by the number of worms that
normally found in the lymphatic system of
infected person.

Infectious agent:
• Wucheriria Bancrofti (vectors are culex,
Anopheles and Aedes species)
• Brugia malayi (vector is mansionia species)
• Brugia timori (vector is anopheles)
 Cont…
Occurrence:
• Widely prevalent in tropical and subtropical areas of
Africa, Asia, Pacific region, Central and South America.
• It is found in Gambella region (western Ethiopia)
Reservoir:
• Humans are definitive hosts.
Mode of transmission:
• By bite of mosquito harbouring infective larvae.
Incubation period:
• One month
 Cont…
Period of communicability:
• Humans may infect mosquitoes when microfilariae are
present in the peripheral blood; (for 5-10 year or longer
after initial infection).
• The mosquito becomes infective about 12-14 days after
an infective blood meal.

Susceptibility and resistance:

• Universal.
• Repeated infections occur in endemic regions and lead to
the severe manifestations such as elephantiasis.
 Life cycle
• An infected mosquito bites and introduces third-stage
filarial larvae onto the skin of the human host (during a
blood meal).
• The larvae develop into adults (reside in the lymphatics)
• The adults produce microfilariae (sheathed and have
nocturnal periodicity).
• The microfilariae migrate into lymph and enter the blood
stream reaching the peripheral blood.
• A mosquito ingests the microfilariae during a blood meal.
• After ingestion, the microfilariae develop in to larvae and can
infect another human when the mosquito takes a blood.
 Clinical manifestation:

• The presence of worms in the lymph vessels

gives rise to a foreign-body reaction.

• After the death of the worm, more proteins

are released and make the reaction even
more severe.

• Three phases may be distinguished.

 Clinical manifestation:

1. Acute phase:
• Starts with in a few months after infection
• It is mainly due to a hypersensitivity
reaction:
– Lymphadenopathy
– Fever
– Eosinophilia
– In this stage microfilariae are not
demonstrable in the peripheral blood b/c the
worms are not yet mature.
 Clinical manifestation:

2. Sub acute phase

• This occurs after about one year following acute
phases.
• In this phase worms have matured and
microfilariae are present in the peripheral blood:
• Reactions to the adult worms cause:
– Attacks of fever
– Lymphangitis
– Epididymitis
– Recurrent attacks - lead to hydrocele.
 Clinical manifestation:

3. Chronic phase:
• Repeated attacks result in lymphatic
obstruction and cause lymphedema.
– Lymphedema in the legs or scrotum =
elephantiasis
– Later elephantiasis of vulva and hands etc.
– Since the adult worms have usually died,
microfilariae are not seen in the blood.
 Diagnosis:
• Clinical and epidemiological grounds
• Obstructive signs with history and travel to and residence
in endemic areas.
• Blood film to identifying microfilaria in the peripheral
blood.
– Microfilarial appears in the peripheral blood during the
night (nocturnal) in most parts of the world and during
day (diurnal) in the south pacific region.
– Single dose of diethylcarbamazin citrate (DEC)
causes the sequestered microfilaria to emerge to blood
45-60 minutes later. This test is said to be the Mazoti
Test.
 Treatment:
1. DEC (diethylcarbamazin citrate):
• Results in rapid disappearance of most
microfilaria from blood but may not destroy the
adult worm.
• Because of this we need to repeat DEC annually
for some years.
• Dosage (DEC) (Hetrazan):
– Day 1 – 50mg
– Day 2 – 50 mg Po TID
– Day 3 – 100 mg Po TID
– Day 4-14-2mg/kg Po TID
 Treatment:
2. Ivermectin (Mectizan) 150-200 mcg/kg/d PO as
single dose; repeat every 2-3months.

3. Surgical treatment of hydrocele.

Prevention and control:

• Reducing the vector population.
• Mass and selective treatment.
• Personal protection against mosquito bite.
 SCHISTOSOMIASIS
Definition:
• It is a trematode infection with adult worms living within
mesenteric or vesicle veins.
Infectious agent:
• The major schistoma species are:
– Schistosoma mansoni
– Schistosoma hematobium
– Schistosoma japonicum
• Others in limited areas are:
– S. mekongi
– S. intercalatum
– S. malayesis
– S. mattheei
 Snail vectors are:
• Bulinus-S. hematobium

• Biomphalaria-S. mansoni

• Onchomelania-S. japonicum
 Epidemiology:
• S. mansoni is found in South America, Caribbean Islands, Africa
and the Middle East.

• S. hematobium is found in Africa and the Middle East.

• S. Japonicum is found in the Far East.

• The disease occurs worldwide and 2 million people are expected to

be infected.

• However, most infected individuals show few or no signs and

symptoms, and only a small minority develop significant disease.
 Cont…
Reservoir:
• S. mansoni, S. hematobium and S. intercalatum -
man.

• S. japonicum - dog, cat, pig, cattle, water buffalo,

horse and wild rodents

Mode of transmission:
• Infection is acquired from water containing
free-swimming larval forms (cercariae) that
have developed in snails.
 Cont…
Incubation period:
• Acute systemic manifestations (katayama fever) may
occur in primary infections 2-6 weeks after exposure.
• The infection in humans can persist up to 10 years.
• Snails release cercariae as long as they live (from several
weeks to 3 months).

Susceptibility and resistance:

• Susceptibility is universal.
• Resistance is poorly defined.
Life cycle:

Cercaria
penetration
Enter snail Migrate to
becomes Lungs and
cercaria liver

Pass in feces Becomes

 hatch to
miracidia adult fluke

Burrow wall Migrate to

and enter the Mesentric
lumen plexus
Lay eggs
 Clinical Manifestation
The stages of schistosomiasis are:
A. Invasion stage
B. Maturation stage
C. Established infection and
D. Late stage
 Clinical Manifestation
A. Invasion stage:
– It is when cercariae penetrate skin:

– Cercarial dermatitis with itching papules

and local edema

– Cercariae remain in skin for 5 days before

they enter the lymphatic system and reach
the liver.
 Clinical Manifestation
B. Maturation Stage:
– It is the stage during which schistosoma mature
in the liver:
• Fever
• Eosinophilia
• Abdominal pain
• Transient generalized urticaria (known as katayama
syndrome)
– This stage may be diagnosed as clinical
malaria or may pass unnoticed.
 Clinical Manifestation
C. Established infection Stage:
– This is a stage of egg production and eggs
reach to the lumen of bladder and bowel.
– Some eggs penetrate the tissue; reach the
bladder and intestinal wall are discharged with
urine and feces.
– Eggs that could not penetrate the tissue are
carried with blood to the liver and lungs.
– Other eggs that fail to reach the lumen of the
bladder or bowel provoke an inflammatory
reaction resulting in:
 Clinical Manifestation
–In S. mansoni infection:
• Bloody diarrhea

• Abdominal cramps

–In S. hematobium infection.

• Terminal haematuria

• Dysuria
 Clinical Manifestation
D. Late stage:
– This is the stage of fibrosis which occurs where there are eggs
in the tissues around the bladder this may result in:
• Stricture of urethra leading to urine retention or fistula.
• Dilatation of ureters (hydroureter) and kidney
(hydronephrosis) possibly leading to kidney failure
• Calcification of bladder.
– In the liver portal hypertension leads to:
• Hypersplenism and anemia
• Esophageal varices and bleeding.
– In the lungs fibrosis results in pulmonary hypertension which
leads to congestive cardiac failure.
 Cont…

Diagnosis:
• Demonstration of ova in urine or feces
• Biopsy of urine and feces are repeatedly negative
(liver biopsy, bladder biopsy).

Treatment:
• Praziquantel and oxamniquine are the drugs of
choice
• But in Africa praziquantel is best because of
resistance strain of oxamniquine.
 Prevention and control:
• Treatment of cases.
• Intermittent irrigation.
• Drainage of water bodies.
• Clearing of vegetation in water bodies to deprive snails of
food and resting place.
• Flooding.
• Educating the public about the mode of transmission and
ways of prevention.
• Proper disposal of human faeces and urine.
• Avoid swimming in water bodies known to have the
infection.
• Use rubber boots to prevent exposure to contaminated
water.
Thank you!!!