Microbiology and Parasitology

1. Major bacteria infecting the Hematology System

• Bartonella Henselae (Cat scratch disease)
2. Major parasites infecting the Hematologic
System
• Plasmodium species: Malaria
• Babesia species: Babesiosis
3. Major viruses infecting the Hematologic System
• HIV
• Parvovirus B19: aplastic anemia
 Cat Scratch Disease
• Cat scratch disease involves fever for a few days,
prolonged malaise, and localized swelling at the site of
infection and nearby lymph nodes for several months
(FIGURE ).
 Cat Scratch Disease
Pathogen and Virulence Factors

• Bartonella henselae , a Gram-negative aerobic

bacillus, causes cat scratch disease.

• Its primary virulence factor is endotoxin (lipid A)

found in the outer membrane of bacteria.

• Bartonella can grow and reproduce inside red

blood cells and in cells lining blood vessel walls.
 Pathogenesis and Epidemiology
• Cat scratches or bites, particularly wounds by
kittens, introduce the bacterium into the skin.

• Blood-sucking arthropods such as fleas may also

transmit the bacterium from cats to people.

• In the skin, the bacterium grows intracellularly.

 Pathogenesis
• Bartonella releases endotoxin when it dies, which
can trigger fever, blood clotting, inflammation,
and possibly shock

• Though carried by cats, Bartonella apparently

causes disease only in people
• it is not known to cause disease in animals.
 Diagnosis, Treatment, and Prevention

• A positive indirect fluorescent antibody test

against Bartonella antigens confirms a
diagnosis of cat scratch disease in
individuals who exhibit the characteristic
signs and symptoms following exposure to
cats.
 Diagnosis, Treatment, and Prevention

• Physicians prescribe antimicrobials—

typically rifampin, ciprofloxacin, or
gentamicin—to treat cat scratch disease.

• Prevention involves avoiding cat-inflicted

wounds and adequate cleansing of bites or
scratches that do occur.
 Major parasites infecting the
Hematologic System

1. Plasmodium species: Malaria

2. Babesia species: Babesiosis

MALARIA : Plasmodium species
 Plasmodium species
• Causative agent of Malaria: an acute and/or chronic
infection caused by protozoans of the genus
Plasmodium

• Four plasmodium species causing human malaria

• Plasmodium falciparum (P. falciparum)
• P. vivax
• P. malariae
• P. ovale
• Widespread species
• P. falciparum: most prevalent in the hotter and
more humid regions of the world.
• P. vivax: more common in temperate region than in
the tropics
• Less widespread species
• P. malariae: confined mainly to tropical Africa
(25%)
• P. Ovale: Low & restricted distribution
 Occurs primarily in tropical west Africa (10%)
General feature of Plasmodium species

• Intracellular obligate parasites. (liver cell & RBC)

• Life cycle,
• Alternation of generation ~ alternation of hosts

• Requires two hosts:

 Man (IH)
Female Anopheles mosquitoes (DH)

• Sexual and asexual reproduction

• No animal reservoir host except P. malariae

 Burden of malaria
• Endemic in 109 countries, 45 within African region
in 2008
• An estimated 3.3 billion people were at risk of in 2006

 2.1 billion were at low risk (< 1 reported case per

1000 population), 97% of whom were living in
regions other than Africa
 1.2 billion at high risk were living mostly in the WHO
African (49%) & South-East Asia (37%)
• Estimated 247 million malaria cases in 2006, 86%
of them were in the African Region
• 80% of the cases in Africa were in 13
countries, and
•over half were in Nigeria, Democratic
Republic of the Congo, Ethiopia, United
Republic of Tanzania and Kenya.
Estimated deaths from malaria per 1000 population, 2006
• Kills in 1 year what AIDS killed in 15 years

• 16% growth in malaria cases annually (WHO)

• Every year ~ 30000 visitors to endemic areas

develop malaria
• 1% of them may die.
Burden of malaria in Ethiopia
• ¾ landmass malarious

• 68% of the population at risk

• Annual clinical cases estimated 4-5 million

• 10-40% of all outpatient consultations

• 13-26% of all inpatient admissions

• Plasmodium species
• P. falciparum =60%
• P. vivax = nearly 40%
• P. malariae =1% cases ,focal distribution like
in Humera
• P. ovale = less than 1% cases , found in Setit
Humera , Gambela & Arbaminch
Epidemiology of Malaria in Ethiopia
 The risk of malaria varies highly from season to
season and from place to place
• Transmission- seasonal (Unstable)
• Mainly depends on rain fall and Temp
• Two major transmission periods
• Major - September to December after main rainy season
• Minor- April to June following small showers of rain in
autumn.
Epidemiology of Malaria in Ethiopia
• Dega zone(> 2,500 m) mean annual temperature of 10-
150C , is malaria free

• Weyna dega zone( 1,500 - 2,500 m) mean annual

temperatures range from 15-20o c
• Malaria most often occurs below 2,000 meters, with
short-lived transmission following the rains

• Kolla zone (< 1,500 m), mean annual temperatures are 20-
25oc, malaria transmission is endemic
Morphological stages
• Sporozoite: develops in the mosquito salivary gland

• Hepatic schizont   actively dividing, multinucleated,

parasite form in hepatocytes

• Trophozoite: metabolically active form living within the

RBC
• Sometimes called the ring form

22
Morphological stages

• Erythrocytic schizont: multinucleated stage in a

RBC resulting from asexual multiplication of
trophozoite
• Each schizont contains a species determined
number of meroziotes

• Merozoite: infective schizont components that

break out of hepatocyte or RBC
23
Morphological stages
• Gametocyte: morphologically distinctive sexual (male
or female) form which develops from some
trophozoites in RBCs
Sta
ges
in h
um
ans
Terms in malaria
• Prepatent period
• An interval between infection and the first detection
of parasites in the blood) is a function of the species
involved and is modified by factors such as the
method of detection and the skill of the
diagnosticians.
• For P. falciparum it is 5.5 to 6 days

26
Terms in malaria
• Incubation period:
• Following the infective bite by the Anopheles mosquito, a
period of time (the “incubation period”) goes by before the
first symptoms appear. The incubation period in most cases
varies from 7 to 30 days. 

27
Terms in malaria
• Recurrence:
Relapse:
Recrudescence:

In malaria, a recurrent infection can occur due to either

recrudescence or relapse.
Relapse means an infection is activated from its
dormant state in the liver called "hypnozoites".
This is applied to malaria strains that have hypnozoites such as
P. vivax

28
Terms in malaria
• Recurrence:
Recrudescence:
recrudescence means parasite infections are detected after
persisted in the bloodstream at undetectable levels for a
period of time.
This term is applied to malaria species that have no
hypnozoites such as P. falciparum, P. malariae.
This is also applied to drug-resistant strains of malaria P.
vivax and P. ovale where the parasites remained in the
bloodstream despite treatment.
29
Transmission and life cycle of
Malaria
• Principal mode Transmission
• bites of female anopheles
mosquito
60 species of mosquito
sucks the gametocytes during
blood meal
bites between 5 PM and 7
AM, with maximum intensity
Anopheles
at midnight.
Mosquito transmission depends

• Susceptibility of anopheles species

 More than 200 known species of Anopheles , 60 of them are
considered to be vectors of malaria

• Feeding habits
• Density
• Longevity (Life Span. Once ingested by a
mosquito, malaria parasites must undergo development within
the mosquito before they are infectious to humans. )
• climatic factors
• temperature, humidity, rainfall, wind, etc
• In Ethiopia : A.gambiae, A.funestus, A.nili,

A.arebiansis & A.pharonensis

are main vectors
• A. arabiensis is responsible for
most epidemics in the country
Other modes of transmission
1. Blood transfusion (Transfusion malaria):

• This is fairly common in endemic areas

• Following an attack of malaria, the donor may
remain infective for:
• 1-3 years in P. falciparum,
• 3-4 years in P. vivax, and
• 15-50 years in P. malariae.
• Most infections occur:
• in blood stored for less than 5 days and

• rare in blood stored for more than 2 weeks

• Frozen plasma is not known to transmit malaria

• blood transfusions malaria

• Infective stage-trophozoites/merozoites

• shorter incubation period,because no exo-

erythrocytic shizogony
 • no relapses possible (vivax/ovale)

• clinical features & management of cases are the

same as naturally acquired infection

• Donor blood should be screened

2. Mother to the growing fetus (congenital malaria)
• occurs in 5 % of new borne whose mothers are
infected
• relatively rare although placenta is heavily infected
• Congenital malaria is more common in first
pregnancy, among non - immune populations

3. Needle stick injury:

• Accidental transmission can occur among drug
addicts who share syringes and needles
Life cycle
• Require two host • Mosquitoes:-
• Man:- • Definite host
• intermediate host • Sexual
reproduction
• Asexual reproduction
• Liver cell
• RBC
• Mosquitoes cycle
• A- Sporogony

• Human cycle
Two phases

B- exo-erythrocytic

schizogony in liver

C- Erythrocytic

schizogony &

gametocytogenesis in

RBC
IN THE MOSQUITO

• During a blood meal on man, female Anopheles

mosquito picks up mature gametocytes

• In the mosquito's mid gut, a micro gamete

(male) penetrates a macro gamete (female) and
form a zygote

• The zygotes in turn become motile and elongated

form called ookinetes
• Invade the midgut wall of the mosquito where they
develop into oocysts

• The oocysts expanding by asexual multiplication, grow,

rupture, and release motile sporozoites , which make
their way to the mosquito's salivary glands

• Inoculation of the sporozoites into a new human host

perpetuates the malaria life cycle
When the female mosquito bites a person, she pierces the skin and injects
saliva (which contains anticoagulants to stop the blood clotting whilst she
takes her meal
Life Cycle:

                                                                    
• Fraction sporozoites escape destruction are carried
rapidly via the blood stream and invade hepatic
parenchymal cells of the liver

• Begin their initial asexual replication : Exo- erythrocytic/

Intrahepatic / Pre-erythrocytic schizogony
• within 5-15 days mature into pre-erytrocytice(PE)
schizonts containing 10,000-30,000 merozoites

• Rupture the swollen liver cells & release merozoites in to

blood stream
• P. falciparum
mature and released simultaneously
from liver, no relapse
• P. malariae

• P vivax
may remain latent in the liver and
relapse
• P ovale
 A proportion of the merozoites are phagocytosed & destroyed

• The remaining enter in to red cells starts erythrocytic

schizogony which to complete takes 36-48 hours (P.
falciparum),48 hours (P. ovale/ vivax) & 72 hours (P. malariae).
• At this time the intracellular merozoites develop in to
trophozoites (‘ring form’)
• When the trophozoites fully developed ,then schizogony
takes place resulting in the formation of schizont containing
8-32 merozoites
• Development to erythrocytic schizont in P. falciparum
takes place in the capillaries of deep tissue ,

• The mature schizont rapture from red blood cells

• releasing merozoites , malaria pigment and toxins
in to plasma
• Merozoites ,which are not destroyed by host
immune system infect new red blood cells,
initiates further cycle of erythrocytic schizogony
with more red blood cells begin destroyed.
• After several erythrocytic schizogony cycle , some
of the trophozoites in the red blood cells develop
in to male female gametocytes

• The gametocytes are now ready to be ingested by

an Anopheles mosquito during a blood meal
Comparison of malarial parasites
Pf Pv Po Pm
 

Tissue schizogony 8 - 27 9 - 17
8 - 25 days 15 - 30 days
days days
Erythrocytic phase
48 hours 48 hours 48 hours 72 hours

Red cells affected Reticulocy Reticuloc

All Mature RBC's
tes ytes

Merozoites per
schizont 8 - 32 12 - 24 4 - 16 6 - 12

Relapse from
No, but blood
Hypanozoites
forms can
No Yes Yes
persist up to
30 years
Clinical Features & pathology
Characterized by acute febrile attacks (malaria

paroxysms)
• caused by the release of toxins (when erythrocytic schizonts
rupture) stimulate the secretion of cytokines from

leucocytes and other cells

Manifestations and severity depend on parasite

species, parasitemia and host status, i,e immunity,
general health, nutritional state, genetics
Prodromal Symptoms

• Malaria paroxysm preceded by Prodromal

period
• 2-3 days before 1st paroxysm
• includes: malaise, fatigue, headache, muscle
pain, nausea, anorexia (i.e., flu-like symptoms)
• can range from none to mild to severe
Febrile Attack (Malaria Paroxysm), 4-8
hr
• periodic febrile episodes alternating with symptom-free
periods

• initially fever may be irregular before developing periodicity

• may be accompanied by splenomegaly, hepatomegaly

(slight jaundice), anemia

• P. falciparum can be lethal in non-immune

• paroxysms comprises of three successive stage: cold stage,

hot stage and sweating stage
cold stage
feeling of intense cold
vigorous shivering, rigor
lasts 15-60 min
hot stage
intense heat
dry burning skin
throbbing headache
lasts 2-6 hours
sweating stage
profuse sweating
declining temperature
exhausted, weak  sleep
lasts 2-4 hours
 Malaria Paroxysm
paroxysms associated with
synchrony of merozoite
release
between paroxysms
temperature is normal and
patient feels well
falciparum may not exhibit
classic paroxysms
continuous fever
24 hr periodicity

tertian malaria
quartan malaria
Complications of acute
malaria
Malaria caused by P. falciparum
• Falciparum/subtertian/malignant malaria

• Most pathogenic of all species

• Almost all deaths are due to falciparum malaria

Factors for Malignance of P. falciparum

• Rapid multiplication

• Infected red blood cells become "stick"

• Infects all age group of red blood cells

• A single red blood cell can be infected by more than one

parasites

• Erythrocytic schizogonic reproduction takes place in the

deep capillaries of organs such as brain, lung, heart, spleen,
bone-marrow, placenta, intestine, etc.
Pathogenecity of P. falciparum
1.Higher Parasitemia in
Falciparum Malaria
• all erythrocytes
invaded
• up to 36 merozoites
• Pv/Po = reticulocytes
• Pm = senescent RBC
P. falciparum.
-Up to 30-40% of RBC
- sever if > 5% RBC are
infected.
P. vivax & P. ovale rarely
exceeds 2%
P. malariae. Usually < 1%
2. Cytoadherence of infected erythrocytes
-trophozoite and schizont stages
-primarily in brain, heart, lungs, and gut
complications
cytoadherence
 SequestrationHypothesis 
cerebral ischemia

hypoxia, metabolic effects

coma

death
 Severe Falciparum Malaria
Features Indicating
Complications Poor Prognosis
cerebral malaria impaired consciousness
blackwater fever repeated convulsions
anemia respiratory distress
hypoglycemia shock
GI and liver syndromes acidosis/hyperlactemia
pulmonary edema hypoglycemia
algid malaria (shock) jaundice or other liver
malfunctions
renal impairment
high parasitemia
(>500,000/mm3)
Predisposing factors for complications of P. falciparum
malaria
(1.) Extremes of age.
(2.) Pregnancy, especially in primigravidae and in
2nd half of pregnancy.
(3.) Immunosuppressed - patients on steroids, anti-
cancer drugs, immunosuppressant drugs
(4.) Splenectomy.
(5.) Lack of previous exposure to malaria (non-
immune) or lapsed immunity
(6.) Pre-existing organ failure.
 Cerebral malaria
• Severe complication of falciparum malaria
• Mortality of 30-50%
• Associated with sequestration in micro-
vasculature of brain

•A diffuse encephalopathy with loss of

consciousness
 Blackwater fever

Blackwater fever (BWF) is a severe clinical syndrome, characterized

by intravascular hemolysis, hemoglobinuria, and acute renal failure that
is classically seen in chronically exposed to Plasmodium falciparum
and irregularly taking quinine.
Malaria caused by P. vivax, P. ovale P. malariae

• Plasmodium vivax is referred to as vivax malaria ,

benign tertian (BT) malaria

• Plasmodium ovale is referred to as ovale malaria,

ovale tertian malaria

• Plasmodium malariae is referred to as malariae

malaria , quartan malaria
• Infections caused by P. vivax, P. ovale or P. malariae are rarely
life threatening
 no Cytoadherence of parasitized cells
 parasitic densities are lower
• Relapses are a feature of vivax and ovale malaria

• Recrudescences are a feature of P. malariae

• P. malariae is nephritic syndrome which may progress to renal

failure.
 
 Hyper-reactive malaria splenomegaly (Tropical
splenomegaly syndrome)
• massive and chronic splenomegaly with
• high levels of IgM ,

• malaria antibody,

• circulating immune complexes

• a moderately enlarged liver with hepatic sinusoidal

lymphocytosis
• The patient is usually
• anaemic (normocytic)
• low white cell and platelet counts
Hyper-reactive malaria splenomegaly
 Genetic factors That Provide Protection Against
Malaria
1. Nature of hemoglobine
• Hgb S (Sickle cell anemia trait) –p.f
• Thalassemia Hgb-P.f
• Fetal Hgb – all sps
• Hgb E – P.v

2. Enzyme content of erythrocyte

• Glucose-6-phosphate dehydrogenase deficiency ,-P.f

3. Presence or absence of certain factor

• Ovalocytosis -P.f & P.v
• Duffy blood group antigens (i.e., Fya and Fyb) negative RBCs-P.v
Laboratory Diagnosis
MALALRIA Diagnostics approaches

Clinical Diagnosis

Malaria Diagnosis

Laboratory diagnosis

Microscopic Molecular
Thin film Immunological PCR
Thick film Ag /enzyme
 QBC •RDT.ICT Malaria Pf etc.
ParaSight F
OptiMAL
Ab- ELISA
Clinical diagnosis

• Based on clinical signs and symptom:

• Fever, Chills, perspiration, anorexia, headaches,
vomiting, and malaise
• It is inexpensive to perform and requires no special
equipment or supplies.
• Are non-specific and symptoms overlap with those of
other febrile illnesses.
• A Dx of MAL based on Clinical grounds alone is
therefore unreliable-Overdiagnosis
 Laboratory diagnosis Techniques
I. Microscopy examination
• Peripheral smear study
• Detecting and identifying malaria parasite in direct blood films
• CONCENTRATING MALARIA PARASITES
• Concentrating parasite in venous blood by centrifugation when note
found in blood films
1.Buffy Coat preparation
2. Quantitative buffy coat( QBC) system
II. Immunologic/Biochemical techniques
• detection of malaria antigen, antibody & parasite products
III. Molecular diagnosis techniques
I. Microscopy examination
 Microscopic examination of blood film
• Established method for
confirmation of malaria- the gold
standard.
• Requirements:
Carefully collected blood
specimen/sample
Well prepared blood films
Well stained
smears( Romanowsky
stains)
Careful examination of the
smears
 Collection of Blood Specimen
I. Collect sufficient quantity of blood
1. Capillary blood from finger prick , toes, or ear
lobes –best
2. Venous blood.(EDTA anticoagulant)
3. In obstetric practice, cord blood and placental
impression smears can be used
II. Time of collection
When the patients feels febrile
Before anti-malaria drugs are given to the
patients
Note:-
• A negative test DOES NOT rule out malaria.
• Repeated tests may have to be done in all
doubtful cases

1. Preparation of blood film

I. thick blood film
II. thin blood film
I. Preparation of thick films

I. slides must be clean, free from

dirt, grease and fingerprints
II. Mix the blood
III. Using an applicator stick, apply 4
drops of blood on to a
microscope slide
IV. Spread the blood without
excessive stirring to form a smear
approximately a cm2, through
which newspaper print can be
red.
V. This should be approximately 5
red blood cells thick.
VI. Allow to air dry horizontally
(without using heat).
VII. Label slides.
II. Preparation of Thin Films

1. The microscope slides must

be clean as for thick films
otherwise the blood will not
adhere and the smear will
be irregular.
2. Apply 1 drop of blood to the
end of the slide, pace
another slide at an angle of
45o and bring it towards the
drop of blood.
3. As soon as it touches it, the
blood will disperse along the
width of the slide.
5.Before it reaches the edges, pull the drop along
the length of the slide.

6. the correct amount of blood in the drop the film

will form a good tail before the end of the
slide. The film here should be 1 RBC thick.
Make 2 slides for each test.
7. Air dry, Label slides
 Preparation and processing the blood film

1 2 3 4

5 6 7 8

9 10 11
Thick blood film
• Good for rapid detection malaria parasites ,
particularly when they are few
 In P.malariae parasitaemia is normally low

• About 30 times more sensitive (detecting about 20

parasites/µl)

• In a thick film the blood is not fixed

 Thin blood film
• required to confirm the plasmodium species

• enabling the parasites to be seen in the red cells

• greatly assists in the identification of mixed infection

• value in assessing whether a patient with falciparum malaria

is responding to treatment

• gives the opportunity to investigate anaemia and white cell

abnormalities
Staining With Giemsa
Immediately before use dilute the Giemsa as required
3% for 30 min
10% for 10 min
 Thin films must be fixed in absolute methanol for at
least 30 seconds(1-2min)
Stain
Wash
Drain & dry vertically/ at an angle.
Microscopic examination of blood films

Focus on the film with the X10 objective.

Examining the film first with 40x objective to select a

well stained area

Apply a drop of immersion oil on the slide and switch to

the oil-immersion objective(100).

Examine at least 100 fields(100Xobjective)

*P.malariae exam approximately 200 fields

Microscopic differentiation
 Microscopic differentiation of species depend on
Host cell and Parasite characteristics

1. Feature of infected red cell and ghosts

 change in size, shape and colour
 Presence of dots, maurer's clefts (not on ghost
cell) on infected red cell
 Single or multiple infection of each cell
2. Parasite morphology at specific stages
 Number and size of chromatin beads

 Shape and size of cytoplasm

 Degree of pigmentation within cytoplasm

 Stages of parasite seen together

Microscopic features of three blood stages
-trophozoites, schizonts, gametocytes
 All these three stages have:
Red nuclear chromatin, blue cytoplasm and
pigment (except young troph)
What are the key features of :
trophozoites?
single (Sometimes double) chromatin bead
Cytoplasm as a ring uniform or fragmented mass
Pigment absent from young (ring) form
 Schizonts?
2-32 chromatin beads
Cytoplasm-typically irregular, amoeboid
Pigment in early and late form
• Gametocyte?
 Single chromatin bead (diffuse in male)
 Round or crescent shaped
 Solid cytoplasm
 Pigment in early and late stage
Notes: the mature gametocytes of Pv, Po and Pm
are hard to distinguish from mature troph of these
species.
Artefacts
Potential source:
• Vegetable spores, yeast, pollen, algae and
bacteria in the stain or on the slide
• Platelets
• Howell-jolly bodies in anaemic patients
• Ghosts of immature red cells mimicking
schuffner's stippling
Examining Microscopic feild
Examination

P.falciparem
Young Trophozoite (Ring
forms)

• Stage frequently found

in blood film
Mature Trophozoite

• Stage rarely seen in

peripheral blood

• RBC unaltered in
size, sometimes
stippled, pale
Schizont stage

• Not usually seen in

peripheral blood

• RBC unaltered in size ,

sometimes stippled, pale.

• Merozoites: 8-32; average

24

• Pigment: clumped black

Gametocytes
• RBC is distorted.
• Fairly frequently found
• Size: larger than red cell
• Shape: crescent or banana
• Male:- Bluntly round ends
• Female:-Rounded/pointed ends
• Cytoplasm: Reddish blue(Male)/Dark
blue(female)
• Chromatin:
• Male:-fine granules scattered
• Female:-compact masses near center
• Pigment: black granules
• Rounded forms may be seen if film dries
slowly
Plasmodium vivax

Young Trophozoites
• Stage frequently seen
•
Mature Trophozoite
• Not frequently seen
Schizonts
• Quite frequently seen
• RBC much enlarged
• Size: Almost fills red
blood cells
• Shape: amoeboid or
segmented, parasite
large, filling enlaged RBC
• Cytoplasm: pale blue
• Merozoites: 14-24;
average 16
• Pigment: Golden brown
central loose mass
Gametocytes

• Are round to oval with blue stain

• May almost fill the red blood cell

(RBC).

• Rbcs are enlarged 1 1/2 to 2 × and

may be distorted.

• Difficult to differentiate from late

trophozoites
 
Reporting blood films for malaria parasites

A. REPORTING THICK BLOOD FILMS

• plus sign scheme :
Parasites
1 – 10 per 100 high power fields ………………… +
11 -100 per 100 high power field…………………++
1 – 10 in every high power field…………………+++
More than 10 in every high power field ………. ++++

• Example: P. falciparum trophozoites +++, gametocytes +,

with malaria pigment in white cells
 If no parasites are found after examining 100 fields
(or if indicated 200 fields), report the film as:
Malaria thick film: NPF (No parasites found)

 
RDTS procedures

1. 50 µl of blood from finger prick

 A blood specimen is mixed in a buffer
 The labeled Ag – Ab complex migrates up the test
strip

Sample origin Detection line Absorbent pad

Control
anti-Pf Ab Ab

Ant-MAL Abs
(all species)
Treatment
Antimalarial drugs like
Chloroquine
 Widespread resistance has now rendered it virtually
useless against P. falciparum

Artemisinin - active against all Plasmodium species

Pyrimethamine in combination with a sulfonamide

 Effective against all four human malarias

And other can be used

108
 Prevention and Control

1. Avoid mosquito bites by

• Using impregnated bed nets
• Wearing protective clothes
• Using mosquito repellents
• screens, house spraying

2. Destroy adult mosquitoes by

• Indoor residual regular effective spraying
3.Preventing breeding of mosquitoes by
• environmental modification
• Spraying breeding places with effective larvicides
• Biological control
4. Treatment
• Active infection
• Chemoprophylaxis

5) Health education

6) Blood screening for malaria  

Babesia species
 Babesia species
• Causative agent of Babesiosis , piroplasmosis, thick
fever, or red fever

• More than 100 species have been reported

• known as parasites of domestic and wild animals

• Humans are accidental host

• Four species known to infect humans

Name Normal parasite

B. bovis Ox
B. divergens Ox
B. equi Horse
B. microti microtus Rodents
 Transmission and life cycle
Transmission

• By bite of infected ixodid or hard –bodied tick (definitive

host )

• blood transfusion

Life cycle
•   During a blood meal, a Babesia-infected tick
introduces sporozoites into the mouse host

• Sporozoites enter to erythrocytes and undergo

asexual reproduction (budding)

•   In the blood, some parasites differentiate into male

and female gametes

• The gametes ingested by appropriate tick

• gametes unite and undergo a sporogonic cycle
resulting in sporozoites

• Babesia-infected tick introduces sporozoites into the

human host during a blood meal

• Sporozoites enter erythrocytes and undergo asexual

replication (budding)
• Humans are, for all practical purposes, dead-
end hosts
 Clinical feature

• Multiplication of the blood stage parasites is

responsible for the clinical features

• chills, sweating, fatigue, hemolytic anemia, jaundice,

fever and hepatomegaly, usually 1-2 weeks after
infection

• it is self-limiting disease infection in human

Laboratory Diagnosis

1. Examination of stained smear

• identifying poleomorphic ring like intra-
erythrocytic parasite in Giemsa -stained blood
films

• The small parasites appearing much like

P.falciparum

• can be differentiated from malaria parasite by the

absence of pigment in the infected erythrocytes
2. Serologic test: IFA
3. Molecular technique: PCR

Treatment
Clindamycin and quinine or Atovaquone plus
Azithromycin
Prevention and control
1. Tick control through acarcidal treatment ( animal
host )

2. Chemotherapy to infected animal and host

3. Avoidance of exposure to tick