MALARIA

DR Mohammedyassin Redi

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 Etiology
• Plasmodium protozoa
• Five species:
P. falciparum
P. malariae
P. ovale
P. vivax
P. knowlesi

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 Epidimology
• Malaria is a worldwide problem with transmission occurring
in over 100 countries

• The principal areas of transmission are Africa, Asia, and

South America.
• P. falciparum and P. malariae are found in most malarious
areas
• Rainy season ,tropical and subtropical areas
• Malaria is mainly seasonal in the highland fringe areas, and
of relatively longer transmission duration in lowland areas,
river basins and valleys

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 epidimology continue….
an estimated 300 million cases and more than
1 million deaths occur each year.

Most malarial deaths occur in infants and

young children.
In Ethiopia,malaria affects 2/3 of population

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 Transmission
• Malaria is transmited to human by bite of
female anopheles mosquitoes
• Other rare way of transmission

– By blood transfusion
– From mother to child during
pregnancy(congenital malaria).

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 Life cycle

• The life cycle alternates between the sexual cycle

in the female Anopheles mosquito and the asexual
in human

• In human under go a 2 step process with

- the 1st phase in hepatic cells(exoerythrocytic

phase) and
- the 2nd in the red blood cells (erythrocytic phase
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 Life cycle

• The exoerythrocytic phase

–Entry of sporozoites into the bloodstream by a female
Anopheles mosquito
– sporozoites enter the hepatocytes develop and multiply
asexually as a schizont
–After 1–2 wk, the hepatocytes rupture and release
merozoites
–The tissue schizonts of P. falciparum and P. malaria rupture
once and do not persist in the liver
–The tissue schizonts for P. ovale and P. vivax.
• The primary type ruptures in 6–9 days,
• The secondary type remains dormant in the liver cell in the
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hypnozoite form as long as 5 yr
 The erythrocytic phase
–Merozoites enter to erythrocytes
–Then transforms into the ring form, which then
enlarges to become a trophozoite (both are seen on
Giemsa stain on blood smear)
–Asexual multiplitcation of trophozoites => release of
merozoites in to bloodstream results in fever
–Merozoites develop into male and female
gametocytes => ingested by mosquito
–Gametocytes fuse to form a zygote in the stomach
cavity of the mosquito

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08/09/2021 9
 pathology

• Four important pathologic events:

• Fever occurs when erythrocytes rupture and release
merozoites.
• Anemia is caused by hemolysis, sequestration of
erythrocytes in the spleen and other organs, and bone
marrow suppression.
• Immunopathologic events- excessive production of
proinflammatory cytokines (TNF); polyclonal activation; and
immunosuppression.
• Tissue anoxia- Cytoadherence

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• Cytoadherence of infected erythrocytes to
vascular endothelium
• obstruction of blood flow
• Capillary damage =>vascular leakage of blood,
protein and fluid=> tissue hypoxia & edema in the
brain, heart, lung, intestine and kidney
• Anaerobic metabolism=>Hypoglycemia and
lactic acidosis

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• Genetically inherited conditions
– Sickile cell resist P. falciparum
– RBC lacking Duffy b/d Ag resistant to P. vivax,
– Fetal hemoglobin resistant to P. falciparum
• Severe disease
– Children 3 mo to 2–5 yr of age have little specific immunity
to malaria
– Pregnancy
– Patients from outside the endemic region
– P.falciparum infection

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 CLINICAL FEATURE DIAGNOSIS OF
SEVER & COMPLICATED MALARIA
• most severe and complicated malaria is
usually due to P. falciparum
-high parasiteamia >60%
-‘sequestration’ in which mature parasites
specifically adhere to endothelial cells in the
post capillary venules of critical organs such
as the brain, heart, liver, kidney

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Severity is considered
• if the asexual form of P.falciparum on blood
smear and the presence of one or more of the
following clinical features
• Prostration
• A change in behavior or altered mental status
• Multiple convulsions

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• Severe anemia with hematocrit <15%      
• Hypoglycemia RBS<40mg/dl
• Jaundice
• Pulmonary edema, or adult respiratory
distress syndrome     
• Renal failure due to acute tubular necrosis  
• Circulatory collapsse or   “Algid” malaria
(septic shock–like)   
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 Severe anemia due to
complicated malaria

Jaundice due to
complicated malaria

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 Signs and symptoms of severe malaria
in adults and in childrena
Sign or symptom Adults Children
• Duration of illness 5–7 days Shorter(1–2
• RD/(acidosis) Common Common
• Convulsions Common (12%) common (30%)
• Posturing ( Uncommon Common
• Prostration/
obtundation Common Common
• Resolution of coma 2–4 days Faste
• Neurological sequelae
after cerebral malaria Uncommon(1%) Common
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• Jaundice Common Uncommon
• Hypoglycaemia Less common Common
• Metabolic acidosis Common Common
• Pulmonary oedema Uncommon Rare
• Renal failure Common Rare
• CSF opening p Usually normal Usually raised
• Bleedingdisturbances Up to 10% Rare
• Invasive bacterial
co-infection Uncommon Common
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The classic presentation of malaria
• consists of paroxysms of fever alternating with
periods of fatigue but otherwise relative
wellness
• Febrile paroxysms are characterized by
 high fever, rigors, sweats, and headache, as
well as myalgia, back pain,
 abdominal pain, nausea, vomiting, diarrhea,
pallor, and jaundice

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• Paroxysms coincide with the rupture of
schizonts that occurs every 48 hr with P. vivax
and P. ovale and result in every other day
fever spikes.
• Rupture of schizonts occurs every 72 hr with P.
malariae and results in fever spikes every 3rd
or 4th day. Periodicity is less apparent with P.
falciparum and mixed infections

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 Diagnosis of malaria
• Clinical:
• consider malaria on any child with fever or
unexplained systemic illness and has traveled or
resided in a malaria-endemic area.
• Geimsa stain:
• Thick smear- to scan large no. of erythrocytes
• Thin smear- to identify the malaria species
• Immunochromatographic test (rapid tests)
• PCR
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 History
• chills, malaise, fatigue, diaphoresis, headache, cough,
anorexia, nausea, vomiting, abdominal pain, diarrhea,
arthralgias, and myalgias
• travel hx or from endemic area
• Transfusion history and use of contaminated needle
• Hx of information on residence
• Hx of differential diagnos
–sepsis, pneumonia, meningitis, encephalitis,
– relapsing fever, typhoid fever
–viral infections such as influenza and hepatitis
–endocarditis, gastroenteritis, pyelonephritis,
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 Physical findings
• tachycardia, tachypnea fever pallor,
• jaundice, hepatomegaly and/or splenomegaly.
Splenic rupture has been described
• Altered consciousness with or without seizures
• Respiratory distress or acute respiratory
distress syndrome (ARDS) very
• dark urine
• severe jaundice

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 Investigation
• Blood film :
-thick blood film
-thin blood film
haematocrit ,
blood sugar
Serum electrolytes
Renal function test
lp
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 Plasmodium blood smears

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 Con...
Rapid diagnostic tests (RDT) to detect ag
Polymerase chain reaction is even more
sensitive

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Important criteria that suggest P. falciparum
malaria include
 symptoms occurring <1 mo after return from
an endemic area,
 intense parasitemia (>2%),
 ring forms with double chromatin dots, and
 erythrocytes infected with more than 1
parasite
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 SEVERE MALARIA
 Malaria may become a medical emergency by
rapidly progressing to complications and death.

 Early diagnosis & proper management can

prevent serious complications.

 Most complications have similar pathogenesis .

 Predisposing factors for
complications

Immunosuppressed - patients on steroids, anti-

cancer drugs, immunosuppressant drugs. patients
with advanced tuberculosis, HIV and cancers.

Splenectomy

Lack of previous exposure to malaria (non-immune)

or lapsed immunity

Pre-existing organ failure

• Complications of P. falciparum • Complications of P. vivax / P.
malaria malariae
– Severe anemia
– Cerebral malaria ( coma ) – Rupture of spleen
– Metabolic (Lactic) Acidosis – Hepatic dysfunction
– hypoglycemia – Thrombocytopenia
– Convulsions – Severe anemia
– renal failure – malarial nephropathy
– Algid Malaria(CR-Collapse
– Pulmonary odema & ARDS
– Hypotention & shock
– Bleeding & clotting disorder(DIC)
– haemoglobinuria
– hyperparasitemia
– Hyperpyrexia
– Jaundice
– Prostration
 Complications of P. Falciparum MalariaSEVERE MALARIA
• WHO has identified 10 complications of P.
falciparum malaria that define severe malaria
severe anemia, impaired consciousness
(including cerebral malaria), multiple seizures,
respiratory distress (due to metabolic acidosis),
prostration, hemoglobinuria, abnormal
bleeding ,pulmonary edema ,circulatory
collapse and jaundice.
 Cerebral malaria
• is defined as the presence of coma in a child with P. falciparum parasitemia and an
absence of other reasons for coma.

• Children with altered mental status who are not in coma fall into the larger
category of impaired consciousness.

• Cerebral malaria is most common in children in areas of midlevel transmission and

in adolescents or adults in areas of very low transmission.
• It is less frequently seen in areas of very high transmission.

• Cerebral malaria is associated with a fatality rate of 20-40% and

• is associated with long-term cognitive impairment in children.

 Con...

• Physical findings may be normal or may include

• high fever, seizures, muscular twitching, rhythmic
movement of the head or extremities,
• contracted or unequal pupils, retinal hemorrhages,
hemiplegia, absent or exaggerated deep tendon
reflexes,
• a positive Babinski sign.
 Management
• Treatment of uncomplicated malaria:
P. falciparum: artemether-lumefantrine (coartum)
Bid for 3 days (1.7/12mg/kg/per dose).
P.vivax, P.malariae or P. ovale: first-line drug of
choice is chloroquine.
Second line- oral quinine plus doxycycline or
clindamycin.
Supportive treatment
 Treatment of severe malaria
• Artesunate 2.4 mg/kg im or iv then at 12 hr,
24 hr if necessary daily then after
• Artemether 3.6mg/kg im then 1.6mg/kg daily
• quinine salt 20mg/kg loading followed by 10mg/kg
TID starting 8hrs after loading. Dilute with 5%
dextrose to run over 4hr.
• Treat complications and supportive care
 Childhood malaria
PREVENTION
Mosquito control
Insecticide treated nets (ITN), LLIN (pyrethroids)
Indoor residual spray (IRS)-DDT, Malathion
Larval control (Larva killers, fish, damp closure)
Personal protection:
• Mosquito repellents (applied over the skin--DEET)
Chemotherapy (prophylaxis for travelers)
Adequate clothing during the dusk and night
Vaccine on trial (RTS,S/ASO1)
 Malaria prophylaxis
General guide line on the use of chemoprophylaxis
• P.falciparum:
Mefloquine,doxycycline,atovaquone/proguanil
• Vivax and Ovalae: chloroquine, premaquine and
agents used for falciparum
• Pregnant ladies: mefloquine and chloroquine
• Children: all except doxycycline (use > 8years)
• Hyponozoite: Premaquine
• Weekly: chloroquine, mefloquine
• Daily: doxycycline, premaquine,atovaquone/proguanil
Typhoid fever
 Definition

• An infectious feverish disease caused by the bacterium Salmonella

typhi(Salmonella enterica Serovar Typhi ) and less commonly by
Salmonella paratyphi.

• Acute generalized infection of the

reticulo endothelial system,
intestinal lymphoid tissue, and the gall bladder.

• The infection always comes from another human, either an ill person or a
healthy carrier of the bacterium. The bacterium is passed on with water
and foods and can withstand both drying and refrigeration.
 Definition

• An infectious feverish disease caused by the bacterium Salmonella

typhi(Salmonella enterica Serovar Typhi ) and less commonly by
Salmonella paratyphi.

• Acute generalized infection of the reticulo endothelial system,

intestinal lymphoid tissue, and the gall bladder.

• The infection always comes from another human, either an ill person or a
healthy carrier of the bacterium. The bacterium is passed on with water
and foods and can withstand both drying and refrigeration.
 Epidemiology

♦  strongly endemic
♦  endemic
♦  sporadic cases
 Carl Joseph Eberth who discovered the
typhoid bacillus in 1880.

Georges Widal who described the  

‘Widal agglutination reaction’ of the blood in 1896.
1. The best known carrier was "Typhoid
Mary“; Mary Mallon was a cook in Oyster
Bay, New York in 1906 who is known to
have infected 53 people, 5 of whom died.

2. Later returned with false name but

detained and quarantined after another
typhoid outbreak.

3. She died of pneumonia after 26 years in

quarantine.
 Causes

1. Caused by the bacterium Salmonella Typhi .

2. Ingestion of contaminated food or water.

3. Contact with an acute case of typhoid fever.

4. Water is contaminated where inadequate sewerage systems and poor sanitation.

5. Contact with a chronic asymptomatic carrier.

6. Eating food or drinking beverages that handled by a person carrying the bacteria.

7. Salmonella enteriditis and Salmonella typhimurium are other salmonella bacteria,

cause food poisoning and diarrhoea.
 Pathophysiology
Ingestion of contaminated food or water

Salmonella bacteria

Invade small intestine and enter the bloodstream

Carried by white blood cells in the liver, spleen, and bone marrow

Multiply and reenter the bloodstream

Bacteria invade the gallbladder, biliary system, and the lymphatic tissue of
the bowel and multiply in high numbers

Then pass into the intestinal tract and can be identified for diagnosis in
cultures from the stool tested in the laboratory
 Clinical manifestation

- if only a mild exposure; some people become "carriers" of typhoid.

• Poor appetite,
• Headaches,
• Generalized aches and pains,
• Fever, Lethargy, Lethargy,
• Lethargy,
• Diarrhea,
• Have a sustained fever as high as 39 to 40 degrees Celsius,
• Chest congestion develops in many patients, and abdominal pain and
discomfort are common,
• Constipation, mild vomiting, Bradycardia.
 Time frame
• Occurs gradually over a few weeks after exposure to the bacteria.
Sometimes children suddenly become sick.
• The condition may last for weeks or even a month or longer without
treatment.

First-Stage Typhoid Fever

The beginning stage is characterized by high fever,fatigue, weakness,
headache, sore throat, diarrhea, constipation, stomach pain and a skin
rash on the chest and abdominal area. According to the Mayo Clinic,
adults are most likely to experience constipation, while children usually
experience diarrhea.
 Second stage
Second-stage typhoid fever is characterized by weight loss, high fever,
severe diarrhea and severe constipation. Also, the abdominal region
may appear severely distended.

Typhoid State
When typhoid fever continues untreated for more than two or three
weeks, the effected individual may be delirious or unable to stand and
move, and the eyes may be partially open during this time. At this point
fatal complications may emerge.
 Diagnosis

Diagnosis of typhoid fever is made by

• Blood, bone marrow, or stool cultures test

• Widal test

• Slide agglutination

• Antimicrobial susceptibility testing

 Medication
Antibiotics
 Antibiotics, such as ampicillin, chloramphenicol, fluoroquinolone
trimethoprim-sulfamethoxazole, Amoxicillin and ciprofloxacin etc used to
treat typhoid fever.

 Prompt treatment of the disease with antibiotics reduces the case-

fatality rate to approximately 1%.
 Cephalosporins

 Ceftriaxone: 50-75 mg per kg per day one or two doses

 Cefotaxime: 40-80 mg per kg per day in two or three doses

 Cefoperazone: 50-100 mg per kg per day

 Prevention

 Be vaccinated against typhoid while traveling to a country where typhoid is common.

.

. Avoid risky food and drinks

.
 Eat food that have been thoroughly cooked and that are still hot and steaming.
.
 Avoid foods and beverages from street vendors.
 Treating carriers
.

Typhus
The Organism
 Rickettsia prowazekii
 Obligate intracellular bacteria
 Pleiomorphic rods
 Susceptible to moist heat and dry heat
Epidemiology
 United States
 30 cases since 1975
 Africa
 Burundi 1997,Ethiopia and Rwanda
 Most common in people
living under unhygienic conditions
 Refugee camps
Epidemiology
 Ethiopia, the number of cases reported
annually has ranged between 7,000 and
17,000. Most of these cases have not
been confirmed in a laboratory.
Transmission
 Human body louse
 Pediculus humanus corporis
 Infective for 2-3 days
 Infection acquired by feeding on infected
person
 Excrete R. prowazeki in feces
at time of feeding
 Lice die within 2 weeks
Clinical Symptoms
 Incubation: 7-14 days
 High fever, chills, headache,
cough, severe myalgia
 May lead to coma
 Macular eruption
 5-6 days after onset
 Initially on upper trunk, spreads to entire
body Center for Food
Security and Public
 Except face, palms and soles of feet Health Iowa State
University -
Diagnosis
 Initial diagnosis
 Clinical signs and history
 Laboratory tests not diagnostic
 Confirmatory diagnosis
 Culture
 Serology
 Biopsy
 PCR
Center for Food Security and
Public Health Iowa State
University -
Treatment
 Chloramphenicol
 Doxycycline 200mg
 Response within 48 hrs. usually
 Vaccine
 Not commercially available

Center for Food Security and

Public Health Iowa State
University -
Prevention and Control
 Treat clothing and bedding
 160 degrees for one hour
 Chemical control
 Permethrin (0.5%) temephos (2%),
popoxur (1%) and carbaryl (5%)
 Proper hygiene

Center for Food Security and

Public Health Iowa State
University -
.

Thank you