VECTOR-BORNE DISEASES

By: Dereje G. (MSc. Infectious & Tropical Diseases))

 Learning Objectives

At the end of this chapter, the student will be able to:

 Describe what vector-borne disease means

 Identify the common vectors which transmit disease to man

 List the common vector-borne diseases

 Participate in diagnosis and treatment

 Implement the common preventive and control methods

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 What is it?

 Vector
 Insect / any living carrier - transmits an infectious agent

 vector -required for part of the parasite's developmental cycle-

also transmits the parasite directly to subsequent hosts

 Insects form a major group of disease vectors - mosquitoes, flies,

ticks, lice and fleas & many are haematophagous

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 Malaria
 Malaria is a mosquito-born diseases

caused by genus Plasmodium

 Plasmodium species are apicomplexa

parasites

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 Infectious agents
• Four plasmodium species causing malaria
– Plasmodium falciparum
– P. vivax •The four human parasite species differ in
regards to their morphology, Epidemiology,
– P.malariae details of their life cycles, and their clinical
– P. ovale manifestations

NB. Currently the new plasmodium specie called

knowlesi ( simian parasite) has been reported
Malaysia, Thailand

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 Epidemiology

 Malaria, sometimes called the “King of Diseases”

• One child dies of malaria in Africa every 20 sec and one

malarial death every 12 sec in the world

• Kills in 1 year what AIDS killed in 15 years

• Every year ~ 30000 visitors to endemic areas develop malaria

1% of them may die

Causes direct costs and indirect costs

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 Epidemiology…
 The four human malarial species exhibit an overlapping
geographical distribution
 Widespread species
• P. falciparum: most prevalent in the hotter and
more humid regions of the world
• P. vivax: common also in temperate region

• Less widespread species

– P. malariae: confined mainly to tropical Africa (25%)

– P. Ovale: Low & restricted distribution

 Occurs primarily in tropical west Africa (10%)

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 Epidemiology of Malaria in Ethiopia
The risk of malaria varies highly from season to season and from
place to place (altitude dependant)
• Transmission- seasonal (Unstable)

– Mainly depends on rain fall and Temp

 Two main transmission periods ?

– Major - September to December after main rainy

season
– Minor- April to June following small showers of

rain in autumn
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 Bur. Mal. Eth.
– 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

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 Predisposing factors

 Climate

 Anopheles capable to transmit the parasite

 Socio-economic factors like immigration, war, agricultural

irrigation farms, etc.

 Susceptible recipients

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 Life cycle Note: P.vivax & p.ovale become
dormant hypnozoites in liver

Life Cycle:

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 Mode of transmission
 Bite of an infective female anopheles mosquito

 Blood transfusion ?
Infective stage- trophozoites / merozoites
Shorter incubation period, because no exo-
erythrocytic phase
no relapses possible (vivax/ovale)
clinical features & management of cases are the same
as naturally acquired infection

 needles sharing

 organ transplantation

 mother to fetus transmission is possible

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 Mode of transmission con…

In Ethiopia :
 A.gambiae,
 A.funestus,
 A.nili,
 A.arebiansis
 A.pharonensis are main vectors

A. arabiensis is most common and responsible for most

epidemics in the country

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 Basic pathogenesis
 Immunological

 RBCs changes

 Parasite itself

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 Immunopathogenesis

CMI Tc
TH1 IL2

IL1 NK
IFNγ TNF
APC
Mq
ROI
IL1 NO

IL4
Hum
TH2 B-cell Abs
15 IL5
 Immunopathogenesis
 TH1 produces IFN γ which activates the macrophages to

produce TNF, NO and ROS which help to kill the parasite,

on the other hand, if these molecules are excessive tissue
damage will occur.

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 Immunopathogenesis
TH2 will produce IL4 & IL5 activate the B cells

into plasma cells  Abs which prevent RBCs invasion

by the parasite, on the other hand, if excessive Abs
produces  Ag/Ab complex which deposit in tissue 
activate complement tissue damage, also Ag/Ab
complexes stimulate the macrophage to release their
products  more tissue damage
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 RBCs changes
 Cytoadherance and sequestration
 Rosetting
 Deformability

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 Uncomplicated Malaria

 Anemia:

 Hemolysis of parasitized RBCs

 BM suppression by IL1

 Splenomegaly:

 Due to RE hyperplasia

 Jaundice:

 Due to hemolysis

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 Complicated Malaria

 Metabolic Acidosis, Anemia, Hypoglycemia

 CNS Cerebral Malaria
 CVS Algid Malaria
 Lung ARDS
 GIT Vomiting, diarrhea, abdominal pain
 Liver hepatic failure
 Spleen rupture spleen
 Kidneys Black water fever, ARF
 Obstetric- fetal distress, still birth, low birth weight

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 Clinical Manifestation

 Chills, rigor, fever, head ache, diarrhea, hallucinations,

abdominal pain, aches, renal or respiratory symptoms,

jaundice, etc.

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 Febrile Attack (Malaria Paroxysm)
• Periodic febrile episodes alternating with symptom-free
periods

• May be accompanied by splenomegaly, hepatomegaly (slight

jaundice), anemia

• Paroxysms comprises of three successive stage: cold stage, hot

stage and sweating stage

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 cold stage
• feeling of intense cold
• vigorous shivering, rigor
• lasts 15-60 min

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 hot stage
• intense heat
• dry burning skin
• throbbing headache
• lasts 2-6 hours

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 sweating stage
• profuse sweating
• declining temperature
• exhausted, weak  sleep
• lasts 2-4 hours

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 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
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 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.

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 Diagnosis
 Clinical diagnosis and epidemiological grounds
 Blood film for hemoparasite
 RDTs
 PCR

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 Treatment
Chloroquine
 Widespread resistance has now rendered it virtually
useless against P. falciparum
Artemisinin - active against all Plasmodium species
Coartem (artemether-lumefantrine)
Fansider (Pyrimethamine-a sulfonamide) - Effective against
all four human malarias
Primaquine destroys primary and latent hepatic stages of P.
vivax and P. Ovale and thus has great clinical value for
preventing relapses of P. vivax or P. ovale malaria.
Quinine remains a main stay for treating attacks of
chloroquine- and multidrug-resistant P. falciparum malaria

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 Flow chart for the diagnosis and treatment of malaria at health center and hospital level
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 RX

First line treatment for severe malaria due to P. falciparum at

the health center and hospital level is either:

• IV or IM artesunate (preferred) OR

• IM artemether (alternate) OR

• IV/IM quinine infusion (if artesunate is not available)

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 Danger signs of severe malaria
• Altered consciousness (e.g. sleepiness, confusion, drowsiness, coma)
• Prostration, i.e. generalized weakness so that the patient is unable to
walk or sit up without assistance
• Unable to eat or drink
• Repeated vomiting, resulting in inability to retain oral medication,
• Severe dehydration
• Convulsion or recent history of convulsions
• Difficult breathing
• Jaundice (yellowish discoloration of the eyes)
• Anemia (paleness of palms is most reliable symptom in children)
• Hemoglobinuria (cola colored urine)
• Abnormal spontaneous bleeding
• No urine output in the last 24 hours

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 Treatment

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 Coartem® Dosage Schedule

Source: WHO, 2007

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 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

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 Prevention and Control
3.Preventing breeding of mosquitoes by
 environmental modification
 Spraying breeding places with effective larvicides

4. Treatment
 Active infection
 Chemoprophylaxis

5) Health education

6) Blood screening for malaria

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 Yellow fever
Definition

 An acute infectious viral

disease of short duration and

varying severity

Infectious agent

 Yellow fever virus

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 Epidemiology
 Mainly found in West Africa and S America
 Yellow fever occurs in 2 major forms:
1. Jungle (sylvatic) Yellow Fever
 the natural reservoir of the disease in a cycle involving
nonhuman primates and forest mosquitoes
 Man may become incidentally infected on venturing into
jungle areas
2. Urban YF
 transmitted between humans by the Aedes aegypti
mosquito
 Found in southwest Ethiopia (Gambella region)

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 Reservoir
 Urban areas- humans

 Forest areas- Vertebrates other than humans

(mainly monkeys)

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 Mode of transmission

 By the bite of infective Aedes aegypti mosquitoes

Transmission cycle
Jungle YF Urban cycle

Monkey Monkey Human Human

Ae. Africanus Ae.simposni Ae. aegypti

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 Incubation period – 3 - 6 days

Period of communicability

 Blood of patients is infective for mosquitoes shortly before

onset of fever and for the first 3-5 days of illness

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 Signs & Symptoms
Stage One (3-6 days after exposure)

 High fever  Loss of appetite

 Chills  Nausea
 Headache
 Jaundice (yellowing
 Muscle aches of eyes and skin)

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 Signs & Symptoms

Stage Two: Remission

 3-4 days
 Recovery possible

Stage Three: Toxic period

 Vomiting
 Hemorrhage
 Kidney and liver failure
 Delirium, seizures
 Heart damage – Coma
– Death
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 Diagnosis
 History of residence and/or travel to endemic area
 Clinical manifestation
 Serology

Treatment
 No specific treatment

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 Prevention and control

 Active immunization
 Eradication or control of Aedes aegypti mosquitoes in
urban areas
 Notification of the disease to the concerned health
authorities

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 Relapsing Fever

 An acute infectious bacterial disease characterized by

alternating febrile periods (recurrent pyrexial attacks)

 Infectious agent

 Borrelia recurrentis- cause of louse-borne RF

 Borrelia duttoni- cause of tick-borne RF

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 Epidemiology

 Occurs in Asia, eastern Africa (Ethiopia and

Sudan), central Africa and South America

 It occurs in epidemic form when it is spread by lice

and in endemic form when spread by ticks

 It is a disease of poverty, overcrowding, poor

personal hygiene, and infestation with lice

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 Reservoir

 Humans for Borrelia recurrentis

 Wild rodents and soft ticks through transovarian

transmission for tick borne RF

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 CLINICAL FEATURES

SYMPTOMS SIGNS
 Fever  Temperature
 Headaches  Tachycardia
 Arthralgia/ myalgia  Hepatomegaly
 Dry cough  Splenomegaly
 Epistaxis/gum bleeding  Jaundice
 Confusion

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 Mode of transmission
 Acquired by crushing an infected louse so that it
contaminates the bite wound or an abrasion of the skin
Incubation period
5-10 days usually 8 days
Period of communicability
Louse becomes infective 4-5 days after ingestion of
blood from an infected person and remains so for life
(20-40 days)

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 Diagnosis
 Clinical and epidemiological grounds
 Giemsa or Wright stain (blood film)
 Dark field microscopy of fresh blood
Treatment
 Tetracycline N.B: Jarisch-Herxheimer reactions occur
following antibiotic Rx for a number of
 Penicillin
spirochetal and bacterial infections; include
 Doxycycline rigors, fever, and hypotension
 Erythromycin
Prevention and controls
 Personal hygiene
 Delousing
 Health education
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 Epidemic Typhus
 An acute rickettsial disease often
with sudden onset
Infectios agent
 Rickettsia prowazekii
 Obligate intracellular bacteria
 Susceptible to moist heat and dry
heat

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 Epidemiology
 United States
 30 cases in 1975
 Africa
 1997: Burundi 1997
 20,000 cases from Jan. to March

 Most common in people living under unhygienic conditions

 Refugee camps

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 Transmission
 Human body louse
 Pediculus humanus corporis
 Infection acquired by feeding on infected person
 Excrete R. prowazeki in feces at time of feeding

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 Transmission
 Louse feces rubbed into bite or
superficial abrasions
 Inhalation of feces
 Sylvatic typhus
 Flying squirrel
 30 human cases in eastern and central
U.S.

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 Transmission
 Humans or flying squirrel required for life cycle
 Not transferred transovarially
 No person-to-person transmission

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 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
 Except face, palms and soles of feet

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 Diagnosis
 Initial diagnosis
 Clinical signs and history
 Confirmatory diagnosis
 Culture
 Serology((weil-felix agglutination test)
 PCR

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 Treatment
 Chloramphenicol
 Tetracycline
 Doxycycline 200mg
 Response within 48 hrs. usually
 Vaccine
 Developed after WWII
 Not commercially available

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 Prevention and Control
 Treat clothing and bedding
 Chemical control
 Permethrin (0.5%) temephos (2%), popoxur (1%) and carbaryl
(5%)
 Proper hygiene

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 Leishmaniasis

a disease caused by protozoan parasites of the

genus Leishmania

Causative agent is Leishmania parasites

obligate intracellular protozoa

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Leishmaniasis can easily classified clinically as:

1. Visceral leishmaniasis These different forms

2. Cutaneous leishmaniasis of the disease is caused
3. Mucocutaneous leishmaniasis by the different species
of Leishmania
4. Diffuse cutaneous leishmaniasis

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 Epidemiology

 350 million people are at risk in 88 countries around the

world
72 of which are developing countries
In Ethiopia
 Four species of Leishmania is found, namely,
 L. aethiopica,
 L.major
 L. tropica
 L. donovani

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 Visceral leishmaniasis (VL)
 Occurs mainly in arid and semiarid lowlands
 Important endemic foci include
 Gelana focus at lake abaya,
 the segen valley (Aba- Roba focus)
 the Omo river plains and
 the Metema and Humera plains

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 Cutaneous leishmaniasis
♠ Endemic at altitudes between 1400 and 2700 m

♠ Prevalence rates of 5.5 – 40% were reported from villages in

Shewa , Wello and G.Gofa with the highest rate in Ocholo

village in G. Gofa
♠ hyraxes serving as the primary reservoir host

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 Mode of transmission

 Common mode of transmission

 Bite of sand fly
 Uncommon modes of
transmission:
 Congenital transmission
 Blood transfusion

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69 Dereje G.(BSc, MSc in ITD)
 Clinical features and pathology

1. Cutaneous leishmaniasis (CL)

 Relatively benign self-healing skin
lesions (localized or simple CL)
 chronic ulcerated, papular, or nodular
lesion
 lesion is painless, non-tender, non-
pruritic and usually clean
 Sores can leave significant scars and be
disfiguring if they occur on the face
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 Diffuse Cutaneous
Leishmaniasis

• Lesion develop over large areas

of the body
• Scaly, not ulcerated, nodules
• Chronic and painless
• Numerous parasites in lesions
L. aethiopica • Seldom heal despite treatment

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 Con…
3. Mucocutaneous Leishmaniasis
(MCL)
- simple skin lesions that metastasize
to mucosae especially nose and
mouth region.
• variable types and sizes of lesions
• chronic and painless
• ulcerative type
• rapid and extensive mutilation

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 Visceral Leishmaniasis
(Kala-azar or dumdum fever)
 caused by the Leishmania donovani complex,
 L.d. donovani
L.d. infantum
L.d. chagasi
• reticuloendothelial system affected
• spleen, liver, bone marrow, lymph nodes
• onset is generally insidious
• progressive disease
• 75-95% mortality if untreated
73 • death generally within 2 years
 Clinical Presentation
• Incubation period
• generally 2-6 months
• can range 10 days to years
• fever, malaise, weakness, wasting
• Splenomegaly, hepatomegaly,
enlarged lymph nodes
• depressed hematopoiesis
• severe anemia
• leucopenia
• thrombocytopenia

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 Enlarged spleen and liver in an autopsy of an
infant dying of visceral leishmaniasis

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 Diagnosis of CL, MCL, DCL
• suspected because of:
• geographical presence of parasite
• + skin lesion:
• chronic, painless, ‘clean’ ulcer
• nasopharyngeal lesions
• nodular lesions

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 1. Demonstration of parasite
amastigotes (scrapings, biopsy, aspirates)

2. culture from ulcer material

3. Leishmainin test

4. serology??

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Diagnosis visceral leishmaniasis

(i) Demonstration of parasite in tissues by

 light microscopic examination of the stained
specimen,
 culture
 animal inoculation
(ii) Detection of parasite DNA in tissue samples

(iii) immunodiagnosis by detection

Antigen detection
 antibody detection
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 1.Demonstration of the parasite

 Finding of amasigote from aspirate

Aspirate %positive
Spleen …………………………………….95-98%
Bone marrow …………………………….64-86%
Enlarged lymph node …………………About 64%
Buffy coat (India) ………………………….67-99%
Buffy coat (Africa)……………….........About 50%

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 Treatment
Treatment

• Sodium stibogluconate

• Pentamidine isethionate

• Amphotericin B

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 prevention and control

 Early detection by serological diagnosis (VL) and

treatment of infected persons
 Personal protection from sand fly bites
 Vector control by the use of light traps, sticky paper
traps, or residual insecticide spraying of houses
 Destruction of reservoir
 vaccination???

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 Onchocerciasis
 Commonly known as river blindness

 Is a filarial disease caused by

OnchocercaVolvulus

 Not fatal, it does cause disfigurement

& blindness in many cases

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 Epidemiology

 The world’s second leading infectious cause

of blindness

 WHO estimates the global prevalence is 17.7

million, of whom about 270,000 were blind

 Foci are also present in Southern Arabia,
Yemen and in S. & C. America
 Occurs most widely along the courses of fast
running rivers in the forests & Savannah
areas of west and central Africa

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Mode of transmission

 By the bite of infected black flies

(simulium species)

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Life cycle of Onchocerca volvulus

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 Onchocerca volvulus
 Habitat:

 Adult:

 Subcutaneous nodules and in the skin

 Adults can live ~ 8 – 10 years in nodules

 Microfilariae:

 Skin, eye and other organs of the body

 Infective larvae in:

 Gut, mouth parts and muscles of black fly

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Clinical feature
Onchocerciasis
 Acute onchocerciasis:
 Itchy (pruritic)
 Erythematous
 Papular rash with thickening of
the skin

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Clinical feature
 Chronic onchocerciasis:
 Elephant or lizard skin Hanging groin

- Leopard skin river blindness

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Diagnosis
 Mf in skin snips

Skin biopsy

 Mf in urine, blood & most body fluids (in heavy infection)

 Wet mount preparation Staining

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Treatment

 Ivermectin:

 Paralysis of worms

 Reduces the microfilarial load

 Surgical Care:

 Nodulectomy

 Removes adult worms

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Prevention and control

 Destruction of vector (Larvae of Simulium)

 Personal protection (Avoiding Simulium bites)

 Treatment of communities

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Any