VECTOR-BORNE DISEASES

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• Vectors are living organisms that can
transmit infectious diseases between
humans or from animals to humans
• Vectors includes insects (mosquitoes,
ticks, fleas)
• Many of these vectors are bloodsucking
insects
• They ingest MOs during a blood meal
• Later inject it them into a new host
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 1. Malaria

 Definition :An acute infection of the blood

caused by protozoa of the genus
plasmodium.
 protozoan parasites-genus Plasmodium
 five plasmodium species develop in humans
 P. falciparum (life-threatening malaria)
 P. vivax
 P. ovale
 P. malariae
 P. knowlezi
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• the commonest causes of Malaria in Ethiopia
are - P. Falciparum and P. vivax
• P.falciparum is the commonest species
throughout the tropics
• up to 80–90% cases in sub-Saharan
African are due to P. falciparum

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• Reservoir—Humans; except P.malariae,
the African apes and some South American
monkeys
• Mode of transmission—Bite of an
infective female Anopheles mosquito
• Most species feed at night; some at dusk
or in the early morning
• transfusion of blood and occasionally from
mother to fetus
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• Incubation periods
– 7 –14 days for P. falciparum
– 12–18 days for P. vivax and P. ovale
– 7 – 40 days for P. malariae

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 Period of communicability
• Humans infective-gametocytes in the blood
– varies with parasite species and with response
to therapy
• Untreated or insufficiently treated patients
– several years in malariae
– up to 5 years in vivax
– generally not more than 1 year in falciparum
malaria
• the mosquito remains infective for life
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 Clinical Manifestations of uncomplicated malaria

• Fever, Chills, Rigors, Sweating

• Severe Headache, Generalized body and
joint pain
• Nausea and or vomiting, Loss of appetite,
Abdominal pain (especially in children)
• Irritability and refusal to feed (in infants), flu-
like symptoms, fever above 38°C
• Splenomegaly, Pallor (lack of colour on the
skin)
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 Diagnosis

• Clinical manifestation and epidemiological

grounds
• Blood film
• White blood cell count
• Blood culture to rule out sepsis
• Chest X-ray to rule out pneumonia.

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 Treatment

• First line- P.falciparum or mixed–

uncomplicated
– Artemether + Lumefantrine, 20mg + 120mg in a
fixed dose combination
• Treatment of uncomplicated P. Vivax malaia
– First line Chloroquine phosphate, 1 g, then 500
mg in 6 hours followed by 500 mg p.o QD for 2
days or
– 1 g at 0 and 24 hrs followed by 0.5 g at 48 hrs P.O
– Followed by Primaquine, 15mg base P.O.QD for
14 days
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 Clinical features of complicated malaria

• Inability to take in fluids (or breast milk in

children)
• Circulatory collapse or shock
• Dark or 'cola-coloured' urine
• Spontaneous unexplained heavy bleeding
• Difficulty in breathing
• Generalized weakness, inability to walk or sit
without assistance
• Sleepiness, change of behaviour
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• Repeated generalized convulsions
• Altered consciousness
• confusion, delirium, convulsions, coma
• Tachypnoea, respiratory distress and/or cyanosis
• Oliguria, renal failure
• repeated vomiting
• Hypoglycemia
• severe anaemia
• Hyperpyrexia (axillary temperature >38.5°C)
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 Treatment
• Administer drugs parenterally to ensure
adequate blood-serum concentrations
• First line
– Artesunate: 2.4mg/Kg IV or IM given on
admission (time = 0), then repeat at 12 hours,
and 24 hours, then once a day for up to 5 days

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 Prevention and control measures
• Rapid diagnosis and effective case management
– important in reducing malaria transmission.
• Insecticide-treated mosquito nets (ITN)
• Permethrin-sprayed blankets, sheets
• Permethrin-treated outer clothing worn in the
evening or in bed
• Indoor residual spraying of insecticide (“house
spraying”)
• Environmental control
• Chemoprophylaxis
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 2. lymphatic filariasis

• A disease caused by the reaction of the

body to worms in the lymphatic system
• Agents
– Wuchereria bancrofti
– Brugia malayi
– Brugia timori

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• Reservoir—Humans are definitive hosts
• Mode of transmission-by bite of
mosquito harboring infective larvae
• Incubation period-one month
• Period of communicability—Not directly
transmitted from person to person
– Humans may infect mosquitoes when
microfilaria are present in the peripheral blood

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 Clinical Manifestation
Three phases may be distinguished
A. Acute phase
• Starts within a few months after infection
• Inflamatory manifestations-due to hypersensitivity
reaction
• toxic products of living or dead worm
• Lymphadenopathy(neck and axilla)
• Fever, chills
• Eosinophilia
• In this stage microfilariae are not demonstrable in the
peripheral blood because the worms are not yet mature.
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 B. Sub--acute phase

• ƒThis occurs after about one year

• microfilaria-peripheral blood
• ƒ Reactions to the adult worms cause
attacks of fever with lymphangitis or
Epididymitis
• Recurrent attacks lead to hydrocele
• ƒ Lesions associated with
hypereosinophilia
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C. Chronic phase
• ƒ lymph vessels and glands-obstructed
• as a result lymph edema develops
• Lymph edema mostly in legs or scrotum
(elephantiasis)
• Hard, thick, rough and fissured skin
• worms died, no microfilariae in the blood

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Diagnosis
• ƒ Obstructive signs with history and
residence in endemic areas
• ƒ microfilariae in the peripheral blood
(blood film)

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Treatment
I. Diethyl carbamazin Citrate (DEC) 8 to 10
mg/kg for two to three weeks for filarial
infections
II. Ivermectin(200 mcg/kg), albendazole
III. Doxycycline
IV. Refer the patient for surgical treatment of
hydrocele
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 Prevention and control

• Reducing the vector population

• Mass and selective treatment
• Personal protection against mosquito bite

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 Flea-Borne Diseases
Endemic Typhus(Flea-borne typhus)
• resembles louse-borne typhus, but is
milder
Infectious agent
• Rickettsia typhi
Reservoir— Rats and mice

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Mode of transmission—Infective rat fleas defecate
rickettsiae while sucking blood
• this contaminates the bite site and other fresh skin
wounds
Incubation period—From 1 to 2 weeks, commonly
12 days.
Period of communicability
• Not directly transmitted from person to person
• Once infected, fleas remain for life (up to 1 year)
• transfer it to their progeny
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 Clinical Manifestation

• Prodromal symptoms of headache,

myalgia, arthralgia, nausea, and malaise
developing 1 to 3 days before the abrupt
onset of chills and fever
• Rash is present in only 13% of patients
• Pulmonary involvement: non-productive
cough and pneumonia

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Diagnosis
• Epidemiological ground
• Weilfelix agglutination test (Serology)

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 Treatment
1. Doxycycline-adults 100 mg orally twice a
day or
2. Chloramphenicol 50 mg/kg per day orally in
four divided doses for seven days
Prevention and control
1. Destroy rats from burrows and harborages.
2. Use insecticides to abolish flea
3. Treatment of patients

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 Louse-Borne Diseases

A. Epidemic Typhus
• is a potentially lethal, louse-borne disease
caused by Rickettsia prowazekii
• The principal vectors are Pediculus humanus
corporis (the body louse) and P. humanus
capitis (the head louse)
Mechanisms of transmission
• During a blood meal, the louse defecates
highly infective feces at the site of its feeding
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• skin irritation at the site of a louse bite
• Rickettsiae in feces then introduced into
abraded skin
• Lice feces may remain infectious for as
long as 100 days
• Transmission occur from sharing clothes
or transfer of feces

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 Symptoms
• The majority experience the abrupt onset
of fever and severe headache
• Cough
• Tachypnea
• Muscle tenderness
• Abdominal tenderness
• Arthralgias

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Diagnosis
• in a suspected epidemic laboratory testing
to confirm the diagnosis for the first cases
• after confirmation clinical
• Serological techniques are used

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TREATMENT
• The drug of choice is doxycycline
• tetracycline and chloramphenicol are
effective agents for epidemic typhus

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 PREVENTION

• Delousing — Eradication of human

infestation with lice using permethrin
powder 0.5%
• Antibiotic prophylaxis-
chloramphenicol or tetracycline
• Vaccination
• Clothing and bedding that have not
been used should also be treated

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B. Relapsing Fever
• Relapsing fever occurs in two major forms:
tick-borne (TBRF) and louse-borne (LBRF)
• caused by spirochetes of the genus
Borrelia
• characterized by recurrent episodes of
fever that accompanies spirochetemia

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• louse-borne relapsing fever is caused only by
B. recurrentis
• TBRF caused by –B. duttoni other causes
possible
• The vector of B. recurrentis is the body louse,
which only feeds on humans
• Humans are probably the only reservoir of B.
recurrentis
• B. recurrentis is currently endemic in Ethiopia
and Sudan
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• The highlands region of Ethiopia may have
hundreds to thousands of cases of LBRF
annually
• The highest incidence during the rainy
season when the poor gather together in
shelters
• Lice move from one person to another,

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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

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 CLINICAL MANIFESTATIONS
• presents with the sudden onset of fever,
punctuated by an intervening afebrile period
• The temperature may be as high as 43ºC and is
usually above 39ºC
• first episode of fever is unremitting for three to six
days
• After 4-5 days the temperature comes down, the
patient stays free for 8-12 days and then a relapse
follows with the same signs but less intense.
• In untreated cases there may be up to ten relapses.

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 Diagnosis
• Clinical and epidemiological grounds
• Giemsa or Wright stain (blood film)
• Dark field microscopy of fresh blood.
TREATMENT —
– Penicillins and tetracyclines are the antibiotics
of choice

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 PREVENTION AND CONTROL
1. Control of vectors (louse)
2. Personal hygiene
3. Health education about hygiene and
modes of disease transmission
4. Delousing of patient’s clothes and his/her
family
5. Chemotherapy of cases and
Chemoprophylaxis for contacts
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 Snail-Borne Diseases

Schistosomiasis
• referred to as “bilharziasis”
• parasitic blood fluke (trematode) infection
• adult worms living within mesenteric and
bladder veins over a lifespan of many years
• Fluke=a parasitic flatworm typically having
suckers and hooks for attachment to the
host

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• Three major species produce infection in
humans
– S. mansoni and S. japonicum provoke
intestinal and hepatic complications
– S. haematobium predominantly leads to renal
and bladder sequelae

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• Reservoir-The principal reservoir for S.
mansoni and S. hematobium man
• S. japonicum-dog, cat, pig, cattle are hosts
• Mode of transmission
– acquired from water containing free swimming
larval forms (cercariae)

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 CLINICAL MANIFESTATION

• The stages of schistosomiasis are:

A. invasion
B. maturation
C. established infection and
D. late stage.

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 A. Invasion stage
• 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.

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 B. Maturation
• Schistosoma mature in the liver.
• Fever, eosinophilia, abdominal pain and
transient generalized urticaria (known as
katayama syndrome)
• Worms descend the portal vein. S. manson;
migrates to mesenteric veins in the intestinal
wall and S. haematobium to bladder plexus.
• This stage may be diagnosed as clinical malaria
or may pass unnoticed.
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 C. Established infection
• 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.
• The inflammatory reaction, resulting in fibrosis, causes signs and
symptoms of schistosomiasis.
• Sign of colitis with bloody diarrhea and cramps in S. mansoni
infection. Terminal haematuria and dysuria in S. haematobium
infection.
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 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, eosophageal varices and bleeding.
• In the lungs fibrosis results in pulmonary hypertension,
which leads to congestive cardiac failure.
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 Diagnosis
• Demonstration of ova in urine or feces,
• Biopsy of urine and feces are repeatedly
negative (rectal snip, liver biopsy, bladder
biopsy).

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 Treatment
• Praziquantel and oxamniquine are the drugs
of choice
• But in Africa praziquantel is best because of
resistance strain of oxamniquine.

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 PREVENTION

• Treatment of cases
• Intermittent irrigation
• Drainage of water bodies
• Clearing of vegetation in water bodies to deprive snails of
food and resting place
• Straightening and deepening margins of water bodies
• Educating the public about the mode of transmission and
ways of prevention
• Proper disposal of human feces and urine
• Avoid swimming in water bodies known to have the infection
• Use rubber boots to prevent exposure to contaminated water.

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 Leshmaniasis

• Vector-borne disease caused by genus

leishmania, intracellular protozoa
• Vectors – Phlebotomus and Lutzomyia
• Zoonotic form, dogs as main reservoir in the
Mediterranean basin, China, the Middle East,
and South-America; cause is L. infantum
• The anthroponotic form, humans as reservoir,
is caused by L. donovani ; prevalent in East
Africa and the Indian subcontinent
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Major forms:
• Visceral– L. donovani, L. infantum
• Cutaneous– L. aetopica, L.major, L.
tropica
• Mucocutaneous-- L. aetopica

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 Transmission VL
• Female sand flies (Phlebotomus and
Lutzomiya Spp.) get infected after sucking
blood from infected reservoir eg. human or
other mammals
• Amastigotes transform to promastigotes in
sand fly gut
• promastigotes are regurgitated and
injected into the skin during subsequent
blood meal
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 Epidemiology in Ethiopia

• Lowlands of Ethiopia with varying endemicity

– N.West. - Metema and Humera, Wolkayit,
Libo/Fogera
– N.East – Ethio-Djibouti Awash Valley
– S. West –Dawa, Genale, Woito, Konso, Omo,
Gambella Sudan border
• Main risk factor - population migration
• VL cause - by species of the Leshmania
donovani complex - L. donovani and L.
Infantum
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 Visceral leishmaniasis

Presentation
• Kala-azar (Black fever in Hindu)
• Fever, night sweats, weakness ,weight loss
• Cachexia (Severe malnutrition, weakness,
and muscle wasting resulting from a chronic
disease),Pallor
• Non tender, soft massive splenomegaly
• Hepatomegaly + LAP

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• Darkening of face/ashen grey appearance
• Bleeding 20 to thrombocytopenia
• Susceptibility for 20 infection
• Pancytopenia (Anemia, Thrombocytopenia,
Leukopenia, Neutropenia)
• Marked eosinopenia
• Hypergammaglobulinemia
• Hypoalbuminemia
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 Diagnosis

• Gold-standard: Demonstration of
amastigotes in tissue aspirates
• Diagnostic sensitivity – Spleen - > 95%;
Bone marrow  70%, Lymph nodes 
58%
• Detection of Rk 39- Sn 72%, Sp 82%
• Culture

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 Treatment

• Sodium stibogluconate (SSG) 20mg/kg

iv/im for 30 days
• Alternative: Amphotericin B 1mg/kg every
other day for 30 days/total 15 doses.
• AmBisome 4mg/kg for 5-7 doses: 1-5days,
10th, 14th

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 Prevention and control
1. The avoidance of outdoor activities
2. The use of mechanical barriers such as
screens and bed nets
3. Wearing of protective clothing
4. Application of insect repellent
5. Treatment of cases
6. Vector control and elimination of reservoir
host (e.g. domestic dogs)
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 Thank You

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