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Public Health

Pharmacy
Students

2022-2023
 Lecture 2

Maisra Mohammed El-Bouseary

Lecturer of Microbiology
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ARTHROPOD- BORNE –DISEASES

 ARTHROPOD - BORNE – DISEASES
Arthropods account for over 85 % of all known animal species,
and they are the most important disease vectors.
Vector-borne diseases are prevalent in the tropics and
subtropics and are relatively rare in temperate zones, although
climate change could create conditions suitable for outbreaks
of diseases such as Lyme disease,

Rocky Mountain spotted fever, malaria, dengue fever, and viral

encephalitis in temperate regions.

Arthropod-borne diseases include viral, bacterial, protozoal and

rickettsial diseases
A) Arthropod-borne VIRAL disease
They are caused by group of viruses called
arboviruses.
Each is specific for a viral disease.
The term arboviruses (arthropod borne = arboviruses)
is used to describe viruses from various families which
are transmitted via vertebrates arthropods.
Many are transmitted by means of an infected, blood-
sucking, arthropod vector.
Others may be transmitted by inhalation, or
conjunctival contact with infected excretions, or by
direct contact with infected animal.
There are several types of life cycles, but many
arboviruses have a sylvatic cycle while some also have an
urban cycle.
1. Urban cycle; the virus cycles between man and an
arthropod.
2. Sylvatic cycle (jungle cycle); the virus cycles between
an arthropod and a mammalian host. Man is a dead-end
host infected by the arthropod

Urban cycle Sylvatic cycle

(jungle cycle)
 Recovery involves the cell-mediated immune system; the
arboviruses are generally good inducers of interferon,
which may partially explain early influenza-like symptoms
common to so many of these viruses (fever, headache,
fatigue and myalgia).
Antibody can be important in resistance to arboviruses
reinfection and limiting disease.
Diagnosis is difficult because many other agents cause
similar symptoms.
Arboviruses infection is usually confirmed by
immunological methods (complement fixation, ELISA,
immune fluorescence assay, etc) or by PCR of the viral
nucleic acid.
Diseases caused by arboviruses include encephalitis,
febrile diseases (sometimes with an associated rash),
and hemorrhagic fevers.
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WEST NILE ENCEPHALITIS

 1- West Nile encephalitis (Flavivirus family)
West Nile virus is found in Africa, west Asia/ Eastern
Europe, America and Middle East. The natural reservoir of
the virus is birds and the virus is transmitted by culex
mosquitoes (most likely by Culex pipiens, and Culex
quinquefasciatus.
The incubation period is 3 to 14 days.
Epidemics occur usually in spring and summer. The spread
of the virus is likely to be due to migration patterns of birds.
Most (75%) of people who become infected show none
specific signs and develop protective immunity. symptoms
are flu-like (fever, headache and general malaise)
Sometimes there is lymphadenopathy and also rash
In less than 1% of patients, the infection is
life-threatening as a result of
encephalitis: The symptoms are high
fever, headache, and stiff neck. These are
followed by confusion, coma, tremors,
convulsions, paralysis.
In very severe cases, there are a respiratory
failure and death.
West Nile poliomyelitis, similar to that
caused by the poliovirus, due to the virus
causes flaccid paralysis (an inflammation of
the spinal cord).
In Egypt, two encephalitis
arboviruses are known:
- West Nile virus
- Sindbis virus

Transmitted by culex, and the disease is

usually mild, and may pass unnoticed
(inapparent infection).
Treatment is usually by supportive
therapy, although ribavirin may be
effective.
YELLOW FEVER
 2- Yellow fever:
Epidemiology:
Yellow fever (from jaundice that affects some patients).
The causative agent is yellow fever virus and is
transmitted by biting of mosquitoes.

There are two main types of transmission cycles.

1- Sylvatic (or jungle) yellow fever: In tropical
rainforests, yellow fever occurs in monkeys (the
reservoir) and can be transmitted to man by biting of
mosquito Aedes africanus.
2- Urban yellow fever: mosquitoes Aedes aegypti
vector transmit the virus from man (the reservoir) to
another one.
Clinical findings:
Infection can cause severe illness and death. Up to
50% of severely affected persons without treatment
will die from yellow fever.
After incubation period in the body for 3 to 6
days, infection occurs in one or two phases.
a - First acute phase; fever, muscle pain,
headache, loss of appetite, and nausea or
vomiting. Symptoms disappear after 3 to 4 days.
b - Second phase, is more toxic, in which 15% of
patients enter within 24 hours of the initial
remission.
It characterized by;
-High fever returns, rapidly develop hepatitis
(jaundice) and abdominal pain with vomiting.

-Bleeding can occur from the mouth, nose, eyes

or stomach, the blood appears in the vomit and
faeces.

-Kidney function deteriorates. Half of the

patients who enter the toxic phase die within 10 to
14 days, the rest recover without significant
organ damage.
Clinical findings of Yellow fever
Diagnosis:
-Diagnosis, especially during the early stages is
difficult. It can be confused with malaria, typhoid,
dengue, and hepatitis as well as poisoning.
Rising of IgM
-signs titer with epidemiology and clinical
is effective.

Treatment and Prevention:

There is no specific treatment for yellow fever, only
supportive care to treat dehydration and fever.
Associated bacterial infections can be treated with
antibiotics. Supportive care may improve outcomes for
seriously ill patients, but it is rarely available in poorer
areas.
A- Vaccination: By 17 D vaccine made of
attenuated 17 D strain (one dose SC). It gives
absolute protection after about 10 days, and for
at least 10 years to prevent outbreaks throughout
endemic regions.
Vaccination coverage must reach at least 60% to
80% of a population at risk.
Few countries in Africa currently have this level of
coverage.
B- International Sanitary Regulations:
a- A valid international vaccination certificate is
required for
- Travelers between endemic and receptive areas
- Crew of aircrafts using airports of endemic areas,
and the employees

Validity of Certificate begins 10 days after date of

vaccination, and lasts for 10 years.
But if no certificate is available: the traveler is isolated
for 6 days form the date of leaving the infected area.
If the traveler arrives before 10 days of vaccination
i.e. the certificate is not valid yet, traveler is isolated
until the certificate becomes valid, with a maximum of
6 days.
b- Disinfection of any aircraft leaving and infected
area for a receptive area, shortly before departure, and
also on arrival if necessary
c- Quarantine of imported monkeys at receptive
areas.
In Egypt protection against introduction of yellow
fever takes place through
- Strict quarantine measures.
- The developed immunity against West Nile fever
gives cross immunity with yellow fever.

C- Mosquito control: The risk of yellow fever

transmission in urban areas can be reduced by
eliminating potential mosquito breeding. Concerning
Jungle yellow fever Mosquito control is impossible
DENGUE FEVER
 3- Dengue fever:
Dengue fever is caused by dengue virus. The
hosts are monkeys and man. Mosquito Aedes
aegypti is the vector.
The four serotypes (1 - 4) of dengue virus spread
worldwide with yearly outbreak in Asia, Africa and
Americas.
The virus has an urban and a jungle cycle.
The incubation period is 4 -7 days; however its
extrinsic incubatory period (in mosquito) is 4 –
14 days.
There are two types of dengue fever:
A- Classical dengue fever
It is characterized by acute onset of flu -like
signs as high-grade fever ,frontal headache,
myalgia, arthralgia, and often a maculo-papular
rash and change in taste sensation.
Symptoms tend to be milder in children than in
adults, and may be clinically indistinguishable
from rubella, measles or influenza.
The acute phase may last up to one week,
with a prolonged convalescence characterized
by weakness, malaise, and anorexia.
Encephalitis is reported in some cases.
Dengue fever rash
B- Dengue Hemorrhagic Fever (DHF)
DHF is potentially a deadly complication of dengue.
It appears to be an immuno complex of infection of a
person who has already has immunity to one serotype
of dengue virus with a virus of another serotype.
The increases vascular permeability is a major
problem results in subcutaneous hemorrhage e.g.in the
upper arms.
Disease is more severe in children and the presence
of maternal antibody in infants may result in DHF even
from a first infection.
DHF may resemble classical dengue in the first few
days (2 to 7 days) of illness. However, the patient
becomes restless and lethargic before development of
hemorrhagic manifestations
A child with dengue
hemorrhagic fever or dengue
shock syndrome may present
severely hypotensive with
disseminated intravascular
coagulation

Dengue hemorrhagic fever

SANDFLY FEVER
 4- Sandfly fever
Sandfly fever appears epidemically in
tropics and subtropics; Sandfly virus is
transmitted by biting from the Sandfly
vector Phlebotomus papatasii.
Recovery from the disease is followed
by a long lasting immunity.
Sandfly bites
B- ARTHROPOD- BORN BACTERIAL
DISEASE
Several bacterial arthropod born diseases
are known.

Relapsing fever :
Relapsing fever is an infection caused by
sprocheate borrelia and the vector is louse
or tick bites.
a) Tick-borne relapsing fever
Tick-borne relapsing fever is caused by Borrelia
duttoni, B. hermsii, and B. parkerii.
The Reservoir is rodents.
The soft- tick vector, genus can transmit relapsing
fever spirochetes to humans through their saliva
while feeding, through secretion of infectious fluids
from their coxal glands and in faeces.
Clinical findings:
Similar to that of lice-borne relapsing, except, for
more multiple episodes of fever (10 or more) occur
and each may last up to 3 days. Individuals may be
free of fever for up to 2 weeks before it returns
b) Louse-borne relapsing fever
It caused by Borrelia recurrentis. The vector is lice
(Pediculus humanus) acquires the borrelia when feed
on infected humans reservoir.
Then the sprocheate multiply in the gut of the louse
and gains access to invade the bloodstream after
crushing the louse or scratching the area while louse
is feeding on an uninfected human.
No animal reservoir exists. Neither the louse bites
nor faeces cause infection.
Clinical findings:
After incubation period of 3-12 days sudden fever
occurs. That lasts 3-6 days and is usually followed by a
single, milder episode (4 or 5 relapses). Each relapse
consists of shaking chills, followed by intense
sweating, falling temperature & low blood pressure
Diagnosis:
Clinical picture not diagnostic in both types,
but suggestive during epidemics. Borrelia is seen
by dark field illumination in a blood smear as
large light coiled with straight ends
spirochaete. It is stained with Giemsa or Field's
stain and by prolonged Gram staining (Gram
negative).
Treatment:
Relapsing Fever is easily treated with 1-2
weeks of antibiotics, most often tetracycline,
doxycycline, erythromycin, or penicillin.
Prevention and Control:
No vaccination and personal hygiene and
use lice killer are very important.
 Wearing proper clothing will help prevent
control infection
 Eradication of ticks and rodents
 Limit tick bites by using insect repellent
 Use rodent-proof buildings in areas where
the disease is known to occur-Identify and
remove any rodent nesting.
C- ARTHROPOD-BORN PROTOZOAL
DISEASES
The arthropod –born protozoal diseases
including trypanosomiasis filariasis and
leishmaniasis were discussed in the course
of parasitology, second year
D-ARTHROPOD- BORN RICKETTSIAL
DISEASES
Rickettsia is non-motile, Gram-negative,
non-spore forming and highly pleomorphic
bacteria that can present as cocci, rods or
thread-like.
It is obligate intracellular parasites and
cannot live in artificial nutrient media but
grown either in tissue or embryo cultures
except Rochalimeae quintana (Trench
fever) which can grow on blood agar
under 5% C0 .
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All rickettsiae are transmitted to humans
through arthropods vector (ticks, fleas, and lice)
from animal or human reservoir except Coxiella
burnetii (Q fever) which is transmitted by
inhalation of aerosols of cattle milk
(Occupational zoonoses).
All rickettsiae cause skin rash- fever - headache
and malaise.
Rash is due to hyperplasia and inflammation of
vascular epithelium, thrombosis is small blood
vessels, EXCEPT Coxiella burnetii which
cause pneumonia and low fever.
Rickettsiae are classified on the basis of
clinical features and immuno-logical
characters into THREE groups
 Spotted fever

Typhus
 Others

There in no cross immunity between different

diseases.
Diseases causes by rickettsiae include:
Mammalian Arthropode
Disease M.O.
reservoir vector
1) Spotted fever gp.
a) Rocky mountain
Rickettsia rickettsii Rodents Tick
Spotted fever

b) Mediterranean sea
R.conorii Rodents Tick
fever

c) Rickettsial pox R. akari Mice Mite

Mammalian Arthropode
Disease M.O.
reservoir vector
2) Typhus gp.
a) Epidemic typhus R. prowazekii Human Louse
b) Endemic typhus
R. typhi Rodents Flea
(murine fever)

c) Scrub typhus (night

R. tsutsu-gamushi Rodents Mite
fever)
 Mammalian Arthropode
Disease M.O.
reservoir vector
3) others
Non
a) Q fever Coziella burnetii Cattle, sheep
(inhalation)

b) Trench fever Rochalimeas quintana Human Louse

Typhus group rickettsiae usually grow in host
cell cytoplasm. While, spotted fever group
rickettsiae usually grow in host cell nucleus

Diagnosis:
Ascertaining the place and the nature of potential
exposures is particularly important for accurate
diagnosis, as many rickettsial diseases have
strong geographic links or are associated with
exposure to specific animal reservoir species
or arthropod vectors
The diagnosis of rickettsial disease is based
on two or more of the following:
1)Compatible clinical symptoms and
epidemiologic history.
2)The development of specific convalescent-
phase antibodies which is reactive with a given
pathogen or antigenic group.
3)A positive polymerase chain reaction test result.
4)Immunohistologic detection of a microorganism.
5) Isolation of a rickettsial agent.
The following laboratory diagnostic tests are
currently used

1) Weil - Felix reaction (Non specific):

Agglutination reaction between serum of patient and
certain proteus strains (OX-2, OX-19 and OX -K) as an
antigen (negative in case of Q fever and rickettsial
pox).

2) The specific rickettsial antigen of each disease to

detect the corresponding antibody by using
agglutination reaction, complement fixation test or
immunofluorscent test.
Treatment:
Treatments for most rickettsial illnesses are similar
and include antibiotics e.g. chloramphenicol or
tetracycline and supportive care.
Treatment should be initiated on the basis of
epidemiologic and clinical clues, without waiting
for laboratory confirmation.
Prevention and Control:
Cox vaccine (formularized specific rickettsial
antigen) is available.
Tetracycline and chloramphenicol may be used as
prophylaxis.
General Control measures for vector-borne diseases are
important because most are zoonoses that are maintained
in nature in cycles involving wild animals and are not
amenable to eradication. Therefore, control methods
generally focus on targeting the arthropod vector.
These include undertaking personal protective measures by
establishing physical barriers such as house screens and
bed nets; wearing appropriate clothing (boots, apparel that
overlap the upper garments, head nets, etc.); and using
insect repellents.
Environmental modification to eliminate specific breeding
areas, or chemical or biological control measures to kill
arthropod larvae or adults may also be undertaken.
Areas such as ports and airports should be rigidly
monitored, with control measures utilized to prevent
Thanks