The document discusses various arthropod-borne diseases, highlighting key diseases such as yellow fever, dengue fever, and rift valley fever. It outlines their causative agents, modes of transmission, clinical features, and prevention methods, including vaccination and vector control. Additionally, it details the importance of environmental sanitation and health education to mitigate risks associated with these diseases.

1. ARTHROPOD BORNE DISEASES
Dr. Dalia El-Shafei
Assistant Professor, Community Medicine
Department, Zagazig University

2. Arthropods form a major group of disease
vectors with mosquitoes, flies, sand flies, lice,
fleas, ticks and mites transmitting a huge
number of diseases.
Many such vectors are haematophagous,
which feed on blood at some or all stages of
their lives.

3. Viral
Yellow fever
Encephalitis
Dengue
fever
Rift valley
fever
Bacterial
Plague
Parasitic
Malaria
Filariasis
Leishmanias
is
Rickettsi
al
Typhus
Q fever
Spirochet
al
Relapsing
fever

4. ARTHROPOD-BORNE VIRAL
HEMORRHAGIC DISEASES

5. Acute febrile diseases with extensive external
& internal hemorrhage, usually serious & may
be associated with shock & liver damage with
high case fatality.
The most important of these fevers are Yellow
fever, Dengue fever, Rift valley fever &
West Nile fever.

6. YELLOW FEVER

7. A communicable arthropod-borne viral
hemorrhagic quarantinable acute disease of
short duration & varying severity.
Causative agent: Yellow fever virus.

8. Endemic in Africa & South America in zone
between 15° north & 100° south latitude of equator
(yellow fever belt).

9. HOW EGYPT IS PROTECTED FROM
YELLOW FEVER:
Absence of yellow fever in Egypt & its rarity
in other areas such as Eastern Africa despite
wide spread of vector aedes Egypti may be
due to cross immunity from other flavi
virus (e.g. dengue, west Nile, Japanese
encephalitis) in population which may be
providing an (ecological barrier).

10. RESERVOIR:
Sylvatic or Jungle yellow fever: main reservoir in forest area
is vertebrates other than human mainly monkeys & vector is
forest mosquitoes (haemagogus species). Human has no
essential role in transmission of yellow fever.
{Sylvatic is a scientific term referring to diseases or pathogens
affecting only wild (sylvan means forest-dwelling) animals.
The word "sylvatic" is also simply a synonym for "sylvan" = "of
the forest“}.
Urban yellow fever: reservoir is human & vector is Aedes
aegypti mosquitoes.

12. PERIOD OF COMMUNICABILITY:
No man-to-man transmission.
Blood of man is infective to mosquito shortly during
late IP & during first 3-5 days of disease.
In mosquitoes after biting an infected person there is
9-12 days extrinsic IP, then the mosquito becomes
infective all over its life.
There is also trans-ovarian transmission which may
contribute to maintenance of infection.

13. Mode of transmission:
Urban yellow fever: bite of infective female Aedes
aegypti mosquitoes.
Sylvatic or jungle yellow fever: bite of several
species of genus Haemagogus.
IP: 3-I0 days (6 days in international health
regulation).

14. Virus
Transmission
Zoonotic virus
flaviviridea

15. SUSCEPTIBILITY & RESISTANCE:
1-Age & sex: all ages & both sexes are susceptible.
2.Immunity: infection is followed by absolute
immunity, 2nd attacks are unknown. Transient
passive immunity to inborn infant of immune
mother occurs for up to 6 ms.
3.Occupation: Woodcutter, Hunter.

16. IP
3- 10 days
Symptoms
Influenza like
Hepatic
Hemorrhagic
illness
Death
20-50%

17. CLINICAL FEATURES:
- Mild form: sudden onset, FHMA, chills, muscle pain,
prostration, nausea & vomiting.
- Faget sign: slow pulse out of proportion of elevated
temperature.
- Jaundice is moderate early in disease & intensified
later.
- Albuminuria or anuria may occur, leucopenia.
- Most of the manifestations resolve after 5-7 days.
- After a brief remission of hours to a day some cases
progress to severe form (hemorrhagic symptoms
including epistaxis, gingival bleeding, haematemesis
(coffee ground or black) melena, liver & renal failure).
- Fatality rate of jaundiced cases may reach 20-50%.

19. DIAGNOSIS:
1. Isolation of virus from blood by inoculation of
suckling mice, mosquito or cell culture.
2. ELISA “viral antigen in blood”.
3. PCR “viral genome in blood & liver tissue”.
4. Serologic diagnosis “specific IgM in early sera or
rise in titre of specific antibodies”.

20. Prevention & control
Vaccine
17 D vaccine
Personal protective
measures

21. PREVENTION:
General:
1) Environmental sanitation:
A) Eradication or control of Aedes Aegypti:
i. Anti-larval & anti-pupal measures
ii. Anti-adult measures
iii. Jungle mosquitoes “impractical”.
B) Human protection against mosquitoes: e.g.
protective clothing, bed nets, repellents.
2) Health education: modes of transmission.

22. Individual measures for control
of mosquito bite

23. Specific:
1) Immunization:
a) Active Immunization: “most effective preventive measure”
- 17 D vaccine:
■ Live attenuated vaccine “non virulent strain cultivated on chick
embryo & subsequently freeze dried”. Vaccine is stored at -25°C.
■ Single dose, 0.5ml, S.C. injection.
■ 99% immunity: International health regulation considered vaccine
effectiveness to start after 10days & persists for 10 years & then re-
immunization is required.
■ No or minimal reaction “1st 4 ms of life....vaccine associated
encephalitis”.
■ Given to:
- International travelers coming from or going to endemic countries.
- Since 1989 WHO has recommended that at risk countries in Africa
that fall in the endemic belt should incorporate it into their routine
childhood immunization program after 6 month.

24. Dakar vaccine:
- Live attenuated neurotropic virus.
- It is produced in mouse brain & administered by
cutaneous scarification.
- It is not approved by WHO for international use as it
leads to encephalitis.

27. International measures:
It is one of quarantinable diseases & following
measures should be done to prevent introduction of
yellow fever from endemic area (Yellow Fever belt)
into receptive area (areas free of yellow fever, but the
vector is present & population is susceptible e.g. in
Egypt):
* Notification within 24 hs by governments to WHO.

28. * VALID VACCINATION CERTIFICATE:
a. Is required from all international travelers including children
coming from or going to endemic areas "Yellow Fever belt".
b. Validity starts 10 days after primo-vaccination & lasts for 10 ys.
c. Validity starts on same day after re-vaccination & lasts for 10 ys.
d. If no certificate is available: traveler is isolated for 6 days from
date of leaving endemic area.
e. If traveler arrives before 10 days of vaccination, i.e. certificate is
not valid yet: traveler is isolated until certificate becomes valid or
until end of international IP calculated from day of leaving last
endemic area.
f. Traveler is quarantined in mosquito-proof accommodation in
airport.
g. This certificate is required by many countries including Egypt.

29.  Disinfection of any aircraft leaving an endemic area for
receptive area, by aerosol spray of suitable insecticide,
shortly before departure and also on arrival.
 Quarantine of imported monkeys.

32. DENGUE FEVER
(BREAK BONE FEVER)

33. • Communicable arthropod-borne viral
hemorrhagic acute febrile disease of short
duration & varying severity.
• It is endemic in south Asia.
• Dengue 1, 2, 3, 4 are now endemic in Africa.
• In recent years outbreaks of dengue fever has
occurred on east coast of Africa from
Mozambique to Ethiopia to Saudi Arabia.

35. • Causative agent: viruses of dengue fever: 1, 2, 3
& 4 types.
• Reservoir: Man-mosquito cycle in tropical urban
centers. A monkey-mosquito cycle may serve as a
reservoir in south Asia & West Africa.
• Mode of transmission: bite of infective Aedes
aegypti mosquito.

39. CLINICAL PICTURE:
Sudden onset of fever for 3-5 days, intense
headache, rash early generalized erythema
& maculopapular rash.
Minor bleeding “epistaxis, gum bleeding
and peteachia”.
Generalized bleeding & lymphadenopathy.

45. PREVENTION & CONTROL:
1. Environmental sanitation:
b. Eradication or control of mosquito vector.
c. Human protection against mosquitoes.
2. Health education.

54. RIFT VALLEY FEVER

55. Communicable arthropod-borne viral zoonotic disease.
It was introduced to Egypt from East & South Africa
in1977, causing outbreak in animals, that was
transmitted to man.
Causative agent: Rift valley fever virus.
Reservoir: Cattle, sheep, goats.
Mode of transmission:
- bite of some infective Aedes & Culex species.
- Handling diseased animals & their tissues.

60. Aborted animals from infected cow with RVF

61. CLINICAL PICTURE:
Disease is usually mild & self-limited: fever,
influenza like picture (FHMA) & recovery.
Severe cases show hemorrhagic fever, liver
necrosis, damage of retina & encephalitis
May be fatal.

62. PREVENTION AND CONTROL:
1. Measures for animal reservoir:
• Prevention & control in animals “vaccination”.
• Quarantine of imported animals from endemic
areas.
2. Eradication or control of mosquito vector.
3. Measures for man:
• Human protection against mosquitoes

63. VIRAL ENCEPHALITIS

64. An endemic disease in different parts of world.
Usually mild but serious outbreaks have been
reported with involvement of brain, spinal cord and
meninges.
Occurrence:
West Nile virus encephalitis: Africa & Middle
East.
Eastern equine encephalitis: East U.S.A
Western equine encephalitis: West U.S.A
Japanese B encephalitis: Japan, Korea, Philippines
& India.

66. • Agent: specific arbovirus
• Reservoir: Birds & some wild & domestic
animals.
• Vector: Mostly by mosquitoes & some by ticks.
In Egypt, WNV is transmitted by culex.

67. PREVENTION:
1. Eradication or control of vector.
2. Protection of man from vector
3. Quarantine measures for imported birds & animals.

68. OTHER VIRAL
HAEMORRHAGIC FEVERS

69. • Such as: Lassa fever, Marburg disease & Ebola
virus disease
• Highly fatal & manifested by hemorrhagic
maculo-papular rash & bleeding from all orifices
of body in case of Ebola virus disease.

73. EATING THE BUSH MEAT IS BEHIND THE
OUTBREAK

75. WILL EBOLA EVER END IN AFRICA???
WHO confirms new Ebola case in Liberia
On April 1, 2016

76. Viral
Yellow fever
Encephalitis
Dengue
fever
Rift valley
fever
Bacterial
Plague
Parasitic
Malaria
Filariasis
Leishmanias
is
Rickettsi
al
Typhus
Q fever
Spirochet
Relapsing
fever

79. EPIDEMIC TYPHUS
(LOUSE - BORNE TYPHUS)

81. Causative organism: - Rickettsia prowazeki.
Reservoir of infection:-
- Man, case, organisms are found in blood throughout febrile stage.
- Vector: louse, "pediculus humanus".
Modes of transmission:-
1- Contamination of skin with faeces of infected louse. The
organisms find entry through skin abrasions by scratching.
2- Inhalation of dried faeces of infected louse.
N.B.: 1- The louse bite is not infective.
2- There is no transovarial transmission from louse to its generations.

82. CLINICAL PICTURE:-
I.P.: 12-14 days.
Abrupt onset of high fever, rigors, body aches. Face
becomes flushed then cyanotic & patient soon
becomes dull & confused.
Skin rash appears on the 5th day on folds of axilla,
anterior part of forearms then trunk & back.
Complications: Bronchopneumonia, thrombotic
changes, gangrenes of fingers, toes and genitalia.
Diagnosis: C/P & confirmed by lab investigation as
weil-felix reaction (agglutination test).

84. PREVENTION:-
1- Community development.
2- Health education “personal cleanliness”.
3- Measures against lousiness :-
- Providing washing facilities:
- Delousing of population “washing facilities & dusting
with a suitable insecticide”.
4- Specific prevention: -
- Typhus vaccine (live attenuated vaccine),
- Madrid E typhus vaccine “single IM dose, immunity
for 5 years”.

86. CONTROL:
*Cases:-
Notification to LHO.
Isolation in hospital after dusting.
Terminal disinfection by dusting (to kill any lice) &
steam disinfection for clothes & bedding (to kill rickettsia).
Treatment by tetracycline 500 mg / 6hs for seven days.
Release after clinical recovery of the case.
*Contacts:-
Delousing by bathing & dusting.
Surveillance for 2 weeks, for case-finding.

87. *Epidemic measures:-
Delousing of confined groups & underdeveloped
communities by washing facilities & dusting.
Vaccination of high risk groups.
Searching for the source of infection.

88. ENDEMIC (MURINE) TYPHUS
(FLEA-BORNE TYPHUS)

90.  Causative organism: R. mooseri.
 Reservoir of infection: Rat & vector is rat flea.
 Mode of transmission: Contamination of skin
with faeces of infective fleas. Organisms find
entry through skin abrasions.

91. CLINICAL PICTURE:
I. P.: 8 - 14 days.
Resembles mild epidemic typhus.
Diagnosis: Weil-felix reaction.
Prevention:
- Eradication & control of rats.
- Control of fleas.
N.B.: No specific prevention.
Control of cases & contacts: as usual.

93. Q-FEVER

95. Acute febrile rickettsial disease, with minimal
clinical manifestations mainly in form of atypical
pneumonia.
Agent: Coxiella Burnetti is an organism which has
an unusual stability; it survives adverse physical
conditions such as dryness, pasteurization & many
disinfectants.
Reservoir: Ticks, human body lice, small wild
mammals, cattle, sheep, goats, birds and man.
Period of communicability: Direct transmission
from person to person is rare.

96. MODES OF TRANSMISSION:
- Occupational: direct contact with domestic animals.
- Air borne: dust contaminated by placental tissues,
birth fluids & excreta of infected animals.
- Ingestion of raw milk
- Trans-conjunctival
- From person to person.

98. CASE PRESENTATION:
Incubation Period: 14-21 days
Clinical Picture:
Onset is sudden with chills, headache, malaise,
weakness and severe sweats.
Infection may be in apparent or non-specific.
Pneumonitis is found in X-rays.
Spontaneous recovery is common.

99. DIAGNOSIS:
- Culture in eggs or animal inoculation from blood
after onset of disease.
- Serological tests may show a rising titre.
- Weil-Felix reaction is negative.

100. CONTROL:
A- Preventive measures:
1- Animal control:
- Vaccination or antibiotics.
- Milk pasteurization at high.
2-Health education: Adequate disinfection &
disposal of animal products.
3- Immunization: Inactivated vaccine Q 34, “1ml
SC”. For high risk workers as lab workers &
workers in contacts with animals & animal
products.

102. B-Control of cases and contacts:
1- Cases :
a- Notification: to LHO.
b- Isolation: none
c- ttt: Tetracycline or Chloramphenicol is effective.
d- Disinfection: Concurrent of sputum, blood & articles
2- Contacts: no special measures, Search for cases.
C - Epidemic and International measures:
No specific measures.

103. Viral
Yellow fever
Encephalitis
Dengue
fever
Rift valley
fever
Bacterial
Plague
Parasitic
Malaria
Filariasis
Leishmanias
is
Rickettsi
al
Typhus
Q fever
Spirochetal
Relapsing
fever

104. RELAPSING FEVERS

108. TICK- BORNE RELAPSING FEVER
“TBRF”
A systemic spirochetal disease due to infection with
Borrelia duttoni
Transmitted by ticks

109. Agent: spirochete Borrelia duttoni “many different strains
according to areas of isolation and or vector rather than
biological differences”.
Reservoir: In most areas, it affects rodents & accidentally
man but in Central Africa, it primarily affects man.
Period of communicability: Ticks remain infective for
several years & pass infection transovarially to their progony.
Mode of transmission: Bite (through the saliva) or coxal fluid
of an infected tick.

110. CASE PRESENTATION :
IP: 3-10 days
- Periods of fever lasting 2-9 days alternating with
afebrile periods of 2-4 days
- The number of relapses varies from 1 to 10 or
more. Each febrile period terminates by crisis &
disease lasts for more than 16 days.
- Transitory petechial rashes are common.
- Bronchitis, nerve palsies, hepatosplenomegaly &
renal fever can occur.
- Fatality rate: 2-10%.

112. DIAGNOSIS:
Blood films show
circulating Borrelia
duttoni.
Specimen must be taken
during the febrile attack.

113. CONTROL:
A-Preventive Measures:
1) Control of ticks & rodents: treating interiors of houses
by benzene hexachloride or dieldrin to prevent ticks from
infesting human habitations. Cracks & proper housing
construction are very important.
2) Protection of susceptible:
Use personal protection measure including use of
repellents & protective clothes. Also, chemoprophylaxis
with tetracycline after exposure (tick bite) is used when
risk of acquiring the infection is high.
3) International measures: notification to W.H.O.

114. B-Control of cases & contacts:
1) Cases:
Notification: to LHO
Isolation: precautions with blood & body fluids.
Concurrent disinfection : none
Treatment: tetracycline
2) Contacts: Case findings.
C- Epidemic measures: apply insecticides to
clothes & houses.

115. LOUSE BORNE BELAPSING FEVER
“LBRF”
Spirochetal disease caused by Borrelia recurrentis &
transmitted by human louse.
1 or 2 & never more than 4 relapses.
Death is often in the 1st attack.
Agent: Gram negative spirochete (Borrelia
recurrentis).
Reservoir: Man is the only reservoir.

116. Period of communicability: Louse becomes infective
4-5 days after ingestion of blood from an infected person
& remains infective for life (20-40 days)
Mode of transmission:Transmitted from infected person
to new individuals by human louse; Pediculus humanus.
Infection occurs by contamination of wound with louse's
body fluid, following crushing of louse on skin.
N.B.: (1) No transovarian transmission.
(2) Neither bites nor faeces of louse cause infection.

117. CASE PRESENTATION:
- IP: 2-10 days
-C/P: FHMA, skeletal & abdominal
tenderness with palpable liver & spleen,
jaundice & purpura occur. Hyperpyrexia,
hypotension & cardiac failure can be fatal.

118. DIAGNOSIS:
Blood should be taken during febrile period &
examined by dark ground illumination or stained
blood films.
Intraperitoneal inoculation or culture in lab animals
can be used to recover the spirochetes.

119. CONTROL:
A-Preventive measures:
1) Delousing: residual insecticide powder.
2) Protection of susceptible: use of repellents &
protective clothes. Also, chemoprophylaxis with
tetracycline after exposure is used when risk of
acquiring the infection is high.
3) International measures: notification to WHO

120. B- Control of cases and contacts:
1) Cases:
- Notification : to LHO
- Isolation: precautions with blood & body fluids.
- Concurrent disinfection : none
- ttt: procaine penicillin injection followed by oral tetracycline
2) Contacts: Case findings.
C) Epidemic measures: Apply insecticides to clothes &
houses.

121. Viral
Yellow fever
Encephalitis
Dengue fever
Rift valley
fever
Bacterial
Plague
Parasitic
Malaria
Filariasis
Leishmaniasis
Rickettsial
Typhus
Q fever
Spirochetal
Relapsing
fever

123. FILARIASIS
(BANCROFTIAN FILARIASIS)

126. FILARASIS IN EGYPT:
It is endemic in Egypt.
Nile Delta: Qalyobia (Sandanhour), Menoufia (Kafr
al Hemma & Shenawaii), Sharkia (El korain
village), Dakahlia, Kafr el sheikh, Gharbia
Upper Egypt: Giza (Badrashin) & Assuit.
A program for elimination of lymphatic filariasis
started in 2002 & showed successful results.

127. CAUSATIVE AGENT:
Nematode: Wuchereria bancrofti & other long
thread-like worm (male 4 cm & female 7cm). Adult
worm normally resides in lymphatic of infected
people.
Female worms produce microfilaria that reach
blood stream 6-12 months after infection.
The microfilaria appears in large number during
night with maximum density in blood between 10
p.m & 2 a.m (nocturnal periodicity).

128. Reservoir of infection: Human with microfilaria in
their blood.
Man is definitive host & mosquito is intermediate
host.
Period of communicability: Human can infect
mosquito when microfilaria is present in peripheral
blood.
They can persist for 5-10 ys or longer after infection,
mesquite becomes infective after about 2 weeks.

129. MODE OF TRANSMISSION:
Bite of infective mosquito: in Egypt: female Culex
pipiens, but it could be transmitted by bite of
Anopheles gambia & Aedes.
Mosquito cycle begins when microfilaria are ingested
by female mosquito during feeding. Microfilaria
penetrates stomach wall of insect & develops in
thoracic muscles into elongated infective filariform
larva that migrate to proboscis.
When mosquito bites an individual, larvae can enter
punctured skin, then passes via lymphatic where they
molt & become adult.

135. SUSCEPTIBILITY & RESISTANCE:
General susceptibility: Filarial disease appears
only in small % of infected persons.
Immunity: Man may develop resistance only after
many years of exposure to infection.
Environment: Unsanitary planning with inadequate
sewage disposal, where breeding places of culex &
collection of water for other species.

137. CLINICAL FEATURE:
• Asymptomatic
• Acute form: fever, lymphangitis & lymphadenitis
• Chronic obstructive form: due to fibrosis &
obstruction of lymphatic vessels after repeated
attacks, 10 years later, leading to elephantiasis of
limbs, breast & genitalia, hydrocele, chyluria,
paroxysmal nocturnal asthma & severe
eosinophilia.

140. DIAGNOSIS:
 Detection of microfilaria in blood during
maximum presence (nocturnal).
 Live microfilaria can be seen in a drop of blood,
geimsa smears.

141. PREVENTION:
General:
1. Environmental sanitation:
a. Eradication or control of mosquito vector
b.Human protection against mosquitoes: e.g.
protective clothing, bed nets, repellents.
2. Health education: Modes of transmission &
Protection against mosquito bites.

142. SPECIFIC “MASS DRUG ADMINISTRATION
(MDA)”:
WHO recommends MDA in Endemic areas
Annual single dose, diethylcarbamizine citrate
(DEC) 6mg/kg BW + 400 mg albendazole for 4-6
years, or regular use of DEC-medicated cooking
salt for 1-2 years.
- 2 fold purpose: preventing future cases of
lymphatic filariasis & helping those people who are
already suffering from disease.

144. CONTROL:
Control of cases:
1. Notification: to LHO.
2. Isolation: not practical. As far as possible,
patients with microfilaria treated with anti-filarial
drugs should be protected from mosquitoes to
reduce transmission.

145. 3. Specific ttt: DEC (Banocid, Hetrazan).
ttt results in rapid suppression of most or all
MF from blood, but may not destroy all adult
worms.
Low level of MF may reappear after ttt.
Therefore, ttt must usually be repeated at
yearly interval, & lab follow up should be
done for treated cases.

146. ELIMINATION OF LYMPHATIC FILARIASIS IN
EGYPT
WHO has launched a global program for elimination of
lymphatic filariasis worldwide.
Elimination of lymphatic filariasis means a reduction of
disease incidence close to zero as a result of continued &
coordinated activities.
WHO's strategy comprises 2 components: interruption of
transmission, & care for those who already have disease.
To interrupt the transmission, the entire population at risk
must be covered by MDA for a period long enough to ensure
that level of MF in blood remains below that which is
necessary to sustain transmission.
Egypt started the program for elimination since 2000
following WHO recommendation of administering DEC &
Albendazole.

149. LEISMANIASIS

150. Group of diseases due to infection with
Leishmania which is transmitted by sandflies.
Reservoir: man, dogs, wild rodents & foxes.
Vector: several species of sandflies.

153. LEISMANIASIS IN EGYPT:
A focus of visceral leishmaniasis was discovered in El
Agamy, in 1982 .
The last case there was reported in 2005.
Only one more case of visceral leishmaniasis was reported,
in the Suez region in 2008.
However, due to a lack of awareness among medical
practitioners, visceral leishmaniasis is suspected to be
underreported.
Import of cases from Libya and Sudan may occur regularly
& go unnoticed.

155. Cutaneous leishmaniasis has been an increasing problem
in Egypt.
Known foci are among nomads in North Sinai.
Reported number of cases is estimated to be 4-5 times lower
than the real number of cases.
People at risk are soldiers, laborers, & immunocompromised
adults.

156. CUTANEOUS LEISHMANIASIS (ORIENTAL SORE)
New world cutaneous Leishmaniasis: L. mexicana.
Old world cutaneous Leishmaniasis: L. tropica, L. major & L.
aethiopica.
Modes of transmission:
1. Bites of infective sandfly.
2. Contact with skin lesions of case.
Occurrence:
 L. Mexicana: Mexico & Peru.
 L. tropica: Central Asia, India & West Africa. In Egypt it is
found in Alexandria region.
 L. major: Mediterranean & Southwest Asia.
 L. aethiopica: Ethiopia & Kenya.

157. CLINICAL PICTURE:
Starts with a papule & enlarges to become an
indolent ulcer on exposed parts of body which
either heals or lasts for many years.

159. MUCOCUTANEOUS LEISHMANIASIS
 Causative agent: L. braziliensis “central & south
America”.
 C/P: nasopharyngeal destruction & deformities.

161. VISCERAL LEISHMANIASIS (KALA AZAR)
Causative agent: L. donovani
C/P: Chronic infection with fever,
hepatosplenomegaly, lymphadenopathy & anaemia.
There is progressive emaciation & weakness with
generally fatal outcome if not treated

163. DIAGNOSIS OF LEISHMANIASIS:
1. Demonstration of Leishmania bodies in stained
smear of ulcer, organ or blood.
2. Culture if necessary.

164. CONTROL :
Prevention:
General:
Vector control e.g. by insecticides.
Protection of man from sandflies: e.g. repellents,
protective clothes.
Proper control of domestic animals especially dogs
Rodent control
Health education.

165. Specific:
Active immunization: live attenuated vaccine to
minimize severity of disease in some endemic
areas.
International measures: non

166. CONTROL OF CASES & CONTACTS:
Cases: - Early case finding & treatment.
- Skin lesions must be covered to avoid infection of
vector & contact infection of exposed individuals.
Contacts: - Health education.
- Examination.

167. MALARIA

168. A parasitic re-emerging
disease
1 million deaths/year in world
“mostly young African
children”
Recently multiple foci of drug
resistant malaria are
encountered in different areas.
Tropical & subtropical areas.

169. Tropical Africa
Southwestern Pacific
Forested areas of South America
Southeastern Asia
Indian sub-continent

170. CAUSATIVE AGENT:
Protozoan parasites with asexual & sexual phase
“Plasmodium vivax, P. falciparum, P. ovale & P.
malaria.
Mixed infections are not infrequent in endemic
areas.

171. RESERVOIR:
Humans: only important reservoir of human
malaria.
Case may have several plasmodia species at same
time.
Infective stage to vector is gametocytes which have
to be mature, both sexes, sufficient density &
viable.
Antimalarial drugs lose viability of gametocytes.
Female anopheline mosquito is definitive host
Infective stage to man is sporozoite.

173. PERIOD OF COMMUNICABILITY:
As long as infective macro gametes are present in
blood of patients. This varies with parasite species. In
untreated cases it may reach up to 3 years, however,
with antimalarial drugs the period is shortened greatly.
Humans may infect mosquitoes as long as infective
gametocytes are present in the blood, this varies with
parasite species and with response to therapy.
Untreated or insufficiently treated patients may be a
source of mosquito infection for one to several years.
Transfusion transmission may occur as long as asexual
forms remain in the circulating blood. Stored blood can
remain infective for at least a month.

176. MODE OF TRANSMISSION:
1- Bite of infective female anophiline mosquito, where
sporozoite are present in salivary glands. Most species
feed at night; some important vectors also bite at dusk
or in the early morning.
2- Infection or transfusion of infected blood or use of
contaminated needles & syringes (e.g. injecting drug
users) may also transmit malaria.
3- Congenital transmission occurs rarely. However,
pregnant women are vulnerable than others to
falciparum malaria (and possibly other plasmodium
species).

178. INCUBATION PERIOD:
Time between infective bite & appearance of
clinical symptoms is 9-40 days according to type of
malaria species.
With infection through blood transfusion, IP depend
on the number of parasites infused & are usually
short, but may range up to about 2 months.

179. SUSCEPTIBILITY:
It is universal except in human with specific genetic traits.
Age:
- All ages are affected.
-Tolerance to clinical disease is present in adults in highly endemic
areas where exposure to infective anopheline is continuous over
many years.
Sex: -Males are more exposed usually due to outdoor life.
Immunity:
- no natural immunity.
-Infection induces species specific immunity.
-Some sort of active immunity develops in endemic areas.

181. Genetic: Most indigenous populations of Africa show a natural
resistance to infection with P.vivas which is associated with
absence of Duffy factor on their erythrocytes.
Persons with sickle cell trait (heterozyotes) show relatively low
parasitaemia when infected with P. falciparum, so relatively
protected from severe disease; homozygote's suffering from sickle
cell disease are at increased risk of severe falciparum malaria
especially anemia.
HIV infection: increased risk of symptomatic falciparum malaria
& its severe manifestations.
Sociocultural & environmental factors: Low socioeconomic
standard, outdoor sleeping, agricultural societies & vitiated air
contribute to spread of infection.
Suitable environment for mosquito breeding “hot+humid+rainfall”

182. CLINICAL PICTURE:
slowly rising fever, chills, malaise, headache,
nausea, lassitude, muscle & joint pain, then rigor
sensation & rapidly rising temperature ending by
profuse sweating.
The cycle of fever, chills, sweating is repeated
either daily or every other day or every 3rd day or
irregularly according to malaria species.
Relapses may occur after a period of cure without
parasitaemia at irregular interval up to 5 years.

184. COMPLICATIONS:
- Anemia.
- Splenomegaly.
- Abortion & fetal infection.
- Falciparum malaria may be associated with
respiratory distress, jaundice, liver failure,
encephalopathy, pulmonary & cerebral edema,
coma & death.

185. DIAGNOSIS:
• Malaria parasites in thick blood film.
• Repeated microscopic examination every 12-24 hs
may be necessary to cover all parasite species.
• Several tests have been developed: The most
promising are:
- Rapid diagnostic tests: plasmoidal antigens in blood.
- PCR: most sensitive method.
- Demonstrating antibodies which appear after 1st week
of infection but may persist for years denoting past
malaria infection.

188. PREVENTION:
1. General preventive measures: of arthropod borne disease.
- Environmental sanitation, vector control and Health education:
* Elimination of the breeding sites of mosquito.
* Eradication of larval stages by spraying crude oil & larvicides on water
surface.
* Destruction of adult mosquitoes by using suitable insecticides (liquid
aerosol, pyrethrium).
- Human protection:
* Screening of windows and doors, using bed nets and animal barrier
between breeding places and human habitation.
- using protective cloths.
- Apply of repellents to exposed skin between dusk
- Avoid going outdoors & down when anopheline mosquitoes commonly
bite.
- Health education: public, at risk groups and travelers.
- Avoid taking blood from any individual giving history of malaria or a
history of travel to, or residence in, a malarious area.

189. 2. Specific measures:
Chemoprophylaxis for international travelers going to
endemic areas.
■ Chloroquine or hydrroxy chloroquine 5 mg /kg/week
or chloroquine phosphate (500 mg for average adult).
■ Continued for 4-6 weeks after leaving endemic areas.
■ In areas with chloroquine-resistant P. falciparum,
mefloquine is recommended (5mg/kg/week) for adults,
1-2 week before travel, during stay & 4 weeks after
leaving endemic area.

190. CONTROL:
Case: Early case finding:
* By lab examination of clinically suspected persons.
* By periodic survey.
* Through malaria campaign.
ttt: Using antimalarial drugs as chloroquine or
mefloquine etc.
Contacts:
■ Investigation for early case findings.
■ Investigation for source of infection or exposure.

192. MALARIA SURVEY
Field study in endemic areas to find out magnitude of problem, ecological
factors & to plan for prevention and control.
Planning:
■ Mapping area to identify water channels, collections, cultivated lands,
houses & climatic conditions.
■ Study population characteristics e.g age, sex, occupation, habits etc.
■ Study vector; types of mosquitoes, density, species, life span, breeding
places, resistance to insecticides.
■ Choose the suitable representative sample.
Preparation of:
■ Team of work. ■ Equipments (microscope, slides ect) ■ Transportation
facilities.
Investigation: Clinical &lab examination.
Statistical analysis: to show malariometric indices.

193. HUMAN INDICES:
1-Splenic index (non-specific): % of children between 2-6ys
showing splenomegally “excluding other causes”.
Interpretation:
- Below 10% low endemicity.
-10-25% moderate endemicity.
-25-50% hyperendemic.
2-Parasitic index (specific): % of infants below one year
showing malaria parasites in their blood, it is most sensitive
index of recent infection. Gametocytic index; is % of those
having gametocytes in their blood.
3-Vector index: Oocytic index is % of oocytes or ookinetes
in stomach wall of female anopheles.
4-Sporozoite index is %of female anopheles having
sporozoites in salivary glands.

195. MALARIA ERADICATION
Eradication is the highest level of disease control
Aiming at elimination of reservoir of infection, complete cure of
cases & prevention of disease transmission by destruction of
vectors.
To eradicate malaria in certain area 4 phases have to be done:
1. Preparatory phase: preparation, planning surveying to study
vector & magnitude of problem.
2. Attack phase: complete coverage of area by insecticides. D.D.T.
is applies twice a year during period of malaria transmission.
3. Surveillance system for early case finding & presumptive
treatment with chloroquine of any case with fever & completion of
treatment in +ve blood film cases.
4. Consolidation phase: insecticides are stopped & continue with
presumptive & radical treatment.