COMMUNICABLE AND VECTOR

BORNE DISEASE

MR. MUTIRIA
 Course content
• Describe communicable disease in regard to
– Causative organism
– Mode of transmission
– Pathophysiology
– Signs and symptoms
– Diagnosis
– Management
– Prevention and control
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• To include:
– Cholera
– Amoebiasis
– Bacillary dysentry
– typhoid
– Worm infestation
– Ebola
– Rabies
– Shigella
– SARS
– H1N1
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• Describe vector borne diseases
– Mode of transmission
– Life cycle
– Clinical importance
• To include the following
– Malaria
– Plague
– Leishmaniasis (Kalazar)
– Schistosomiasis
– Filariasis
– Chikungunya
– Yellow fever
– Relapsing fever
– trypanosomiasis
 CHOLERA
It is an acute intestinal disease characterized
by sudden onset of profuse watery stool,
vomiting, rapid dehydration and circulatory
collapse.
Clinical cholera is usually seen in the lower
social economic groups. Children but not
infants are more susceptible
 Epidemiology
It is caused by Vibrio cholerae a gram
negative, curved motile organism.
Transmission
Faecal oral route but almost all infections are
water-borne.
Vibrios can live in water for 2 weeks and prefer
brackish(salty) water. In sea water they may
survive for longer periods. Vibrios readily multiply
in foods such as milk and boiled rice.
 Pathogenesis
Vibrio cholerae stays in the intestinal lumen
and produces a toxin that activates formation
of cAMP through stimulation of adenyl cylase,
increased cAMP cause increased loss of
water& electrolytes thus causing diarrhoea.
 Clinical picture
• Incubation period is usually 2-3 days.
• Fever is low grade or absent because the
infection is not systemic.
• The disease develops in three stages
• Stage I
• Lasts for 3-12 hours. Characterised by the
passage of profuse watery diarrhoea.
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Soon fecal matter disappears from the stools which
comprise almost clear fluid with flakes of mucous ,
giving them the classical rice-water appearance.
The patient then starts vomiting food first, later rice-
water appearance.
Severe cramps in the abdomen and limbs develop
from loss of salt.
Stage II
There is collapse from dehydration. The body
becomes cold, the skin dries and is inelastic.
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The blood pressure is low or not recordable, the pulse
becomes rapid and feeble .
Urine production stops and the patient may die of shock.
Stage III
This is the stage of recovery, either simultaneous or with
treatment or patient may die.
The diarrhoea decreases, the patient is able to take
fluids orally and the general condition rapidly improves.
The diarrhoea decreases, the patient is able to take
fluids and the general condition rapidly improves.
 Management
• Patient is admitted to a temporary hospital. Strict
isolation is not necessary as only the vomitus and
stool are infectious.
• Oral rehydration in a patient who is able to drink
and IV fluids if in shock or too weak.
• Adults
– First line treatment is Doxycycline 100mg BD for 7days
– Others include: tetracycline, cotrimoxazole,
erythromycin
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• Children
• Azithromycin is recommended for
children and pregnant women
• Others include Erythromycin,
chloramphenicol

N.B. A stool culture will assist in the

selection of correct antibiotics.
 Prevention and control
Disease surveillance -It involves continuous monitoring of
the disease i.e. morbidity &mortality reports, field
investigations of epidemics or individual cases and lab
investigations such as culture.
Water for drinking should be made safe.
In case of a cholera outbreak, large quantities of water can
be treated with bleaching powder ( chloride of lime)
Milk should be pasteurized and uncooked food avoided or
washed in safe water.
Left over foods should be protected against contamination
by flies
 Prevention and control
• If you suspect an outbreak in your catchment
area do the following:
– Open a temporary hospital in a school or church
– Notify regional or district medical officer in charge and plan to
inform the public and give health education on prevention.
– Protect the main water supply; treat with bleaching powder or
chlorine
– Take stool specimen for culture
– Do not refer suspected cases
– Prepare large amounts of rehydration fluids to be taken orally.
– Give IV fluids for a short period, only to patients in shock.
– Have cholera beds prepared.
 AMOEBAISIS
It is an infection caused by a pathogenic amoeba,
Entamobea histolytica.
Infection with amoeba is in most cases asymptomatic.
Under certain circumstances, the amoeba may invade
the bowel wall causing amoebic dysentery.
It is acquired when the cysts are ingested. The
emerging trophozites takes up residence in the
ascending large bowel where it can live as a commensal
or begin penetrating the intestinal wall causing small
mucosal ulcerations which result in dysentery.
The parasite penetrates through the sub mucosa and
into the muscularis layer of the colon.
 Epidemiology
• It is acquired when the cysts are ingested. The
emerging trophozites takes up residence in the
ascending large bowel where it can live as a
commensal or begin penetrating the intestinal wall
causing small mucosal ulcerations which result in
dysentery.
• The parasite penetrates through the sub mucosa
and into the muscularis layer of the colon.
• If the muscularis layer becomes extensively
involved, scarring can result (amoeboma).
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• Invasion of bloodstream by the trophozite may led to
infection of the liver, especially the right lobe. After a
variable incubation period, a liver abscess may form.
• The only infective form of E. histolytica is the cyst. If
trophozites are ingested they are destroyed in the
stomach.
• An asymptomatic cyst-passer forms the main reservoir
for spread of amoebiasis.
• Cysts are passed from person to person by the faecal-
oral route. Amoebiasis can occur in families or spread
through institutions but usually doesn’t occur in
epidemics like Bacillary dysentery.
 Clinical picture
• When amoeba penetrate the intestinal wall, they
multiply in the sub-mucosa causing bottle shaped ulcers.
• From the ulcers the amoeba may be transported to the
liver.
• Amoeboma- this is where by the scar in the colon heals
while the parasite is still in the tissue. This results in an
abscess and keloids.
• Amoebic dysentery is insidious and associated with
abdominal discomfort. There may be mildly loose stool
or frank diarrhoea with or without blood and mucous
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• Amoebic dysentery is insidious and associated
with abdominal discomfort. There may be
mildly loose stool or frank diarrhoea with or
without blood and mucous
Distended colon
Chronic amoebiasis may resemble duodenal
ulcer, gall bladder disease or carcinoma of the
colon.
 Other extra-intestinal manifestation
Amoebiasis of the skin may occur where amoeba
come into contact with the skin, that is:
Around the anus
Around incision wounds
An amoebic skin ulcer is irregular and painful. The
ulcer enlarges continuously because of necrosis of
the edges.
When a liver abscess breaks through into the chest
cavity, a lung abscess or empyema may occur.
 Management
• Diagnosis is through a Stool is checked for cysts
Metronidazole 800mg orally 3 times a day for 5
days.
Metronidazole 25mg/kg/day in children for 3
days-tds should be chewed slowly to reduce
vomiting.
Tinidazole 2g OD for 3 days is an effective
alternative
 Prevention
• Screening of food handlers before
employment.
• Boiling of drinking water.
• Proper disposal of faeces.
• Construction and use of latrines in endemic
areas
 TYPHOID FEVER
• An infectious bacterial disease caused by
salmonella typhi.
• Human beings are the only known reservoir
and host
 Clinical Description
• S. typhi only infects humans; chronic carriers
• Transmitted from person-to-person, usually
via the fecal-oral route
• The incubation period depends upon the
infective dose. Range 3 days to 1 month;
average 8-14 days
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• Typhoid fever is a systemic infectious disease,
symptoms include:
– sustained fever,
– headache,
– malaise and anorexia.
– constipation
– Bradycardia
– Spleenomegally
– Ulceration of Peyer’s patches
– bloody diarrhea
 Treatment
• Fluid replacement due to diarrhoea
• Oral norfloxacin 400mg 12 hourly for 10 - 14 days
• Oral ciproxacin 500mg bd. for 14 days
• Patient should be isolated in fly-proof room
• Contaminated articles should be disposed by
incineration
• Stools and urine should be disposed of in a pit
latrine or septic tank
• Surgical treatment for perforated bowels
 Prevention and Control
• Identification of the carriers especially those
who work as food handlers and treat them
promptly
• Administration of typhoid vaccine
• Safe water supply
 BACILLARY DYSENTERY (SHIGELLOSIS)
• Bacterial disease of the intestines common in areas where
the standards of hygiene are low, particularly, where there
is scarcity of safe water, improper human excreta disposal,
large population of flies and child malnutrition.
• It is caused by a non-motile gram-negative bacilli of the
genus shigella
• The organisms responsible for outbreaks are:
– Shigella sonnei
– Shigella dysenteriae
– Shigella flexneri
– Shigella boydii
 Clinical picture
• Transmitted through oral feacal route
• Incubation period of 1-4 days
• The onset is sudden with:
– fever,
– headache,
– diarrhoea with streaks of blood
– colicky abdominal pains
• After a few motions (usually in a few hours) diarrhoea stops and is
followed by :
– Severe colicky abdominal pain known as dysenteric syndrome
– painful contractions of the sphincter ani which produce an irresistible
urge to defecate (tenesmus).
– Vomiting may also occur.
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• Toxaemia which causes:
– high fever and
– rapid pulse.
• Dehydration with muscular cramps, oliguria
and shock.
• In infants, rectal prolapse may occur as well as
convulsions.
 Management
• Mild bacillary dysentery is self-limiting
• Antibiotics: oral ciprofloxacin 500mg 12
hourly for five to seven days
• Analgesics for colic such as codeine phosphate
and loperamide, belladonna, or paracetamol
• Rehydration due to diarrhoea and fluid loss.
• Oral rehydration using ORS in water is always
useful as an aid to parenteral rehydration
 Prevention and Control
• Safe water supply
• Improvement in personal hygiene
• Digging and use of pit latrines
• Practising food hygiene
• Giving health education that emphasises
environmental hygiene and breastfeeding
• Inspection of public eating places, markets,
boarding schools and camps
 HELMINTHIC DISEASES

• TAENIASIS
• HOOK WORM
• TRICHURIASIS
• ENTEROBIASIS
• HYDATIDOSIS
• STRONGYLOIDIASIS
• ASCARIASIS
 TAENIASIS
• This is an infection caused by the tapeworm Taenia
solium and Taenia saginata. The cysticercus stage of
Taenia solium in humans can cause serious problems
such as epilepsy and death.
• Distribution
– World wide. Most cases of Taeniasis reported in eastern
Africa are caused by T. saginata. In southern & central
Africa, cases of taeniasis is due to T. solium.
• Morphology
– Body is segmented, with a distinct structure that is;
scolex(head), strobila, proglotids
 Life cycle
• The adult ribbon-shaped tapeworm live in the
small intestine of human. Broken segments of
the worm containing the gravid uterus and the
eggs are passed in the stool.
• The eggs are ingested by cows or pigs . In the
tract of the animals, the embryo develops into
a 6-hooked larvae, the oncosphere (also called
the hexacanth), which penetrates the bowel
wall and is carried via bloodstream to striated
muscles. Here the larvae invaginate, grow and
form the infective cysts known as cysticerci.
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• When the meat is ingested, the cysts are
dissolved by the gastric acid in the stomach to
release embryos.
• The T. saginata embryo attaches itself to the
wall of the small intestine by its head and
grows into an adult worm.
• The T. solium embryos behave differently ,
penetrating the bowel wall of the human as it
does the pig. It is carried in the blood stream
to organs like striated muscle or the brain.
Lifecycle
 Clinical manifestation
• T. saginata causes no signs and symptoms. In
some people they cause;
• Loss of weight
• Abdominal discomfort
• Pruritus ani
• T. solium infections are dangerous, especially
when the cysticerci invade the brain. Patients
may present with seizures or other
neurological signs and symptoms.
 Diagnosis
Microscopy of stool. Eggs are not laid singly
and appear only accidentally in the stool. The
segments can migrate out of the anus and
found on the buttocks.
 Management
Praziquantel 25 mg/kg three time a day for 2
days; albendazole 400mg once daily for 3 days
Niclosamide 2 tabs(11-34kg), 3 tabs <34kgs is
an alternative effective against both T.
saginata and T.solium
 Prevention
Proper fecal disposal
Cooking meat thoroughly, deep freezing of
meat kills all cyticerci though doesn’t protect
against salmonellosis, brucellosis and anthrax.
Health education on dangers of eating
uninspected meat.
 Roundworm (Ascariasis)
• Caused by Ascaris lumbricoides, which infects
the small intestine
• Multiplication in large numbers in the
intestinal lumen may cause intestinal
obstruction at the ileocaecal valve.
• They can contribute to severe malnutrition
and vitamin A deficiency
 Clinical picture
• Once the eggs are passed out in faeces, they
require embryonation in the soil before they can
become infective, this takes 8-50 days.
• Embryonated eggs can be carried away from the
contaminated place into houses by feet,
footwear or in dust by the wind.
• Human beings may ingest the eggs as they eat or
drink using contaminated hands and utensils, or
through eating raw contaminated foods like fruit.
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• Once the eggs are ingested by a human being
they
hatch into worms. In order to reach maturity,
the larvae need to pass through the lungs and
trachea to the pharynx.
• Once in the pharynx they are swallowed and
return to the gastrointestinal tract where they
can live for about a year.
Life cycle
 Symptoms
• It is asymptomatic
• Vague abdominal pains
• Worms may be expelled through vomitus or
stool
• Cough during migration
 Treatment
• Oral mebendazole 100mg 12 hourly for three
days
• Oral levamisole (3 tabs or 5mg/kg body wt)
single dose
• Oral piperazine 150mg/kg body wt single dose
 HOOKWORM
Most infected individuals( carriers) are
asymptomatic.
Hookworm disease develops from a
combination of factors;
Heavy worm burden
Prolonged duration of infection
Nutritional state of patient
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• Morphology
• Ankylostoma duodenale are grayish white or pinkish with the
head slightly bent in relation to the body.
• Females are often longer & stouter.
• They posses well developed mouths with two pairs of teeth.
• Mode of transmission
• Skin penetration by the filariform larva
• Life cycle
• The eggs are already embroynated when passed out with
faeces.
• The larvae leave the faeces and bury themselves in moist
damp soil. These larvae are called rhabditiform form.
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• And are not infective before they have changed into a
sheathed filariform, this occurs after about 5 days.
• The filariform larvae may attach themselves to grass or hide
in the soil.
• As soon as they are touched by something they attach
themselves to it. When this happens to be a human leg or
foot they penetrate actively through the skin and reach the
lungs via the blood stream through the venous system and
the right side of the heart .
• In the lungs, they penetrate the alveoli and are then carried
up passively through bronchial, bronchi and trachea to the
larynx-pharynx.
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• Next they are swallowed and reach the
duodenum 3-5
• days after penetrating the skin.
• The worms are attached to the mucous with
hook like teeth in their buccal cavity.
• The whole cycle is complete in ≈ 40 days.
 Clinical manifestation
• Asymptomatic in vast majority.
• Pruritic maculorpapular dermatits ‘ground itch’
• Larvae migration through the lungs-coughing,
wheezing & esinophilia
• In GIT-dyspepsia, abdominal pain, distention
and sometimes diarrhoea.
• The major sequence of hook worm infection is
iron-deficiency anemia.
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The hook worm sucks blood from the
intestines leading to loss of RBCs, iron &
protein, especially albumin.
When the host’s iron stores are depleted,
iron-deficiency anemia sets in & symptoms
related to anemia appear
LIFE CYCLE
 Diagnosis
Characteristic hookworm egg in feaces.
Differentiation of Necator and Ankylostoma is
not possible from the eggs but the adult worm
can be distinguished.
If the faeces are left to stand for long, the
eggs hatch and the larvae may be mistaken for
strongyloides larvae.
 Management
• Albendazole 400mg STAT or
• Levamisole 2.5mg/kg
• In iron-deficiency ferrous sulphate 200mg
once or twice for at least 2 months.
 Prevention and control
• Wearing of shoes
• Deworming campaign
• Proper faeces disposal.
• Appropriate action includes the following
– Health education on personal protection.
– Health education on balanced diet to prevent anemia when
iron intake is borderline.
– Mass treatment campaign when everyone has and uses
latrines
– Regular examination ,by mothers and health workers ,of
children’s mucosa to detect anemia
 STRONGYLOIDIASIS
• As hookworm
 TRICHURIASIS
• It is a nematode of the large intestine
• Distribution
– hot, humid climates and is most common in
children from low income families.
• Morphology
– Has a narrow anterior esophageal end and shorter
and thicker posterior anus.
– They are pinkish –whitish . They attach to their
host through their anterior end.
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• Mode of transmission
– Transmission is indirect, as the eggs passed in the
faeces require embryonation in the soil.
• Life cycle
– Eggs are deposited from human feces to soil where,
after 2-3 weeks, they become embryonated and enter
the infective stage.
– when embryonated eggs are ingested, they hatch into
the duodenum, releasing larvae that mature before
migrating to the large intestine bowel.
– The mature worms attach themselves to the mucosa of
the caeum and colon and may live for several years.
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• Clinical presentation
– Tissue reaction to whipworm is mild.
– Most infected individuals are asymptomatic.
– Heavy infection may result in abdominal discomfort,
loss of weight, anemia, prolapse of the rectum and
eosinophilia.
• Diagnosis
– Stool examination. Eggs are easily recognized under
microscopy.
• Management
– Albendazole 400 mg Stat
• Prevention
– Sanitary disposal of faeces and personal hygiene.
 ENTEROBIASIS
• It is caused by Enterobius vermicularis ( pin
Worm)
• Distribution
– world wide, more common in temperate countries
than tropics and especially in school children.
• Morphology
– It is a small delicate nematode.
– The adult female has a sharply pointed posterior end.
– It is 8-13mm long
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• Mode of transmission
– Initial infection occurs by fecal oral route. Infection is
maintained by direct transfer of infective eggs from the anus
to the mouth( auto-infection) or indirect fecal-oral contact
through clothing, bedding, food and other articles. Airborne
through inhalation of dust containing the eggs is also
possible.
• Life cycle
– Adult worms live in caecum & appendix.
– Gravid worms migrate from caecum & appendix into the
perianal area especially at night where they lay eggs which
are not fully embroynated but it takes 4 hours to be
embryonated. When swallowed they hatch and release
larvae which goes to the caecum where they mature. It
takes 15-20 days to mature into adult worms
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• Clinical manifestation
– Pruritus-ani, resulting in excoriation and secondary
bacterial infection
– Disturbance of sleep and restlessness
– Loss of appetite and weight
– Vulvitis and appendicitis
• Diagnosis
– Can not be made from looking for eggs in the faeces
instead, eggs deposited in the perianal region are
detected by application of transparent tape over the
anus early in the morning. The tape is transferred to a
Microscope slide and characteristic pin worm eggs are
searched for
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• Management
– Mebendazole 500mg start as a single dose
– Treatment of household members is also
advocated to eliminate asymptomatic reservoirs of
potential re-infection.
 HYDATIDOSIS (HYDATID DISEASE)
• The hydatidosis disease is actually a disease of
the dogs (zoonotic).
• Human beings become infected only by
accident. The disease is a serious problem
among the communities of northern Kenya
• It is also known as echinococcosis or
hydatid disease.
 Mode of Transmission
• Hydatidosis is caused by the cysts of the dog
tapeworm known as Echinococcus granulosas.

Dogs and other carnivores such as jackals and

lions are the hosts of the dog tapeworm.
• The eggs are passed in the faeces of an
infected dog and ingested by domesticated
animals such as sheep, goats, cattle, camels,
donkeys, and wild antelopes
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• The eggs hatch in the animal’s intestine and
penetrate through the intestinal wall to the
portal circulation. They are then carried to the
liver and lungs where they form many cysts
• When a dog eats the diseased animal it
becomes infected with these cysts, which then
proceed to develop into mature worms.
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• Human beings become infected when they
accidentally ingest eggs from dog faeces.
• The larvae migrate from the intestine to the
liver or lungs causing cysts.
• The larvae can also cause cysts in other tissue
in the body.
 Clinical Features
• In the liver, the cyst grows slowly over time
thereby enlarging the liver. The abdomen may
also become grossly distended.
 Diagnosis
This is done through:
• A chest x-ray or an abdominal ultrasound
investigation.
• A serological test can also be done to assist in
making the diagnosis.
• Diagnostic puncture and aspiration of cyst
content
 Management
• The treatment of hydatid disease can either be medical
or surgical.
• The medical treatment is as follows:
– Oral albendazole 20mg/kg in divided doses twice daily for 30
days (The cure rate with this treatment is 20%). The treatment
can arrest the growth of the cyst and reduce its size
– PAIR (Puncture, Aspiration, Instillation of 95% alcohol and Re-
aspiration). This is the treatment for the liver or spleen. The
ultrasound machine is used to guide the PAIR procedure. This
treatment is very effective and has a high cure rate
 Ctied
• The surgical treatment is known as
endocystectomy. It is the surgical removal of
the cysts contents, especially those cysts that
are easily accessible like abdominal cysts.
 Prevention and Control
• The prevention and control of the hydatid
disease can be achieved by eradicating stray
dogs and deworming them.
• Deworming should be done every six weeks
with praziquantel
• Provide health education on the dangers of
close contact with dogs (licking), especially
among children.
• Infected meat should not be fed to dogs.
 Complications
• Cysts with fistulas
• Billiary / bronchial obstruction
• Bacterial infection
• Compression syndromes
• Cyst rupture leading to anaphylaxis
• Venous/arterial embolism
 MALARIA
• An acute infection of the blood caused by
protozoa of the genus plasmodium.
 Epidemiology
• Malaria is caused by the plasmodium (parasite) that is
transmitted to human beings by the bite of the infected
female anopheles mosquito
• There are four plasmodium species and any of them can
cause malaria
– Plasmodium falciparum
– Plasmodium malariae
– Plasmodium ovale
– Plasmodium vivax
• Plasmodium falciparum is the predominant species
98.2% while P. malariae, P.ovale is 1.8%
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• Kenya has four malaria epidemiological zones
– Endemic: around Lake Victoria in western Kenya
and in the coastal regions
– Seasonal transmission: Arid and semi-arid areas of
northern and south-eastern
– Epidemic prone: areas of western highlands of
Kenya
– Low risk malaria areas: This zone covers the
central highlands of Kenya including Nairobi
 Transmission and Life Cycle of Malaria
• Malaria parasites develop in two cycles:
• Asexual Cycle
– Takes place in the body of the infected human being and
starts when the infected female anopheles mosquito bites
a person.
– Upon biting humans, the infected female mosquito injects
sporozoites via its proboscis into the blood stream.
– The sporozoites circulate in the blood for about one hour
and then they enter the liver cells.
– In 10 - 14 days the sporozoites develop into liver schizonts
while still in the liver.
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– The liver schizonts later burst releasing large numbers of
merozoites.
– The merozoites leave the liver and enter the blood stream
where they penetrate the red blood cells.
– Inside the red blood cells, the merozoites develop into
trophozoites. The trophozoites then develop into
erythrocytic schizonts.
– These erythrocytic schizonts burst releasing a shower of
merozoites, which invade fresh erythrocytes.
– Some of the released erythrocytic merozoites form male and
female gametocytes, which are sucked by the feeding
mosquito.
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• Sexual Cycle
– Takes place in the body of the female anopheles
mosquito.
– The mosquito sucks blood containing the male
and female gametocytes.
– In the stomach of the mosquito, the male
gametocytes mate with the female gametocytes.
– The fertilized gametocyte is called the ookinete.
 Ctied
– The ookinete stays in the stomach of a mosquito for
about 12 - 18 hours after which it penetrates the
stomach wall.
– Upon reaching the outer surface of the stomach wall,
the ookinete changes into an oocyst.
– The oocysts grow rapidly and burst releasing large
numbers of sporozoites into the body cavity of the
mosquito.
– Many of the sporozoites move to the salivary glands of
the mosquito from where they are injected into the
body of the next human being when the mosquito feeds.
 Clinical features and classification of
malaria
• Uncomplicated malaria: characterized by
fever in the presence of peripheral
parasitaemia.
• Other features may include chills, profuse
sweating, muscle pains, joint pains, abdominal
pain, diarrhoea, nausea, vomiting, irritability
and refusal to feed. These features may occur
singly or in combination.
 Ctied
• Severe malaria This is a life threatening
manifestation of malaria, and is defined as the
detection of P. falciparum in the peripheral blood
in the presence of any one or more of the clinical
or laboratory features listed below:
– Prostration (inability or difficulty to sit upright, stand
or walk without support in a child normally able to do
so, or inability to drink in children too young to sit)
– Alteration in the level of consciousness (ranging from
drowsiness to deep coma)
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– Cerebral malaria (unrousable coma not
attributable to any other cause in a patient with
falciparum malaria)
– Respiratory distress (acidotic breathing)
– Multiple generalized convulsions (2 or more
episodes within a 24 hour period)
– Shock (circulatory collapse, septicaemia)
– Pulmonary oedema
 Ctied
– Abnormal bleeding (Disseminated Intravascular
coagulopathy)
– Jaundice
– Haemoglobinuria (black water fever)
– Acute renal failure – presenting as oliguria or anuria
– Severe anaemia (Haemoglobin<5g/dl or
Haematocrit< 15%)
– Hypoglycaemia (blood glucose level < 2.2.mmol/l)
– Hyperlactataemia
 Management
• Uncomplicated malaria
– Treated with Artemether (20mgs) and
Lumefantrine(120mgs) (AL)
Weight in Age in Number of tablets of AL( 20/120) to be
kgs years administered at 0 hrs, 8 hrs, 24 hrs, 36
hrs, 48 hrs and 60 hrs

5 - 14 5m-<3 1
15 - 24 3–7 2
25 - 34 8 – 11 3
Above 35 ≥ 12 4
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• Severe malaria
– Treat with parenteral Artesunate preferably
intravenous (IV) but intramuscular (IM) can be
used
– In the absence of artesunate, parenteral quinine
or IM artemether should be administered.
– Administer artesunate as follows: Dosage:
• For children below 20 kg administer 3.0 ml/kg
• For patients above 20 kg administer 2.4 ml/kg
 Prevention
• Chemoprophylaxis
• Using bed nets
• Using mosquito screens in houses
• Using chemical mosquito repellents
• Cleaning drainages and water
disposal systems
• Clearing bushes and burying or burning rubbish
heaps
• Use of larvicides and insecticides
 SCHISTOSOMIASIS
• This disease is commonly known as Bilharzia after
Theodor Bilharz who discovered it in Cairo in 1861.
• The incidence of schistosomiasis is related to water
use, Irrigation schemes or water projects for
electricity provide the habitat for the snail vectors.
• Up to 75% of schistosomiasis is transmitted by
infected humans while 25% is said to be
transmitted by dogs, cows, rats, and baboons.
 Causative organism
• It is caused by a schistosome
– Schistosoma Haematobium
– Schistosoma Mansoni
– Schistosoma Japonicum
– Schistosoma intercalatum
– Scistosoma mekhongi
• The most common on E.A. is Haematobium
and mansoni
 Mode of Transmission
• S. mansoni is spread in infected stool while S.
haematobium is spread in infected urine.
 Life cycle
• When the schistosome eggs in the urine or stool
enter a body of water such as a lake, dam, rice
paddy or pond, they hatch into free-swimming
larvae called miracidia.
• The intermediate host for S. mansoni is a vector
snail of the genus biomphalaria pfeifferi; while for
the S. haematobium it is bulinus africanus. The
miracidia, after being shed from the ovum, must
enter the appropriate snail host within 24 hours or
die.
 Cont..
• Inside the body of the snail host, it takes the
miracidia four to seven days to develop and
multiply into numerous infective cercariae.
• The snail sheds them in water where they can
only live for 48 hours unless they infect a
human. A human being becomes infected
when they enter cercariae-infested water,
such as when bathing, swimming, laundering,
cultivating or fishing.
 Cont..
• The cercariae penetrate the skin and enter the
bloodstream from where they are carried to
the liver or bladder to develop into adult
worms. Within four to six weeks, paired adults
reach mesenteric and pelvic veins.
Cont..
 Clinical Features
• Invasion-There is cercarial dermatitis with itching
papules and local oedema
• Maturation- There is fever, eosinophilia,
abdominal pain and generalised urticaria known
as katayama syndrome.
• In established infection
– In S. mansoni there is bloody diarrhoea and abdominal
cramps.
– In S. Haematobium there is terminal haematuria and
dysuria
 Ctied
• In Late Stage
• Urinary Bladder:
– Obstruction to and dilation of ureters leading to
hydronephrosis which may cause kidney failure
– Pyelonephritis
– Bladder polyps
– Calcification of bladder
– Cancer of bladder
 Ctied
Liver:
– Portal vein fibrosis leading to portal hypertension
– Portal hypertension leading to oesophageal varices which may cause
massive haematemesis
– Caput medusae and ascites
– Hepatomegally
• Lungs:
– Pulmonary fibrosis leading to pulmonary hypertension, causing
congestive heart failure
• Bowel:
– Bowel fibrosis and glanulomas
– Gastric varices
– Haemorrhoids
 Diagnosis
• The diagnosis of schistosomiasis is confirmed by:
– Finding eggs in stools or urine during a microscopic
examination.
– Performing a colonic or urinary bladder biopsy
– Serological tests are also highly sensitive and yield
specific results.
 MANAGEMENT
• The main aim of treatment is to kill the adult worms
and to stop their egg-laying activity.
 Prevention and Control
• Prevention of ova-containing urine and stool
from reaching the water by:
- Digging and using pit latrines
- Safe water supply
- Treating the infected persons
• Attacking the intermediate host (the snail)
using molluscicides such as copper sulphate
which kills snails and their eggs.
 Cont..
• Avoiding contact with infested water by using
protective clothing when laundering,
cultivating, swimming and wading. Bathing
should be done at home (storing water at
home for three days will kill the cercariae).
• Conducting mass treatment campaigns for
communities at risk using oral praziquantel,
especially school-going children.
 FILARIASIS
• This is a disfiguring disease caused by a tiny
worm (nematode).
 Species causing Filariasis
1. Wuchereria bancrofti- vector is mosquito
2. Onchocerca volvulus- Vector is simulium ( black
fly)
3. Brugia malayi- Vector is mosquito
4. Loa loa- vector is chrysops (deer fly)
5. Brugia timori- Vector is mosquito
6. Mansonella perstans- Vector is culicoides (biting
midges or fly)
7. Mansonella streptocerca- Vector is culicoides
 Ctied
8. Mansonella ozzard- Vector is culicoides
9.Dracunculus medinensis- Vector is
copepods(crustacean found in water)
 BANCROFTIAN FILARIASIS
• This is a disfiguring disease caused by a tiny
worm (nematode) called wuchereria bancrofti.
• It is transmitted by culex quinquefasciatus
mosquito found in heavily contaminated water
especially in the urban areas and the culex
pipiens and the anopheles mosquito in rural
areas
 Cont..
• These mosquitoes transmit the worm from
person to person in the same way as malaria.
The parasitic worm lives in the lymphatic
system of the patient causing inflammation of
the lymphatic vessels and lymph glands
(lymphangitis, lymphadenitis), filarial fever,
and eventually elephantiasis of the arms, legs
and genitals.
 Mode of Transmission
• Through a bite from a mosquito which injects
the microfilaria into the blood stream.
• Has an incubation period of 10 to 12 days
 Life cycle
• The microfilariae ingested by the feeding mosquito
lose their sheath in the stomach and become first
stage larvae.
• They then penetrate the mosquito stomach wall
and migrate to the thorax muscles where they molt
twice and develop into the infective stage larvae.
• Mature infective microfilaria
migrate to the mouthparts (Proboscis) of
the mosquito ready to transmit it to the next person
 Ctied
• Once injected they develop into adults that
reside in the lymphatics
• The adults produce microfilariae which are
sheathed and have a nocturnal periodicity
Cont..
 Clinical Features
• Acute Phase
– Fever
– Eosinophilia
– Enlarged lymph nodes
– Inflamed lymph vessels (lymphangitis)
 Ctied
• Sub Acute Phase
– Fever
– Eosinophilia (severe)
– Attacks of dyspnoea (asthma-like)
– Funiculitis (pain and swelling of the spermatic cord/s)
– Epididymitis
– Hydrocele
– Lymphadenitis (tender lymph nodes)
 Ctied
• Chronic Phase
– Lymphoedema
– Elephantiasis
– Chyluria ( Presence of chyle in urine)
– Hydrocele
– Oesinophilia
– Monoarthritis
 Diagnosis
• Fluid aspirated from swollen lymph glands or from
hydrocele can be examined under a microscope to show
the microfilariae.
• Thick blood slides for microfilariae should be taken
between 10:00pm and 2:00am. This is because
microfilariae are not present in the peripheral blood
during the day.
• Blood slides for microfilariae may be taken 45 minutes
after administration of a provocative dose of
diethylcarbamazine 100mg.
• Through clinical features
 Treatment
• The drug of choice for filariasis (adult worms and
microfilariae) is diethylcarbamazine (DEC, hetrazan,
benocide, notezine) 6mg/kg body weight daily in divided
doses (150mg) eight hourly for 12 days for an adult.
• Diethylcarbamazine may be combined with levamisole
(Ketrax). This combination kills microfilariae and reduces
the parasite worm count in the body more rapidly.
• Ivermectin and albendazole can be given
• General nursing care
 Prevention and Control
• Use of larvicides such as polystyrene powder
in the pit latrine
• Reduction of human-mosquito contact
including the use of insecticide treated bed
nets.
• Clear bushes
• Drain stagnant water
 LEISHMANIASIS (KALA AZAR)
• This is an infection caused by a parasite of the
leishmania group.
• Transmitted by a bite of female sandfly (phlebotomus) is
the vector.
– Phlebotomus martini
– Phlebotomus orientalis
– Phlebotomus longipes
– Phlebotomus pedifer
• In Kenya, the main vectors are phlebotomus martini
which transmit the parasite leishmania and donovani,
responsible for visceral leishmaniasis
 Ctied
• P. orientalis is common in Sudan
• P. longipes and P. pedifer are commonly found
in Ethiopian and Kenyan highlands. Together
they transmit the parasite leishmania
aethiopica which is responsible for cutaneous
leishmaniasis.
Cont..
 Disease process/cycle
• The sandfly bites an infected person and ingests
amastigotes.
• On reaching the sandfly’s stomach, the amastigotes
change into promastigotes.
• After four to seven days, they migrate to the foregut
where they develop into infective promastigotes.
• The infective promastigotes are then conveyed in the
saliva of the sandfly during feeding.
 Ctied
• From here the promastigotes enter the
bloodstream and into the macrophages.
• On entering the macrophages, the parasites
escape detection by the body’s defences and
are spread to various body tissues
LIFE CYCLE OF LEISHMANIASIS
 Visceral Leishmaniasis
• Visceral leishmaniasis is found in many areas
of the North Eastern region of Kenya, in
Machakos, Kitui, Masinga, Tseikuru (Mwingi),
Makueni and Kibwezi
• It has an incubation period of 4-10 months or
longer, before definitive signs and symptoms
manifest.
NB: Most of the patients (96%) are killed by
secondary bacterial infections of the lesions.
Clinical Features of Visceral Leishmaniasis

• Fever
• splenomegaliy
• hepatomegally accompanied by anaemia and
weight loss.
 Treatment
• Using IV or IM sodium stibogluconate
20mg/kg daily for 20 - 30 days.
• The drug of choice for visceral leishmaniasis
caused by leishmania aethiopica is IM
pentamidine isothianate 3 - 4mg/kg once or
twice a week.
• Prevention or early detection and appropriate
treatment are preferred. Corrective surgery
can be done where need arises.
 Cutaneous Leishmaniasis
• Found in West Pokot, Turkana, Baringo,
Laikipia and Kerio valley.
NB: It is characterized by single or several
painful chronic ulcers in those parts of the
body
 Clinical Features
• In about 2-8 weeks following a bite from an
infected sand fly, a small itchy papule appears
at the site of the bite.
• Over several weeks, the papule grows in size
expanding to form a single indolent ulcer or
multiple ulcers. The disease may be mistaken
for leprosy.
 Ctied
• There may be enlargement of the local lymph
nodes.
• The lesions begin to heal spontaneously two
to twelve months later.
NB: Cutaneous leishmaniasis does not spread to
other body organs.
Cont..
 Management of Cutaneous Leishmaniasis

• Small lesions may be treated surgically by

curettage or by freezing, using liquid carbon
dioxide or by infiltrating them with 1 - 2ml
sodium stibogluconate.
• Large disfiguring or multiple skin lesions are
treated in the same way as for visceral
leishmaniasis using IV or IM sodium
stibogluconate 20mg/kg daily for 20 - 30 days.
 Mucocutaneous Leishmaniasis
• occurs primarily in the tropics of South America.
• Sometimes these primary lesions heal, other times
they spread and become larger.
• Some years after the first lesion is noted (and
sometimes several years after that lesion has
totally healed), new lesions appear in the mouth
and nose, and occasionally in the area between
the genitalia and the anus (the perineum). These
new lesions are particularly destructive and
painful.
 Clinical Features
• If the lesions spread to the roof of the mouth
and the larynx (the part of the wind pipe
which contains the vocal cords), they may
prevent speech.
• Other symptoms include fever, weight loss,
anaemia (low red blood cell count).
• There is always a large danger of bacteria
infecting the already open sores.
 Prevention and Control
• Use of insecticide treated curtains in homes
(these have been used with success in Baringo
district)
• Destruction of infected dogs and rodents
• Early diagnosis and treatment of the infected
persons
• Health education for communities on
preventive measures
 Plague
• It is a highly infectious disease caused by bacteria
called yersinia pestis (Pasturela pestis).
• It is a disease of rodents, especially rats
• It is spread from rat to rat by a rat flea called
xenopsylla cheopis
• Plague is a very rare but serious disease because
it can spread very rapidly unless the first case is
recognised early and appropriate action taken
• Case fatality rate in absence of treatment is 60%
 Mode of Transmission
• Plague occurs when infected wild rats, especially the
sewer rat (R. norvegicus) die from the disease and their
fleas look for substitute domestic rat (rattus italia) hosts.
• The domestic rat becomes infected and after it dies the
fleas start biting human beings.
• When the first human is infected, the disease causes
bubonic plague.
• People working in the fields may also be bitten by fleas
from the dead infected wild rats and develop bubonic
plague.
 Clinical Picture
• Bubonic: occurs when the bacteria infiltrate
the lymph nodes
– Swelling of the lymph gland (Bubos) which
appears within 24 hours, they are commonly
found in the groin and armpit
 Ctied
• Septicaemic- occurs when the infecting
bacteria infiltrates the blood. Both bubonic
and pneumonic can complicate to septicemic
– The patient is prostrasted
– Febrile
– Weak
– Pale and apathetic
– Stupor, coma and death may occur on the 1st, 2nd
or 3rd day or later
 Ctied
• Pneumonic –occurs when the bacteria first
infiltrates the lungs. It is very infectious and
can be spread by cough
– Patient may cough
– There may be rigors
– Malaise
– Intense headache
– Body aches
– Fever and severe prostration
 Diagnosis and treatment
• By doing a microscopy (staining) of sputum or pus from
the bubo to demonstrate the bacilli.
• Clinical features
• Treat using most common antibiotics except penicillin.
– IM streptomycin 30mg/kg two times daily for seven to ten days
– Oral Doxycycline 100mg twice daily for adults or 5.4mg/kg for
children aged below 8 years for seven to ten days
– Oral cotrimoxazole two tabs twelve hourly for seven days for
adults
– Oral chloramphenicol 500mg six hourly for seven to ten days
and children 50 mg/kg in 4 divided doses
 Prevention and Control
• Early diagnosis and notification so that the
patients are not moved or referred to the
hospital
• Chemoprophylaxis of all contacts of the
patients such as family, visitors and health
care workers using Doxycycline or
cotrimoxazole
• Isolation of the infected and quarantine of the
contacts for ten days
 Ctied
• Use of insecticides to kill fleas
• Eradication of rats, for example using rat
poison
• Vaccination during epidemics using an anti-
plague vaccine
• Health education for communities on
preventive measures
 Trypanosomiasis (sleeping sickness)
• A tropical disease caused by protozoa
– Trypanosoma brucei gambiense (Tbg)
– Trypanosoma brucei rhodesiense
• Trypanosomiasis affects both humans and cattle
and is invariably fatal over varying periods of time
if not treated.
• Trypanosoma brucei gambiense causes an acute,
rapidly progressive illness with death from cardiac
complications within several weeks or months.
 Ctied
• Reservoirs include antelope and pigs. Tbr is
found in eastern Africa, now mostly in south-
east Uganda.
• Trypanasomiasis spreads very rapidly unless
the source (the very first case) is identified
early, isolated and treated properly.
• Trypanasomiasis is found in the same areas in
Africa where yellow fever is found.
 Ctied
• Trypanosomiasis is transmitted by tsetse flies
which live in areas of wooded vegetation
• The incubation period between the tsetse bite
and the onset of fever varies from as short as
a few hours following the chancre to several
weeks.
 Clinical Features
• The early stages of trypanosomiasis are
characterised by irregular episodes of fever
with headaches, malaise, weight loss, muscle
and joint pains, pruritus, anaemia, skin rash,
and deep hyperaesthesia (Karandel’s sign).
• The clinical features of trypanosomiasis
depend on the infecting parasite as follows:
 Ctied
• Trypanosoma brucei gambiense (Tbg) infection causes a
slow chronic sleeping sickness, resulting in death from
the disease
in several months or years. Pigs, dogs and antelopes are
the reservoirs.
• Trypanosoma brucei rhodesiense (Tbr) infection is
acute and rapidly progressive unless prompt treatment
is administered. The parasites damage the heart
causing cardiac complications and death within several
weeks or months. Pigs and antelopes are the reservoirs
for Tb rhodesiense.
 Stages
1. Primary Stage (chancre stage)
– Within a few days of the tsetse bite, a painful
indurated erythematous nodule may appear at the
site of the bite.
– This chancre may last for one to two weeks and
then resolve spontaneously.
– The chancre occurs in 70% of cases in Europeans
but is rare in Africans.
 Ctied
2. Blood Stage (systemic illness)
– During this stage, the trypanosomes spread to the blood,
lymph and lymph nodes.
– There is fever, which does not follow any typical pattern
but recurs at intervals of days or weeks.
– After the fever resolves, the patient develops anaemia,
debilitation and general body weakness.
– The spleen becomes enlarged as well as the lymph nodes.
– The cervical lymph nodes especially of the lower back of
neck become visibly enlarged in 80% of patients - this is
called Winterbottom's sign
 Ctied
– The other signs and symptoms of trypanosomiasis
include:
– Pruritic rash (beginning six to eight weeks after
infection)
– Hepatosplenomegaly
– Poor appetite resulting in weight loss, debility,
pitting oedema of face and lower legs
– Impotence and menstrual irregularities
– Heart failure
 Ctied
3. Cerebral Stage (Sleeping sickness stage)
– This is the terminal stage of trypanosomiasis.
– During this stage of the disease, the parasites invade
the brain leading to mental deterioration and coma.
– Convulsions and localized signs such as hemiplegia
and facial palsy may occur.
– Patients are very weak, they sleep during the day but
are restless at night.
– As the disease progresses, the patients become
severely ill and die if not treated.
 Diagnosis
• Microscopic examination of the chancre fluid
to demonstrate the trypanosomes
• Examination of blood (buffy coat) for
trypanosomes
• Wet blood smear for microscopy
• Thick blood smear for microscopy
• Serological test (card agglutination test)
• Lymph node aspiration (microscopy
 Treatment
• Pentamidine 4mg/kg IM for 10 days for tbg
• Suramin 1gm IV on day 1,3,7,14,21 for tbr
 Prevention and Control
• Chemoprophylaxis; IM pentamidine 250mg single
dose protects against Tb gambiense infection for
six months in those working in endemic bush land
areas such as wildlife personnel.
• Bush clearing (which may harm the environment)
and establishment of agricultural settlement will
in the long run destroy tsetse fly breeding areas.
• Use of baited flytraps which have an efficacy of
95% at reducing the tsetse fly population.
 YELLOW FEVER
• Yellow fever is an acute viral disease caused by
yellow fever virus
• It is transmitted to human beings by the aedes
aegypti mosquito.
• The aedes africanus mosquito transmits in
monkeys
• The mosquito becomes infected after feeding on
the blood of an infected monkey or person on
the third day of fever and transmit to another
 Ctied
• One can be infected also through handling of blood from
an infected individual in the first three days of the
disease or handling infected monkeys in the early stages
of viraemia.
• Laboratory staff may become infected when working on
infected monkeys or infected mosquitoes.
• It takes 18 days at a daily temperature of 18°C and four
days at 37°C.
• The cycle takes four days and once infected, the
mosquito remains infected and infective for its entire life
(about two to four months).
 Clinical Picture
• The onset is sudden with the following signs and
symptoms:
– Fever
– Headache
– Backache
– Nausea and vomiting
– A bleeding tendency (epistaxis, bleeding gums,
haematemesis, malaena)
– Liver cell necrosis (in severe illness) resulting in jaundice
– Nephritis leading to albuminuria which may proceed to
anuria and renal failure
 Management
• Give supportive treatment
• Ensure that the patient is nursed in strict isolation
using ordinary barrier nursing techniques.
• Ensure that the patient has no further contact
with the mosquitoes through the use of
insecticide treated bed nets and ensuring that the
room is well screened.
• This is to prevent further spread of the disease
from the patient to other healthy people.
 Prevention and Control
• Administering yellow fever vaccine to all
travelers coming from or going to yellow fever
endemic areas.
• Spraying aircraft coming from yellow fever
endemic areas with insecticides to kill
imported mosquitoes, which may be infected.
• Isolating all persons who have been in contact
with the infected persons.
 Ctied
• Such individuals should be quarantined in
screened houses for seven days.
• Mass immunisation campaign for the
community in areas infested with the aedes
aegypti mosquito.
• Spraying of larvicides in all possible mosquito
breeding places including water holding plants.
 RELAPSING FEVER
• This is an acute infectious bacterial disease
which is characterized by alternating febrile
periods.
• It is also known as Recurrent fever, Spirillum,
Tick fever, or Tick Bite fever.
• It is transmitted by ticks and lice.
• There are two types of relapsing fever, namely:
– Louse-borne relapsing fever- Transmitted by lice bite
– Tick-borne relapsing fever- Transmitted by tick bite
 Clinical picture
• Sudden onset of fever which ranges between 39.5°C -
40.5°C.
• Rapid pulse, headache, aching joints, vomiting and
infected conjunctiva. potential rash, epistaxis, and herpes
labialis.
• After five to seven days, the temperature drops by crisis.
In about 60% of the patients, a less severe relapse of the
symptoms occurs five to ten days after the first attack.
• A second relapse may occur in about 25% of the patients.
In untreated cases, there may be up to ten relapses.
 Ctied
• The fever and clinical symptoms become less
severe each time after the relapse. Relapsing
fever has a high mortality rate of 40%.
• Common complications of relapsing fever include
meningitis, iritis, optic nerve atrophy (blindness),
myocarditis and liver failure bleeding.
• You can confirm relapsing fever by doing a
microscopic examination of a thick blood smear
for the spirochaetes.
 Treatment
• Patients must be nursed flat, given adequate
fluids and be confined to bed for at least 24
hours.
• The treatment of relapsing fever is IM
procaine penicillin 400,000 units stat, followed
the next day by oral tetracycline 500mg six
hourly for five to seven days. An alternative to
tetracycline is oral doxycyline 200mg once
(single dose).
 Prevention and Control
• Improve their personal hygiene
• Use insecticides to kill lice, for example
malathion powder
• Boil clothes to kill lice and eggs (delousing)
 CHIKUNGUNYA DISEASE
• This is a viral disease transmitted to humans
by mosquitoes.
• It usually occurs in outbreaks
• The Aedes mosquito transmits the virus
 Signs and symptoms
• The symptoms usually start 3-7 days after the
mosquito bite and lasts a few days
– Sudden onset of fever
– Severe joint pain
– Headache
– Muscle pain
– Nausea
– Fatigue
– Rash
 Treatment
• It is a self-limiting disease, meaning there is
no specific medicine to treat the virus.
• There are currently no vaccines to prevent it
either.
– Get plenty of rest.
– Drink fluids to prevent dehydration.
– Take medicine such as paracetamol to reduce
fever and pain.
 prevention
• Clothing which minimises skin exposure to the day-
biting vectors is advised
• Repellents can also be applied to exposed skin or to
clothing
• Insecticide-treated mosquito nets offer good
protection for those who sleep during the daytime,
particularly young children, or sick or older people
• Mosquito coils or other insecticide vaporisers may
also be used to reduce indoor biting
 DENGUE FEVER
• Is a mosquito-borne viral infection transmitted by
Aedes aegypti and Aedes albopictus
• There are two clinical forms of the disease referred
to as:
– Dengue fever – symptoms similar to malaria; headaches,
fevers, joint pains, fatigue, muscle pains, skin rash, pain
behind the eyes and vomiting
– Dengue hemorrhagic fever-more serious form, causes
bleeding which initially appears as tiny spots of blood on
the skin and grows into larger patches causing shock and
death
SEVERE ACUTE RESPIARTORY SYNDROME

• It’s a serious form of pneumonia caused by

corona virus
• It is spread through droplets:
– hugging and kissing
– sharing utensils for eating and drinking
– speaking to someone within a distance of 3 feet
– touching someone directly
 Signs and symptoms
• Symptoms normally appear within 3 to 5 days
after exposure to the virus,
– high fever
– Symptoms common to flu, such as aches, chills,
diarrhea, dry coughing, and shortness of breath.
– Patients pneumonia
• Serious complications may occur like:
– respiratory failure
– Heart failure
– liver failure
 Ctied
• WHO criteria for diagnosis is
• A fever of 38° C
• One or more symptoms of lower respiratory
tract illness:
– a cough
– difficulty breathing
– shortness of breath