TROPICAL MEDICINE

MR. NGUUTU
Bsc Clinmed
 1. HELMINTHIC INFECTION
• NEMATODES (ROUND WORMS)
• CESTODES (TAPE WORMS)
• TREMATODES (FLUKES)
 A. NEMATODES(ROUND WORMS)

–Ascariasis
–Hook worm
–Enterobiasis
–Strongyloidiasis
–Trichuriasis
–Filariasis
»Lymphatic Filariasis
»Onchocerciasis
 1. ASCARIASIS
• Refers to infection of GIT by ascaris lumbricoids 
Aetiology/Epidemiology:
• Ascaris lumbricoides is the largest nematode
(roundworm) parasitizing the human intestine. 
(Adult females: 20 to 35 cm; adult male: 15 to 30
cm.)
• Causes about ¼ of all worm infestations
• About 2 million people are affected worldwide.
• It is the commonest and most widespread
• Children are affected more than adults
• It prefers loose soils with plenty of oxygen, not dry,
Temp. under 150c.

• transmission is Faecal – oral route via:-

 Contaminated soil, unwashed hands.
 Contaminated food, fruits and vegetables.
• Geographic Distribution:
The most common human helminthic infection. 
• Worldwide distribution. 
• Highest prevalence in tropical and subtropical
regions, and areas with inadequate sanitation. 
Occurs in rural areas of the southeastern United
States.
Life cycle
• Adult worms live in the lumen of the small intestine.  A female
may produce approximately 200,000 eggs per day, which are
passed with the feces .  Unfertilized eggs may be ingested but
are not infective.  Fertile eggs embryonate and become infective
after 18 days to several weeks , depending on the environmental
conditions (optimum: moist, warm, shaded soil). 
• After infective eggs are swallowed , the larvae hatch , invade
the intestinal mucosa, and are carried via the portal, then
systemic circulation to the lungs .  The larvae mature further in
the lungs (10 to 14 days), penetrate the alveolar walls, ascend
the bronchial tree to the throat, and are swallowed .  Upon
reaching the small intestine, they develop into adult worms .
 Between 2 and 3 months are required from ingestion of the
infective eggs to oviposition by the adult female.  Adult worms
can live 1 to 2 years.
 Pathophysiology
GIT
• Many jejunum
• Few duodenum
• Causes protein calorie malnutrition
• A mass of worms can cause intestinal obstruction 
Lungs
• During migratory phase – Tissue reaction to foreign protein
(larvae)
• Causes pneumonitis and can lead to fibrosis (patient may present
with fever, cough, allergic reactions, urticaria, eosinophilia).
Liver
• May cause liver fibrosis and lung abscess
• Also can cause obstructive jaundice.
 Clinical S/S
I. Cough – during migratory phase (lung phase)
II. Fever temp. 380c
III. Epigastric discomfort and abdominal
disturbances
IV. Poor appetite (anorexia)
V. Passage of worm in stool/vomiting 
Diagnosis
• Description of adult worm in stool
• Stool for ova/cyst – Ova seen in microscopy
 Treatment
1. Benzimidazoles
• Mebendazole (vermox)
• Thiabendazole (mintezol)
• Cambendazole
• Flubendazole
• Mebendazole 100mgs bd x 3/7 P.O
• Current – 500mgs stat
• Thiabendazole 25mgs/kg bd x 3/7 P.O. 
2. Levamizole (Ketrax) 5mg/kg stat 
3. Piperazine Hydrochloride (antepar)
150mgs/kg od x 2/7 po
max 4gm od x 2/7
4. Pyrantel palmoate 10mgs/kg stat
5. Albendazole (Zentel) 400mgs stat.
 Prevention
• Proper use of latrines/toilets
• Washing of hands after toilet
• Washing of hands before handling food
• Proper disposal of children’s feaces into latrines
• Washing of fruits and vegetables before eating
• Using drying racks – for utensils
• Mass treatment of infected persons – deworming.
 NOTE – Ascariasis
• Has intermediate host - man
• Transmission – feacal – oral.
• Has a lung phase
• Seen on microscopic exam of stool
• Commonest
• Infective stage is the egg
• Eosinophilia is a feature
• Drug of choice Piperazine
• May cause intestinal obstruction
• May cause Loffler’s Syndrome- pulmonary
eosinophilia,
 2. HOOKWORM
• An infection of the GIT by Ancylostoma duodenale or Necator
americanus.
Causal Agents/Etiology:
The human hookworms include two nematode (roundworm)
species, Ancylostoma duodenale and Necator americanus. 
• (Adult females: 10 to 13 mm [A. duodenale], 9 to 11 mm [N.
americanus];
• adult males: 8 to 11 mm [A. duodenale], 7 to 9 mm [N.
americanus]). 
• A smaller group of hookworms infecting animals can invade
and parasitize humans (A. ceylanicum) or can penetrate the
human skin (causing cutaneous larva migrans), but do not
develop any further (A. braziliense, Uncinaria stenocephala).
 Epidemiology
• Geographic Distribution:
The 2nd most common human helminthic infection (after
ascariasis). 
• Worldwide distribution, mostly in areas with moist, warm
climate. 
• Both N. americanus and A. duodenale are found in Africa, Asia
and the Americas.  Necator americanus predominates in the
Americas and Australia, while only A. duodenale is found in the
Middle East, North Africa, and southern Europe.
• Necator Americanus is common in Kenya
• A duodenale is also common and is found along the coast and
lake region. It is common in tropics and subtropics.
• The larvae require warm, moist environment with temp. – 20-
320c
• Mode of infection is through penetration into the skin.
LIFE CYCLE
• Eggs are passed in the stool , and under favorable
conditions (moisture, warmth, shade), larvae hatch in 1
to 2 days. 
• The released rhabditiform larvae grow in the feces
and/or the soil , and after 5 to 10 days (and two
molts/sloughing/shedding) they become filariform
(third-stage) larvae that are infective . 
• These infective larvae can survive 3 to 4 weeks in
favorable environmental conditions. 
• On contact with the human host, the larvae penetrate
the skin and are carried through the veins to the heart
and then to the lungs. 
• They penetrate into the pulmonary alveoli, ascend the
bronchial tree to the pharynx, and are swallowed . 
• The larvae reach the small intestine, where they reside
and mature into adults.  Adult worms live in the
lumen of the small intestine, where they attach to the
intestinal wall with resultant blood loss by the host. 
• Most adult worms are eliminated in 1 to 2 years, but
longevity records can reach several years.
• Some A. duodenale larvae, following penetration of
the host skin, can become dormant (in the intestine or
muscle). 
• In addition, infection by A. duodenale may probably
also occur by the oral and transmammary route. 
• N. americanus, however, requires a Trans pulmonary
migration phase
 Pathophysiology
• Skin
• At the site of entry may cause local irritation and
inflammation.
• Lungs
• cough
• Eosinophilia
• GIT
• Adult worm produce enzymes which destroy the local
mucosa and anticoagulants causing haemorrhage
• The blood loss leads to Anaemia
• There is evidence that hookworm infestation directly
causes malabsorption and malnutrition.
• However chronic blood loss increases the patients
nutritional requirements tremendously and can
indirectly contribute to severe nutritional disease
• Severity depends on iron intake and worm load.

• AD takes 0.2mls of blood daily

• NA takes 0.03mls of blood daily
NOTE
• 26-100 worms – slight infestation
• 100-500 worms – moderate infestation
• 500 and above – severe infestation
 Clinical S+S
• ‘Ground itch’–due to local pruritus & inflammation
• GIT – Epigastric discomfort
– Abdominal distension especially in children
• Systemic
– Fatigue/weakness
– Due to anemia – Pallor
• - CCF – severe anaemia
 Diagnosis

• -Clinical S+S
• -Stool – microscopy
 Eggs - > 100eggs – severe infestion
 Adult worms
 Occult blood
• -Blood for FHG and ESR – show iron deficiency –
anaemia
• DDX
1. Other helminths
2. Other causes of anaemia
3. Gastritis
4. PUD
• Treatment
1. Mebendazole 100mgs bd x 3/7
2. Thiabendazole 200mgs bd x 3/7
3. Alcopar (Bepherium) adult 1gm sachet stat.
Disadvantage – less effective against N. Americanas
4. Pyrentel palmoate 15mgs/kg od x 3/7
• Supportive measures
1. Give Haematinics – Ferrous sulphate 200mg tds x
2/52
2. Step up the diet/nutrition, especially vitamin
3. In severe cases, transfuse the patient with packed
cells.
• Prevention
• Proper use of pit latrines to ensure high
environmental sanitation
• Proper disposal of children feaces to ensure
adequate sanitation
• Health education – schools, community
• Mass treatment of the population
• Protective wear – avoid contact with soil
• NB:
• Other causes of anaemia
– Haemoglobinopathies
– Bone marrow diseases
– Drugs
– leukaemia
• Malaena
– Hookworm
– Gastritis
– Ca Stomach
 3. STRONGYLOIDIASIS
• Infection of man GIT duodenum by strongyloides
stercolaris.
• Similar to Hookworm.
Aetiology/Epidemiology
• The nematode (roundworm) Strongyloides stercoralis. 
• Other Strongyloides include S. fülleborni, which infects
chimpanzees and baboons and may produce limited
infections in humans.
• The worm is endemic in Far East and tropics Generally.
• In Kenya it commonly occurs at the coast.
• Oftenly it occurs with hookworm.
• Summary of life cycle
• The infective form is the filariform. The adult
worm colonizes the mucosa and submucosa of the
small intestines
• Eggs produced contain larvae which hatch in the
intestine and are passed with faeces or re-infect
the colon. In the soil some may develop into free
living adults or may change into filariform.
• When the filariform penetrate the skin, they enter
blood, travel by way of blood to the lungs where
they mature and migrate to the epiglottis. 
• From epiglottis they become swallowed into the
GIT. Once in the GIT they barrow into the .
• Pathophysiology
• Lungs
• – Pneumonitis which may end up with fibrosis
• X-ray – Hilar enlargement
• Pulmonary shadows
– Loeffler syndrome.
– Asthma like features
• GIT
– Granulomatous reaction and duodenitis
– Malabsorption – diarrhea
– Malnutrition due to malabsorption
– Epigastric pain, anorexia, Nausea, vomiting, diarrhoea
– Enterocolitis leading to Gram-ve septicaemia (bactaraemia) especially in
Immuno compromised patients. It is not common in all patients with this
condition.
• Skin
• - Linear urticaria
– Erythema
• Diagnosis
– Stool – 0/c – several larvae in stool
• *25% may be negative.
– Eosinophilia – 20 – 50%.
• Treatment
• Thiabendazole - 25mgs/kg bd x 5/2
• Vermectin 200mg/kg stat
• Mebendazole (vermox) 100mgs bd x 3/7
• Albendazole 400mgs od x 3/7
• Prevention
• As for Hookworm
• Proper sanitation and waste disposal
• Wear shoes. 
• NB: Strongyloides resembles hookworm in eggs, larvae and
adult worm.
 4. ENTEROBIASIS
– Infestation of GIT by enterobius vermicularis
– E. Vermicularis is a small, white, threadlike nematode.
– The female measures appr. 10mm long.
• Aetiology/Epidemiology
• The nematode (roundworm) Enterobius vermicularis
(previously Oxyuris vermicularis) also called human
pinworm. 
• (Adult females: 8 to 13 mm, adult male: 2 to 5 mm.) 
Humans are practically the only hosts of E. vermicularis. 
• A second species, Enterobius gregorii, has been described
and reported from Europe, Africa, and Asia.  For all practical
purposes, the morphology, life cycle, clinical presentation,
and treatment of E. gregorii is identical to E. vermicularis.
• Has a world wide distribution
• Common in temperate zones than tropics
• Children are more affected may affect the whole
family
• Transmission is feaco-oral
• Auto infection can occur.
• Pathophysiology
• The worm which measures about 10mm long live
on intestinal content of large bowel.
• The female emerges at the anus at night and shed
eggs (coated in sticky material around the anus)
which become ambryonated rapidly.
• They cause perianal itching – scratching, which
result in a new cycle of autoinfection or cross
infection to other children in the family or school.
The eggs are resistant to desiccation(extreme
dryness). They also survive in dust.
• CLINICAL S+S  
• No Lung phase and no eosinophilia (due to lack of
intensive contact of worm with tissue).
• Intense pruritis ani is the main symptom.
• Intense scratching – anal excoriation and bacterial
infection.
• Loss of appetite/weight loss
• Restlessness
• Lack of sleep
• Vulvitis/vaginitis – bactariosis
• Appendicitis may occur.
• Diagnosis
• Apply a piece of a clear adhesive tape to the
perianal region – which may then be examined
microscopically for the presence of eggs (typical)
• Adult worms may be seen leaving the anus by
the child’s care taker.
• Treatment
• Mebendazole 100mgs stat RPT after 2/52
• Pyrantel pamoate
• Piperazine
• Albendazole 400mgs stat
 Treat the whole family.
Prevention
• Personal hygiene
– Bathing and washing
– Cut nails short
– Wash underclothes, night clothes and bed
clothes
• Correct over crowding
• Proper faeces disposal
• Treat the whole family.
 5. TRICHURIASIS
• Infestation by the nematode (Roundworm) Trichuris
trichiura, also called the human whipworm.
Aetiology/Epidemiology
• The 3rd most common round worm of humans. 
• Worldwide, with infections more frequent in areas
with tropical weather and poor sanitation practices,
and among children. 
• It is estimated that 800 million people are infected
worldwide. 
• Trichuriasis occurs in the southern United States.
• Affects the large intestine
• Prefers hot, humid climate
• Common primarily in Nyanza, Coast, Central
Provinces.
• Often occompanies ascariasis
• Has no lung phase
• The adult female can produce upto 20,000 eggs per
day.
LIFE CYCLE
• The unembryonated eggs are passed with the stool .  In
the soil, the eggs develop into a 2-cell stage , an
advanced cleavage stage , and then they embryonate ;
eggs become infective in 15 to 30 days.  
• After ingestion (soil-contaminated hands or food), the
eggs hatch in the small intestine, and release larvae that
mature and establish themselves as adults in the colon .  
• The adult worms (approximately 4 cm in length) live in
the cecum and ascending colon.  The adult worms are
fixed in that location, with the anterior portions threaded
into the mucosa.  The females begin to oviposit 60 to 70
days after infection.  Female worms in the cecum shed
between 3,000 and 20,000 eggs per day.  The life span of
the adults is about 1 year.
 Pathophysiology
1. In large infestation
– Malabsorption
– Diarrhoea
– Malnutrition
– Rectal prolapse
2. Secondary infections of colon mucosa. 
 Clinical S+S
 1. Lower abdominal discomfort
2. Diarrhoea – loose/watery stool passed more than 3
times a day.
 usually mucoid and blood stained
3. Weight loss – because of diarrhea
4. Anaemia – microcytic hypochromic – red blood
cells are small in size and don’t have the pink
colour associated with adequate Hb.
5. Finger clubbing.
6. Eosinophilia in heavy infectation.
 Diagnosis
1. Stool – ova
– Presence of >200 eggs in an ordinary specimen
confirms the presence of infestation.
Treatment
• 1. Mebendazole 100mg bd x 3/7
• 2. Thiabendazole 25mg/kg bd x 3/7
• 3. Albendazole 400mg stat.
Prevention
• As for the Lumbricoides
 6. FILARIASIS
DEFINITION – caused by Nematode (Roundworm) that inhabit the
lymphatics and subcutaneous tissues.
Aetiology
• Eight main species affects man
1. Wuchereria bancrofti and Brugia Malayi, B. Timori
Resides in lymphatics
Causes lymphatic filariasis
Arthropods - Mosquito
2. Loa Loa
Resides in subcuteneous tissues
Arthropods – Deerflies (Chrysops)
3. Mansonella Streptocerca
Resides in dermis and subcuteneous tissues
Arthropodes - Midges
4. Mansonella Ozzadi
Resides subcuteneous tissues
Arthropodes – Midges and Blackflies
5. Mansonella Pertisans
Resides in body cavities and surrounding tissues
Arthropodes - Midges
6. Onchocerca Volvulus
Invades the skin and the EYES
Arthropodes – Simulium Damnosum (Black fly)
 Life cycle
• Infective larvae are transmitted by infected biting
arthropods during a blood meal.
• The larvae migrate to the appropriate site of the
host’s body where they develop into Microfilariae.
• These microfilariae then produce adult worms. The
adult worms dwell in various human tissues where
they can live for several years.
• The agents for lymphatic filariasis reside in lymphatic
vessels and lymph nodes.
• The female worms produce Microfilariae which
circulate in blood except O.V. which invade the skin
and the eyes and M.S. which invade the skin.
• The microfilariae infect biting arthropods.
• Inside the arthropods, microfilariae develop in 1 to
2 weeks into infective filariform (third stage)
larvae.
• During subsequent blood meal by the arthropod
(insect), the larvae infect the vertebrate host.
• They migrate to the appropriate site of the hosts
body where they develop into adults. It can take
upto 18 months for OV.
 A. ONCHOCERCIASIS (RIVER BLINDNESS)
Definition– Chronic disease caused by a Filarial
Nematode ONCHOCERCA VOLVULUS
• Mainly present as skin nodules on the body
surfaces 
AETIOLOGY / EPIDEMIOLOGY
• Major cause of blindness in tropical Africa.
• Found in;
– RiverVoltaBasin in west Africa
– Central Africa
– Parts of E.A.
• Cases are under estimated in East Africa
• Transmission is by Simulium Damnosum (Black fly)
• Also called Buffallo gnuts – Because of its
humpbacked appearance.
• Female flies can inflict painful bites and contribute
to a serious pest at certain times of the year.
• The fly covers a distance of 40 KM maximum-
150KM
• Prefers fast running rivers or turbulent areas with a
lot of Oxygen
• The adult female worm is 33-35 mm long and 0.4mm
thick.
• The adult worm live for 11-18 years
• The female produces thousands of microfilariae which
live for approximately 2 years
• The vector (Simulium Damnosum) takes up the
microfilariae when it sucks blood from an infected
person.
• The microfilaria develops into infectious larvae which
are passed to a new host when the fly bites again.
• The simulium damnosum bites people out doors during
the day – but not in bright sunlight. Usually around
sunrise or sunset or on cloudy days and in the shed.
PATHOPHYSIOLOGY 
• The larvae in subcutaneous tissue develop into
worms, where the mature male and female collect
into balls bound together by fibrous tissue --->
formation of nodules on bony skin surfaces e.g.
elbow, shoulder, scapular, skull, ribs and iliac crests.
CLINICAL SIGNS AND SYPMTOMS
1. Skin nodules
 Nodules are caused by adult worm.
 The nodules are non-tender, rubbery and firm
 Measures 3mm to 3 cm in diameter
2. Dermatitis
 Causes by reaction to microfilariae
 Appears as itchy papules or macules
 Later the skin becomes loose, scaly, atrophic and
depigmented
3. Eyes
 There is oedema of the conjuctiva
 Corneal spots
 Pannus – (invation of the outer layer of the cornea-
abnormal tissue) – Forms at the lower limbus unlike
Trachoma which starts at upper limbus. (i.e. Limbus
sclerae – is the junction of the cornea and sclera of
the eye)
• Catarracts
• Iritis -These contributes to BLINDNESS i.e. River Blindness
• Glaucoma
DIAGNOSIS
1. Skin snips for microscopy – microfilariae
2. Mazzotis test – Rash and pruritus after a dose of
DEC (50 or 100mg), resulting to appearance of an
acute rash in 2-24hrs from death of microfilariae
in the skin.
• Used for diagnosis
TREATMENT
1. Microfilariae
 DiEthylCarbamazine (Hetrazan)
– 2mgs/kg tds X 3/52
– No effect on adult worm
 Ivermectin (Mectizan)
– 150mg/kg P.O. stat. (Twelve monthly therapy)
– Is effective when given as a single dose
2. Adult worms
--Surgical removal of the nodules
 PREVENTION
1. Chemotharapy with Ivermectin
2. Addition of insecticides to the rivers where
simulium breeds.
 B. FILARIASIS (Lymphatic Filariasis)
Definition: Infection by the nematode Wuchereria
Bancrofti and Brugia Malayi.

• The pathologic manifestation of the disease result

from inflammation and mechanical obstruction of
the lymph channels
 AETIOLOGY/EPIDEMIOLOGY
• In Africa it is common in Coastal belt and Lake
region
• Not in Highlands High altitudes
• Culey fatigans - Urban
• Anopheles funestes – Rural
• No immunity.
• Adult worm is approximately 4-8 cm long and 0.2
mm thick
• NB:
• The adult worm do not replicate in the human host
• The number of filariae and severity of the disease
depends on the number of mosquito bites
• Mosquito vector is intermediate host
 PATHOPHYSIOLOGY 
• Inflammation at infected site (due to reaction to a foreign
proteins)
• Lymph nodes are the primary site of infection and the
clinical manifestation of the disease depends on which LNs
are affected.
• In LN and connective tissue inflammatory reaction -
>Lymphagitis->Fibrosis -->mechanical obstruction of
lymphatic channels ->Oedema ->Elephantiasis and
secondary infection.
– Inquinal LN –Oedema ->elephantiasis of lower
extremities
– Axillary LN – Oedema -> elephantiasis of upper
extremities
 CLINICAL S+S
1. Acute phase (Infective stage) 1st month
• Due to hypersensitivity reaction
• Starts few months after the infection
• Characterized by; 
 Fever
 Eosinophilia
 Lymphadenopathy
 Lymphagitis
• -There is a negative smear (No microfilaria in blood)
• -The microfilaria are still immature
2. Sub acute phase (Inflammatory stage) 1st year
• Occurs approximately in the first year.
• Worms have matured and microfilarie present in the
peripheral blood (Smear +ve)
• Adult worms cause;
Fever
Lymphadenitis
Funiculitis- inflammation of spermatic cord
Epididymitis
Hydrocele
• Microfilariae cause;
 Hyper eosinophilia – Tropical Pulmonary Eosinophilia
 Asthma like symptoms
 Fever
• Lymphoedema
• Elephantiasis – arm and leg swelling
• Chyluria – (chyle-milky bodily fluid-lymph &
emulsified fats formed in SI )
• Hydrocele
• Breast swelling and fibrosis
• Chylous ascities if thoracic duct is involved
1. Blood Slide
• Take between 10 am to 2.00 pm
• Demonstration of microfilariae in peripheral blood
specimen at night
• or 45minutes after an initial dose of
diethylcarbamazine 100mg (Provocative dose)
2. Lymph node aspirate or hydrocele aspirate
NB:
- LN removal can lead to worse obstruction
 TREATMENT
1. Supportive;
- Elevate affected extremities
- Elastic bandages 
2. Specific therapy
Diethyl Carbamazine citrate(Banocide, Hetrazan) 6mg/kg/day x 12-
21/7 
S/E:- Headache ,Pruritus. 
NB: give antihistamine to take care of S/E
Others
Ivermectin (Mectizan)
Albendazole
PREVENTION 
1. Vector control :-Spraying, Draining stagnant water
2. Mass treatment of affected population
 B. CESTODES (TAPEWORMS)
1. Taeniasis
2. Echinococcosis
 1. TAENIASIS
• [Taenia saginata] [Taenia solium]
• The cestodes (tapeworms)- Taenia saginata (beef
tapeworm) and T. solium (pork tapeworm).  Taenia
solium can also cause cysticercosis (cysts formed in
brain and muscle tissue).
• Infection by: - T. saginata – Beef tapeworm
- T. Solium – Pork tapeworm
- H. Nana – Dwarf tapeworm
(hymenolepis nana)
- D. Latum – Fish tapeworm
(diphyllobothrium latum).
• Intermediate host – cows
• Man is ! R!q host.
 Epidemiology
• Is a cosmopolitan infection, but largely found in
cattle raising regions of East and Central Africa.
• Infection follows ingestion of uncooked meat
(beef/pork) containing cysticercus.
• Both species are worldwide in distribution. 
• Taenia solium is more prevalent in poorer
communities where humans live in close contact
with pigs and eat undercooked pork, and in very
rare in Muslim countries.
Life cycle
• The intermediate hosts – cows – are infected while grazing on
contaminated soil.
• The eggs hatch in the ruminants intestines. The larvae
(oncospheres) penetrate the mucosa – enter lymphatics –
circulation and end up in the muscles.
• The scolex of a future tapeworm forms and when eaten as a
component of uncooked meat, it gets attached on the intestinal
mucosa by its four sackers.
• New segments (proglottides) will develop distally until the worm
is about 12 metres (strobila). 
• The distal proglattides are the most mature containing a branched
uterus full of eggs.
• The human passes about six segments each day, after passing
through the anus, the uteri expel the eggs which can remain in
grass for many months, until ingested by another ruminant to
start the life cycle again.
 Clinical S+S
Weight loss
Colic – abdominal colic – severe abdominal pain usually of
fluctuating severity, with waves of pain seconds, or a few
minutes apart.
Irritability
Insomnia
Psychological upsets the patient
Neurocysticercosis – T.solium – Epilepsy

Diagnosis
• Proglottids can be seen moving at the anus and in the stool.
• Ova in stool
 [

Treatment
1. Praziquantel 10-20mg/kg stat – is effective
2. Niclosamide 2gm stat
3. Zentel (albendazole) 400mgs 0d x 3/7

Prevention
1. Environmental sanitation – difficult with nomadic
people
2. Meat inspection should be strict – infected meat
be condemned.
3. Thorough cooking of meat – boiling sterilizes the
worm.
 2. ECHINOCOCCOSIS
• [Echinococcus granulosus] [Echinococcus multilocularis]
[Echinococcus oligarthrus] [Echinococcus vogeli]
Infection by the larval form of the cestodes
(Tapeworm) Echinococcus granulosus.
Is a disease of animals and man.
Prevalent where man, sheep and dogs live in
close contact.
Causes morbidity (a state of being diseased- No
of diseases – m – rate) and mortality (incidence
of death in a pp), and contributes indirectly to
human disease by its effects on domestic
animals.
Aetiology/Epidemielogy
Causal Agent:
Human echinococcosis (hydatidosis, or hydatid
disease) is caused by the larval stages of cestodes
(tapeworms) of the genus Echinococcus. 
Echinococcus granulosus causes cystic
echinococcosis, the form most frequently
encountered;
E. multilocularis causes alveolar echinococcosis;
E. vogeli causes polycystic echinococcosis; and
E. oligarthrus is an extremely rare cause of human
echinococcosis.
 Dogs are the main source of human infection
 Turkana has the highest incidence in the world
 200-300 new cases each year
 Cysts are demonstratable by 0/c
 Also found among the masai and other nomadic
communities
 About 40-70% of dogs are infected in Turkana
 People at risk include farmers, herdsmen
(particularly of sheep) hunters, skinners, tanners,
and those exposed to dogs.
 The worm is small measuring 3-6mm long.
 Distribution
1. Turkana – most common ‘tumour’
-- 40 – 70% of dogs are infected. 
2. Masai land – affects cattle – more than 40%
are infected
 LIFE CYCLE 
• The main reservoir of hydatid cysts includes dogs
and cattle.
• In man – enters the gut and passes by way of
circulation to reach the liver from where they reach
systemic circulation right side of heart and –
pulmonary circulation
• Cysts develop primarily in liver – 70%
• 10-15% in lungs
• Can also develop in any organ.
Pathophysiology
1. Early inflammation of infected
organ
–Pneumonitis in lungs
–Local hepatitis in liver – enzyme
changes
–Focal seizures in brain.
2. Pathologic changes related to mechanical disruption by
the growing cyst.

(i)Liver– Tissue necrosis

- Portal obstruction
- Obstructive jaundice
- Ascites-cyst in portal hepatic and bile ducts
- Vericosities
- 50 – 70% of the cases
- peritonitis
- acute abdomen
- Abdominal mass or distensions
- eosinophilia
• (ii) Lung – 12 – 30% of the cases
– airway obstruction – atelectasis
– cough, haemoptysis, pleuritic pain,
breathlessness, fever
– obstruction of pulmonary vessels
– rupture of vessels – haemorrhage
– decreased ventilation – decreased absorptive
surface area + blockage
(iii) Brain
– Focal irritation – seizures
– Blockage of CSF flow- hydrocephalus 
(iv)Bone
– Destruction of normal bone structure
– Pathological fractures
– Vertebral collapse - paraplegia
(v)Systemic
– Fever
– Pruritus – generalized.
– Anaphylactic reactions
 Diagnosis
1. Imaging – ultrasound – most convenient
- CT – scan or arteriography PRN
- Plain abdominal X-ray
(i)calcified cysts – outer coat
(ii)Lungs or pleural cysts are seen on x-ray
2. ELISA and indirect agglutination tests
– Useful for diagnosis
– >90% sensitive 
3. Immunoprecipitation and complement fixation tests
– More useful in follow up after treatment
Clinical S+S – is useful
--No aspiration.
Treatment
1. Surgery–excision with removal of cyst intact if
possible
– Inject formalin (40% formaldehyde in water) into
cyst at surgery
– Used as a sterilizing agent
– It is lethal – bacteria, fungi viruses and cysts.
2. Mebendazole
– 12 – 1800mgs/days x 30/7
– The drug limits glucose uptake by the parasite –
depletion – death
3. Albendazole 20mg/kg x 6/52 - 800mg/day
 Prevention
i. Deworm dogs
ii. proper disposal of animal viscera
iii. Avoid dog excrement(waste- feces/urine)
iv. Personal hygiene
• NB: Incase of anaphylaxis – manage
 DDX
1. Amoebic abscess
2. Hepatoma
3. Schistosomiasis
4. Cholecystitis – inflammation of the gall bladder
5. Hepatitis
6. Loculare pleural effusion (small cavity or
compartment within an organ or part of an organism)
7. Cavity lesions – TB, fungal infection
8. Tumours – intracranial tumours
9. Abscess
10.Epilepsy.
Complication
1. Rupture
2. Secondary infection
3. Other organ involvement 
NB: Prognosis – Good
Danger – Rupture.
 C. TREMATODES (FLUKES)

1. SCHISTOSOMIASIS – BILHARZIA 
• Is a chronic disease caused by trematodes of the
genus schistosoma.
• Schistosoma affects the bowel or the bladder
depending on the species.
• The clinical manifestation result from body’s
reaction to foreign protein (eggs of the worm), and
therefore depends on the location of the adult
worm.
AETIOLOGY /EPIDEMIOLOGY 
1. It is the most widespread and serious tropical
disease after malaria in some countries
2. -600 million people are at risk
-200 million people are infected
-¾ is from Africa
DISTRIBUTION IN KENYA
 SH is the most common in Kenya
 Common in Lakes, Coast, Tana River
 Tends to spread into new irrigation projects
3. In Egypt 37% of the population are infected
4. Effects of the disease depends on:-
–Worm load
–Duration of the illness
–Immune status of the patients
–Other concurrent illnesses
5. Anaemia caused by schistosomiasis contributes to
morbidity in children and lack of productivity in
adults.
6. The incidence of schistosomiasis is related to water
use i.e:-
(i)Water project for irrigation and electricity
generation provides the habitat for the snail vector
causing epidemics
(ii)Rise in socio–economic levels with improved
agricultural techniques has often been
accompanied by an increased incidence of the
disease.
7. The main schistosomes which infect man in Africa
are;
i. Schistosoma Mansoni (SM) - intestinal
ii. Schistosoma Haematobium (SH) – urinary
Others
iii. S. Japonicum – Valley of Yougze Kiang – Japan and
S.E. Asia (Far East)
iv. S. Intercalatum – Zaire, Gavon, Cameroon
v. S.Mathei and S. Bovis – sometimes infect man
Schistosoma Haematobium (SH)
 Lives in nervous plexus of the urinary bladder
 The eggs are excreted in the urine
 The vector snail belongs to the genus BULINUS –
which prefer temporary water bodies like ponds,
dams etc
 It adapts the adverse conditions during dry seasons
(aestivation)
 The eggs have a terminal spine
 Schistosoma Mansoni (SM)
 Lives in the mesenteric plexus of the large
intestines.
 Eggs are excreted with faecesgenus
BIOMPHALARIA.
 Prefers permanent water bodies like streams,
irrigation schemes and lakes.
 The eggs have a lateral spine
 LIFE CYCLE
• Eggs in urine or stool are deposited in water
• They hatch into miracidium in water
• They must enter into a suitable fresh snail vector in
24 hrs or they die
• Cercaria on penetration of skin gain entrance into a
peripheral vein -> into systemic veins that lead to the
right side of the heart
• From the right side of the heart, they pass through
the pulmonary circulation to the left side of the heart
• They then enter systemic circulation to messentric
arteries
• They go via mesenteric capillaries to mesenteric veins and
end up in the portal circulation(liver)
• In the liver they develop and become adults
• The adult S. Haematobium, swims upstream from the liver
to come and localize in the urinary bladder wall – afew may
be found in the rectum
• S. Mansoni localize in the rectum – a few may be found in
the bladder
• The eggs may re-enter the circulation veins -> portal
circulation ->liver -> right side of the heart ->lungs. At times
they may be trapped in the liver and lungs causing scarring
• Others may go via anorectal anastomosis and reach the
CNS
NB:
1. Other hosts – Monkeys, Baboons and some
Rodents
2. Requires presence of fresh water snails
3. Adult do not replicate inside the human hosts
4. Therefore, the severity of the infection is
determined by the number of cercaria infecting
the skin
5. There is no immunity to Schistosomes
6. Eggs are extremely antigenic, leading to immune
response and tissue destruction
PATHOPHYSIOLOGY 

In 4 stages 

1: Stage of Invasion (Primary Infestation)

The cercaria penetrates the skin causing;
i. Cercarial dermatitis – Itching papules–‘swimmers
itch’
ii. Cercaria enter the circulation and reach the liver
via the right side of the heart causing pneumonitis.
2: Maturation Stage
• Schistomes mature in the liver
• Is associated with fever, eosinophilia,
abdominal pain and generalized transient
urticaria, known as katayama syndrome
• After maturation the adult worms descend in
the portal vein:
i. S. Mansoni – moves to mesenteric veins of
the GIT
ii. S. Haematobium – moves to venous plexus
of the bladder
3: Established Infection (Stage Of Egg Production)
• Some eggs do not penetrate the tissues, but are
carried by blood to the liver and lungs.
• Other eggs penetrate tissues, but fail to reach
the lumen of bladder or bowel. The eggs
provoke inflammatory reaction causing;
–Formation of granuloma
–Colitis + cramps
–Bloody diarrhea in S. Mansoni
–Terminal Haematuria and dysuria in S.
Haematobium
4. Late Stage
• Due to large numbers of eggs, there is fibrosis and
calcification of tissues leading to:-
i. Urethral structure, bladder outlet Obstruction
ii. Dilatation of the ureter (hydroureter)
iii. Hydronephrosis
iv. Kidney failure
v. Pylonephritis
vi. Bladder calcification – Ca bladder commonest
cause of Ca in Egypt and Mozambique
 Liver
• Periportal fibrosis – portal HTN ->liver failure
• Oesophageal varices + ascities -
>Hypoalbuminaemia 
Spleen
• Hyperplenism and anaemia –> bleeding tendencies
Lungs
• Pulmonary fibrosis –> Hypoxia –> restrictive -> lung
disease
• Pulmonary HTN ->RVH ->CCF
 GIT
• Rectal; scarring, abscess and fistula formation
• Rectal prolapse 
CNS
-Focal scarring in CNS leads to;
1. Epilepsy
2. Dementia
3. Secondary infections – Meningitis
– Encephalitis
Clinical Signs and Symptoms
A: S. HAEMATOBIUM
1. Swimmers itch
2. Incubation Period - 10/52
3. Fever (evening)
4. General malaise
5. Abdominal discomfort
6. Suprapubic pain
7. Terminal Haematuria – bright red blood or
“smoky” urine
8. Dysuria
B: S. MANSONI
1. Swimmers itch
2. Incubation Period - 5/52
3. Prodrome as per S.H – fever, G. malaise
4. Bloody diarrhea
5. Rectal discomfort (tenesmus)
6. Infection of ascending colon + hepatic flexure,
causing RUQ pain
7. Urticaria secondary to Eosinophilia
DIAGNOSIS 
1. Clinical S+S in endemic areas
2. Urine – terminal spine (SH)
3. Stool – Lateral spine (SM)
4. Cystoscopy
5. Rectal Snip Then biopsy is taken

6. Serology – circulating anodic antigens (CAA)

- Circulating Cathodic antigens (CCA)
7. Elisa
8. Proteinuria (dipstic) - SH
9. Eosinophilia - SH
 TREATMENT 
1. Praziquantel (Biltricide) (1 tablet = 600mgs)
-40mgs/kg stat P.O. (1200mgs stat) or 20mgs/kg Bd x 1/7 
NB:
• Is active against all forms of schistomes
• Is well tolerated
• Unwanted effects are mild and trancient 
S/E
• H/A
• Abdominal discomfort
• Slight drowsiness
• Urticaria
• Fever
• NB: Not recommended for use in pregnancy
2. Metrifonate (Bilarcil)
– 10mgs/kg P. O. every 2 weeks for three doses
NB:
• It is an organophosphorous cholinesterase
inhibitor
• Effective against S.Haematobium species
3. Oxamniquine (Vansil)
15-30 m/kg body weight OD P.O x 3/7
or
IM 7.5mg/kg body weight start
NB:
 Is schistosomocidal against both immature and
mature worms
 Effective against S. Manoni
 Can be given IM or PO
S/E
1. Dizziness
2. Somnolence (i.e. almost asleep- makes you feel tired)
3. Fever
4. Eosinophilia
5. Transient pulmonary infiltration
6. Abnormal LFTs
7. EEG – change
8. Hallucinations
9. Seizures 
C/I
10.Pregnancy
11.CCF
12.Renal failure
13.Epilepsy
 COMPLICATIONS 
SH
1. Scarred bladder
2. Ureteral and urethral obstruction
3. Hydronephnosis ->renal failure
4. Ca bladder
5. Pulmonary and liver complication 
SM
1. Rectal scarring –> bowel necrosis
2. Rectal prolapse
3. Cirrhosis of the liver
4. Hypersplenism - Massive Splenomegaly
5. Hypo albuminaemia -> ascites
6. Bleeding tendency
7. Hepatic encephalopathy
8. Pulmonary fibrosis ->pulmonary Hypertension -
>Hypoxia
CNS 
1. secondary infections – salmonella paratyphi
 PREVENTION 
A: Removal of intermediate hosts
1. Spraying – with Copper sulphate or Bayluscide
(Niclosomide)
2. Consult with water engineers to increase water
flow
B: Environmental saniation
– Urination in water should be avoided
– Defaecation
C: Avoid contacts with contaminated
water(i.e. water contaminated by
Schistosoma)
PROTOZOAN INFECTIONS
1. MALARIA
2. AMOEBIASIS
3. GIARDIASIS
4. LEISHMANIASIS
5. TRYPANOSOMIASIS
6. TOXOPLASMOSIS
 1. MALARIA
• The use of the word - Malaria
Refer to the:
 Parasite
 Disease caused by the protozoan -plasmodium
 Socio-economic problem/burden
 Definition- Malaria is a disease caused by the
parasite of the genus PLASMODIUM.
 
 Parasite in human
• 4 human species: P. falciparum, P.malaria, P.
ovale, P. vivax.
• Plasmodium Falciparum is the commonest species
in Kenya and is associated with significant morbidity
and mortality.
• Distribution: P. falciparum – >90% Africa
: P. ovale >70% Far East,
• Optimal growth - body temperature
• multiplication from a single sporozoite
• P.falciparum – 10,000 Merozoites (liver)
• P Vivax, P. ovale, p Malaria3000– 4000
 Transmission  
1. Through bite of a mosquito
2. Blood transfusion/through needles
3. Via the placenta
 NB:
i. There is no liver phase in transmission caused by
transfusion, congenital or sharing needles
ii. EE – exoerythrocytic schizogony = liver stage
iii. P. vivax schizogony – 6-8 days with 10,000
Merozoites from one sporozoite
iv. P. ovale schizogony – 9 days with 15,000 Merozoites
v. P. malariae – 12 – 16 days with 2,000 Merozoites
from each sporozoite.
vi. P. Falciparum takes 5-7 days with 40,000 Merozoites
per sporozoites.
• NB: Merozoites do not re-invade the liver.
EPIDEMIOLOGIC AREAS IN KENYA 
• Endemic – present
– Coast, Nyanza, machakos, Kitui – (Coastal belt and low lying
areas).
– Occur all year round with increased temperature + rainfall

• Epidemic – seasonal
– Rift Valley - increased in temperature & rainfall.
– Nandi
– Kisii

• Not present
– Mt Kenya, Aberderes – those areas above 1500m ASL.
- Very dry areas
Malaria risk areas in Kenya
• High Malaria risk areas – Lakeside, Highlands, and
Arid areas
• Low Malaria risk areas – Highlands within central
and Nairobi provinces

• Assignment: Define – Hypoendemic,

Hyperendemic, Holoendemic, Mesoendemic.
Effect on Health
 Worldwide affects 100-200 million people annually
with 400 million at risk.
 About 2.3 million especially children die every year.
 3rd leading cause of death in Kenya
 Is responsible for 10% of infant mortality
 Splenic rates are approximately 85% in Nyanza and
Coast
 It is a major cause of economic loss through loss of
working and leasing days.
• Who is at greatest risk to Malaria?
1. Children less than five years of age in high risk
areas
2. People of all ages in areas of low risk
3. People returning to highly endemic areas after
prolonged absence.
4. Travelers from areas with little or no malaria.
5. Pregnant women, especially in their first
pregnancy.
6. Patients with Sickle Cell disease.
7. Internally Displaced Persons.
8. People who have had Splenectomy.
 Factors that affect severity of the disease
1. Species of Plasmodium
• Severe malaria is caused only by P. Falciparum
• P.F. is also a leading cause of uncomplicated
2. Endemicity
• Adults and older children who have lived for long in
endemic malaria areas are less susceptible to
severe malaria.
• But still they may suffer from uncomplicated
malaria.
3. Host factors
a) Children and pregnant women are more
susceptible to severe malaria.
b) Sickle cell trait
– Infection by malaria parasite causes a sickle Rbc to
deform (become sickled). The sickled cells are removed
by the spleen and the parasite destroyed.
c) G6PD deficiency
– Rbc breaks down before the parasite has had a chance to
replicate. Therefore protects against malaria.Patients
with G6PD deficiency are prone to severe hemolysis
during treatment with Chloroquine and quinine.
d). Specific immunity to the parasite
– Requires constant sub clinical infection to remain active.
If a patient leaves a malaria endemic area, loses
immunity rapidly.
e). Duffy antigen- Protects against malaria

4. Parasite drug resistance

• Degree of parasite drug resistance that prevails
locally also influences severity of Malaria.
 LIFE CYCLE
• The malaria parasite life cycle involves two hosts. During a blood
meal, a malaria-infected female Anopheles mosquito inoculates
sporozoites into the human host (1) . Sporozoites infect liver
cells (2) and mature into schizonts (3) ,which rupture and release
Merozoites (4) . (Of note, in P. vivax and P. ovale a dormant stage
[hypnozoites] can persist in the liver and cause relapses by
invading the bloodstream weeks, or even years later.)
• After this initial replication in the liver (exo-erythrocytic
schizogony A ), the parasites undergo asexual multiplication in
the erythrocytes (erythrocytic schizogony B ). Merozoites infect
red blood cells (5) . The ring stage trophozoite mature into
schizonts, which rupture releasing Merozoites (6) . Some
parasites differentiate into sexual erythrocytic stages
(gametocytes) (7) . Blood stage parasites are responsible for the
clinical manifestations of the disease.
• The gametocytes, male (microgametocytes) and female
(macrogametocytes), are ingested by an Anopheles
mosquito during a blood meal (8). The parasites’
multiplication in the mosquito is known as the
sporogonic cycle .
• While in the mosquito's stomach, the microgametes
penetrate the macrogametes generating zygotes (9) .
The zygotes in turn become motile and elongated
(ookinetes) (10) which invade the midgut wall of the
mosquito where they develop into oocysts (11) . The
oocyte grow, rupture, and release sporozoites (12) ,
which make their way to the mosquito's salivary glands.
• Inoculation of the sporozoites into a new human host
perpetuates the malaria life cycle.
• Malaria is an infectious disease caused by a one-celled parasite known as
Plasmodium. The parasite is transmitted to humans by the bite of the female
Anopheles mosquito. The Plasmodium parasite spends its life cycle partly in
humans and partly in mosquitoes. (A) Mosquito infected with the malaria parasite
bites human, passing cells called sporozoites into the human’s bloodstream. (B)
Sporozoites travel to the liver. Each sporozoite undergoes asexual reproduction, in
which its nucleus splits to form two new cells, called Merozoites. (C) Merozoites
enter the bloodstream and infect red blood cells. (D) In red blood cells, Merozoites
grow and divide to produce more Merozoites, eventually causing the red blood
cells to rupture. Some of the newly released Merozoites go on to infect other red
blood cells. (E) Some Merozoites develop into sex cells known as male and female
gametocytes. (F) Another mosquito bites the infected human, ingesting the
gametocytes. (G) In the mosquito’s stomach, the gametocytes mature. Male and
female gametocytes undergo sexual reproduction, uniting to form a zygote. The
zygote develops into a mobile ookinate which migrates through the wall of the
stomach to form an oocyst. Oocyst matures and releases sporozoites, which travel
to the mosquito’s salivary glands. (H) If this mosquito bites another human, the
cycle begins again. Inoculation of the sporozoites into a new human host
perpetuates the malaria life cycle.
PATHOPHYSIOLOGY 
 The liver and Rbc are the only human tissues directly
infected by the parasite
 All the pathophysiologic changes of malaria result from
infection of liver and rbcs.
A. Infection of Rbc causes;
i. Hemolysis –>anemia. The anemia is Normocytic
Normochromic Anaemia-(NNA)
ii. RBC sequestration in the spleen –>anemia –>
decrease oxygen carrying capacity.
iii. Splenomegaly
---possible rupture
---Thrombocytopenia
---bleeding tendency
 iv. Increased deformability -> blocked vessels –> Anoxia
-> Liver damage.
v. Increase adhesion –> blocked vessels -> Anoxia
-> Liver damage
Vi. Decrease oxygen transport –> anoxia
vii. Increased fragility –>hemolysis –> anaemia
viii. Local necrosis and ischaemia. Rbcs invasion –> rupture –>
releasing new Merozoites and there is release of vaso active
peptides which activate the immune systems ->damage to vessel
endothelium, causing blockage of capillaries –> local necrosis and
ischaemia –>
-Anoxia –> vasodilation –> Hypotension –> ARF
-Liver damage
-Abnormal metabolic activity (i.e. anaerobic metabolism) –>
lactic acidosis.
 B. Liver infection
 It leads to decreased liver functions
i. Jaundice
ii. Hypoalbuminaemia –> fluid over load –>
– Pulmonary edema
– Cerebral edema
iii. Decreased iron turn over –> anaemia
C. Brain - Local ischaemia and inflammation (In the brain,
there is decrease 0xygen, ↓glucose, ↓blood and edema). –
> cerebral malaria
D. Heart – Myocarditis
E. Kidney – irreversible renal damage
F. Spleen – local necrosis
G. GIT – diarrhea, vomiting, dehydration
Summary
A. In Rbc
1. Increased deformability
2. Increased adhesions
3. Increased fragility
4. Decreased O2 transport
5. Toxin production
6. Antigen release
B. Outside the red cell
1. Blocked capillaries (vessels)
2. Increased permeability
3. Anoxia
4. Anaemia
5. Intravascular hemolysis
6. Haemoglobinuria (Black water
fever)
7. Immune complex formation
8. Complement depletion
 ;

9. Disseminated intravascular
coagulation
10. Liver damage
11. Increased Na+ and K+ ratio
12. Decreased albumin
13. Increased plasma volume
14. Orthostatic hypotension
15. Bone marrow depression
16. Reticulo endothelial cell
hyperplasia
17. Platelet depletion.
C. Organ damage
1. Liver failure :-Jaundice
- Coagulation defects
2. Pulmonary disease:-Pulmonary edema
-Acute respiratory distress syndrome(ARDS)
3. Cerebral Disease:-Coma
-Convulsions
-Delirium
4. Acute Renal Insufficiency - Oliguria
- Isosthenura
5. DIC :- Mycordial failure
-Bone marrow depression
-Still birth.
NB: Oligosuria and Isosthenuria is due to;
- Immunie complex nephritis
- Nephrotic syndrome
- Renal cortical necrosis
- Acute tubular necrosis
- Tubular blockage
REMEMBER
 Two characteristics of PF [Malignant tertian malaria
(subtertian malignant.)]Infection makes it
particularly dangerous and more severe:-
i. Infects all ages (stages) especially young cells of
RBCs and produces more Merozoites. Therefore
cause severe hemolysis.
ii. Causes Rbc agglutination(adherence of infected
cells) and local capillary blockage –>
ischaemia/Anoxia
Clinical S + S
 

A. P. Falciparum
• Incubation period 10 – 14 days
• Insidious progression of symptoms
– Malaise
– Hotness of the body
– Muscle and joint pains
– Anorexia
– Increasing headache
– Nausea and vomiting
– Increasing joint pains
– Cough
– Diarrhea
– Chills with gradual increase in temperature over 10-24 hours
On Examination
1. Fever – have no particular pattern. May be persistent,
a times it may be a periodic or a spiking fever.
2. Jaundice – Due to Hemolysis RBC. Therefore the main
features are those of Hemolytic anaemia.
3. Pale – because of anaemia. Anaemia due to
haemolysis.
4. Splenomegaly – tender
- ↓Platelets, ↓immunity, ↑infections.
5. Hepatomegaly– tender
6. ± Other features of complicated/severe malaria.
Cerebral malaria is the most serious complication.
STAGES OF FEVER IN MALARIA
1. Cold stage – Vasoconstriction –> shivering. May
last up to half an hour.
2. Hot stage – temperature -↑400C
3. Delirium – Lasts 2 – 6 hrs. – Not able to think or
speak clearly
– Délusion, Désorientation, Hallucination, Extrême
excitement.
4. Sweating stage – patient sweats a lot, there is
resolution of fever, patient feels tired, but
otherwise well
Variants (forms) of falciparum
1. Billous remittent fever – characteristic by severe liver involvement.
i. Jaundice
ii. Nausea, vomiting
iii. Dehydration – shock
2. Cerebral Malaria:
 Unarousable coma not attributed to any other cause in a patient with
plasmodium Falciparum (positive blood slide for malaria) malaria.
 The progress is as follows:
i. Usually there is progressive severe headache
ii. Confusion, hallucination, psychosis
iii. Coma – (Due to Ischaemia, anoxia, hypoglycarmia + oedema)
iv. Seizures /convulsions.
NB – children die rapidly without any special symptoms other than fever.
3. Black water fever:-
- There is renal failure characterized by:-
i. Severe hemolysis and Haemoglobinuria
ii. Acute renal failure – Urine output less 400mls/24hrs
- in children < 12mls/kg/24hrs
iii. Oliguria – small volume of urine or Anuria – failure of kidney to
produce urine
NB
• It is said to be black water fever because patients pass dark-brown-
black urine owing to intravascular hemolysis caused by P. Falciparum.
- may be precipitated by small amounts of quinine
- There is abrupt onset of fever, marked hemolysis,
Haemoglobinuria, hyperbilirubinaemia, vomiting, circulatory collapse
and acute renal failure. 
• B/S – MPs negative.
4. Algid malaria (severe GIT involvement)
- This is due to ischaemia of mesenteric capillaries.
- There could be:
(i) Vomiting/diarrhea
(ii) Dehydration
(iii) Shock
(iv)Renal failure
• Fever in malaria could be
– Continuous – fluctuation not >10c
– Remittent – fluctuations not > 20c
– Intermittent – several hours in a day
– Quotidian – 1 day
– Tertian – 2 days
B. P. Malariae – (Quartan Malaria)
– No hypnozoites
S+S are less severe than P.F.
1. Parasitaemia is low because malariae infects mature (older) Rbc.
– I.P is 3 – 4 weeks
– Prodrome as per Falciparum (malaise, mild fever, muscle &
joint pains, anorexia)
2. Fever is periodic (cyclical):
- Occurs daily at first, but spikes every 72 hours
- Patients experiences chills– fever rises over 4-5 hours - –
delirium, then sweats a lot – resolution of fever, patient is tired
but otherwise well.
3. Nephritis (proteinuria) – Nephrotic syndrome
C. P. Vivax (Benign tertian)
– The classic tertian malaria – fever spikes every 48 hours
– Vivax infects only reticulocytes – (single Rbc infection)
– IP- 12 – 15 days
– Prodromal s+s similar to P.malariae.

D. P. Ovale (Ovale Tersian)

– Also infects only reticulocytes, only single infection of Rbc.
NOTE
The occurrence of recurrent or chronic malaria in PF and
PM is due to persistent erythrocytic phase, due to
inadequate treatment.
While occurrence of recurrent or chronic malaria inP.V. and
P.O is due to chronic liver phase.
A patient is said to be having SEVERE
MALARIA/COMPLICATED malaria when there is:-
1.Cerebral malaria
2.Severe anaemia - < 15% or Hb <5g/dl
3.Renal failure – Urine output <400mls/24hrs or
12mls/kg in children.
- Serum Creatinine<265 µmol/l (>3.0mg/dl)
-[NormalCreatinine – (62-124µmol/l) or 0.7-
1.4mg/dl]
-[Normal urea – 2.5 – 6.6 mmol/ltr (15 – 40mg/dl)]
4. Pulmonary edema
5. Hypoglycemia – whole blood glucose <2.2mmol/L
(40mgs/dl)
6. Shock – Hypotension – systolic <70mmHg or <
50mmHg in children with low temp.
7. Spontaneous bleeding from gums, nose, GIT etc. –
evidence of DIC
8. Convulsions – repeated more than twice in 24 hours
9. Acidosis – arterial PH < 7.25 or plasma bicarbonate <
15mmol/l
10. Haemoglobinuria – Because of Black water fever.
11. Hyperparasitaemia – of >5% in Rbc.
12. Jaundice – detectable clinically
13. Hyperpyrexia – 390c
NB:
i. Blood creatinine is more accurate than blood urea
because creatinine levels is not affected by extra
renal factors e.g. Diet in protein
ii. Range of Parasitaemia:
a) 50 – 150 parasites – slight
b) 200 – 250 parasites – moderate
c) >1000 parasites – heavy.
Diagnosis
A. Clinical S+S
-Periodic fever, anaemia, splenomegaly or prolonged rising
fever - (requires a high index of suspicion is important).
B. History of exposure
C. Blood slide for MPs (microscopy – detect Parasitaemia of
0.0004% in the hands of a well-trained microscopist)
-In Falciparum – the smear may be negative depending on
the time the smear was taken, experience of the technician.
- Successive smears should be done at least x6.
NB:
– Thin smear – species all stages
– Thick smear – ring forms
D. Blood for – QBC (Quantitative Buffy coat).
-This is mainly concentration of infected red blood cells by
centrifugation with staining of parasite with Acridine orage.
-Infected red cells have a greater density than uninfected
cells.
-Sensitive than thick film that is can detect one infected red
cell in 100million uninfected cells. 
E. Other investigations
- Species specific DNA probes – for PF and P.V – can detect
parasitaemia of 0.001%
- Ribosomal RNA (rRNA) probes – 0.00001%
- Polymerase chain reaction (PCR)
– Rapid Diagnostic Test (RDT).
REMEMBER INVESTIGATIONS IN MALARIA
i. Microscopy – is the gold standard
ii. QBC - Quantitative Buffy Coat
iii. PCR – Polymerase chain reaction
iv. RDT – Rapid Diagnostic Test.
DDX of Malaria
1. Typhoid Fever
2. Brucellosis
3. Kalaazar
4. Tuberculosis
5. Schiztosomiasis
6. Leptospirosis
7. Lymphoma
8. Leukemia
9. Meningitis
10.Trypanosomiasis
11.Septicaemia
12.U.T.I in pregnancy
Treatment
i. Treatment of uncomplicated malaria.
ii. Treatment of complicated malaria.
iii. Supportive treatment.

1.Treatment of uncomplicated malaria.

A. First line – ACT(Artemisinin-based combination
therapies)
– Artemether Lumefantrine (A.L.) (Coartem)
– Dose – Tabs AL iv bd X 3/7
B. Second Line
-Tabs quinine 600mg tds X 7/7
2. Treatment of complicated malaria
- IV Quinine 600mgs in 5% dextrose eight hourly for
three doses.
-A dose runs for four hours and the patient rests for

four hours, then is given the next dose.

- Change to oral quinine as soon as the patient is able
to take orally (i.e. tabs Quinine 6oomgs tds x 7/7).
3. Supportive Treatment

1. Analgesics – Reduces pain and fever

2. Hb level – correct anaemia
3. Haemataenics – If the Hb is low.
(i) Folic acid
(ii)Ferrous Sulphate – give after Tx- parasites
lives on iron
4. Transfuse packed cells if in failure, give frusemide
with Digoxin during transfusion.
5. Diazepam – PRN – If the patient is convulsing.
6. Assess blood glucose level – Correct hypoglycaemia
if present.
7. Measure urine- output/input daily – to rule out
renal failure
8. U/E/C – electrolyte balance – creatinine levels
9. Lactic acid (csf) > 6mmol/l
10. LP PRN – to rule out Meningitis
11. Do blood slide daily
12. No steroids – delay resolution.
Prevention
A. Personal Protection.
1. Treated mosquito nets and
materials
2. Household products coils/mats
3. Household screening
B. Indoor residual spraying
C. Chemoprophylaxis
- SP – 2 or 3 doses of SP from 2nd
trimester
- Given atleast one month apart
- 3 doses more effective particularly
in women who are HIV positive
Others
• Proquanil 200mgs daily x 6/52
• Mefloquine 250mgs weekly x 6/52
• Primaquine 0.75mgs weekly x 6/52
D. Environmental
- Bushes – Cleared
- Water – Drainage
NB: In TROPICAL SPLENOMEGALY SYNDROME (TSS)
[chronic malaria]
- Give Paludrine 200mgs OD X 6/12 or →
 2. AMOEBIASIS
 Infection by the pathogenic amoeba: E. Histolytica
 Others E. Hastimanii and E. Coli
 Also there is Naegleria and acanthamoeba, causing
fulminating meningitis and granulomatous
encephalitis

AETIOLOGY/ EPIDEMIOLOGY
 Endemic where sanitation is poor
 Common around Arusha / Kilimanjaro
 Patients with dysentery does not spread the disease
 Assignment
LIFE CYCLE 
DRAWING
 NB
1. IP 2/52 – to many years
2. Trophozoits themselves are not infective
3. Trophozoits are invasive (invade host tissues)
and multiply within the human host by cell
division
4. Cysts can be killed by boiling water
5. Cysts are resistant to water treatments such as
chlorination
6. Cysts can survive for long periods in feaces –
upto10/7
7. Cysts are killed by desiccation
8. Transmission is by contaminated water, food,
vegetable / fruits, by human feaces
(excrement) i.e.faeco-oral route
9. Also contamination from a leaking sewage
10. Flies can be vectors
 PATHPHYSIOLOGY 
A: Tissue invasion by trophozoits
  There is invasion of the mucosa of the large
intestines., leading to:- 
i. Granuloma formation
• Flask shaped (bottle shaped) ulcers in muscularis
mucosa, consisting of lymphocytes, plasma cells,
sometimes PMNLs, and with undermined, hanging,
irregular edges. 
ii. Necrosis
iii. Perforation
iv. Mesenteric veins invasion with spread into
the systemic circulation
B: role of intestinal flora 
i. E. Histolitica requires nutrients produced by E.
coli and enterobacter aerogenes
ii. After e. Histolitica infection, secondary bacterial
infections e.g. shigella, clostridia are very common
 COMPLICATIONS
1. Bowel necrosis
2. Perforation
3. Peritonitis
4. Liver abscess
5. Sub phrenic abscess
6. Lung abscess
7. Pleural effusion
8. Lung collapse
9. Atelectasis
10.Brain abscess
 Clinical presentation
A: Chronic carriers are u 85%
 Asymptomatic
 Mild abdominal discomfort
 Flatulence
 Occasional diarrhea
 Constipation
B: Amoebic Diarrhea 
 Recurrent bouts of diarrhea often with mucosand
blood tinged (endemic)
 Patients may complain of tenesmus
 usually they are afebrile
 constipation usually occurs between bouts of
diarrhea
C: Amoebic Dysentery
 Present with severe diarrhea, blood with mucus
 Severe abdominal pains with tenesmus (pain
localized along the caecum, and sigmoid colon)
 Fever and headache
 Symptoms may be due to secondary bacterial
infection
D: AMOEBIC APPENDICITIS 
 there is preceding amoebic diarrhea and
dysentery
 There is per umbilical pain – radiating to the right
iliac fossa
 Nausea and vomiting
 Fever
 NB: Should be treated before surgery
E: AMOEBIC GRANILOMA
 Proceeding S+S of amoebic diarrhea
 Tender mass in left iliac region
 R/o carcinoma
 Secondary infection of the granuloma
F: AMOEBIC LIVER ABSCESS 
• Proceeding S+S of amoebic diarrhea
• Jaundice + - usually obstructive
• Right hypochondria pain. Usually localized
tenderness – pointing to site of aspiration
• Tender fluctuant liver mass – again localized
tenderness, pointing to site of aspiration
• Fever - swinging
 DIAGNOSIS
1. clinical S+S
2. Stool o/c stain flesh stool
a) Formed stool cysts – centrifuged stool, suspended in
formalin / Ethenol
…….Trophozoits
b) Diarrhea – specimen must be examined immediately after
its collection
3. SEROLOGY
• HA Indirect Haem Agglutination Test
• FA Immuno Fluorescent Antibody Test
• LA Latex Agglutination Test
• GDP Gel Dissusion Periciptin Test
• CFT Complement Fixation Test
4. STOOL – Culture/ sensitivity – Bacterial infection
-Microscopy – Help make a diagnosis

5. ULTRA SOUND IN LIVER ABSCESS

--Pushed up one side of the diaphragm
(hemidiaphroagm) and immobile

6. Sigmoidoscopy and Mucosal scrapping

7. Abscess Aspirate – microscopy -- Aspirate 8th – 9th

rib
 DDX
1. Bacillary dysentery
2. Viral GE
3. Crohn’s disease
4. Ulcerative colitis
5. Diverticulitis
6. IIeo-caecal Tb
7. Colitis
8. Carcinoma
 TREATMENT
I: Invasive (intestine) 
i) Tabs Metronidazole 800mg Tds x 5-7/7
or 1.4 gm Od x 5/7
ii) Tinidazole 2gm Od x 3/7
iii) Furanide (Entamizole) 500mgs Tds x 10/7
iv) Geatrim 2gm Od x 3/7
v) If symptoms (cysts) persist add Tetracycline
250mgs Qid x 10/7
2: Hepatic (Extra intestinal) – Abscess, Granulomas 
• Flagyl same as above i.e. 800mgs Tds x 5/7
Or 1.4gm Od x 5/7
• Or Chloroquine 300mgs Bd x 5/7
Then 150mgs Bd 14-21/7 
• NB: Identify and treat secondary infections.
 PREVENTION 
1. Water treatment
2. Proper sanitation
3. Personal hygiene
4. Identify and treat carriers
 THE DIFFERENCE BETWEEN BICILLARY DYSENTRY AND AMOEBIC
DYSENTRY
BACILLARY AMOEBIC  
1. Incubation period---less than 1/52 ------Greater
than 3/52
2. Onset ----Acute ------Insidious
3. Occurrence -------Epidemic -------Endemic
4. Fever------Common ---------Only in complications
5. Clinical Picture --Lying down dysentery---Walking
dysentery
6. Tenderness----Whole abdomen------ Localized,
colonic(More sigmoid)
7. Tenesmus -------Very severe ---------------No usual 
8. Stools 
i)Macroscopic-----Mucus and bloody only-----Stool,
blood + mucus
ii) Microscopic
a) -----Numerous polymorphs--a) Polymorphs
scanty
b) ------Few bacteria ----b) Many bacteria 
c) -----Macrophages ------c) E. Histolitica
d) ----Numerous red cells
with ingested red cells ---d) Numerous redcells

in clumps
 3. GIARDIASIS
Infection with Giardia instestinalis (Lamblia)
Was first recognized in 1681 by ANTONY VAN
LERYWENBOEK
Entamoeba histolytica in 1875
Plasmodium ssp in 1880
Aetiology and epidemiology
• Has a worldwide distribution
• Common where water may be contaminated by
human sewage
• Transmission is direct through soiled fingers or
contaminated water, vegetables, or person to
person.
• Cysts are infective stage – cyst are activated by acid
when ingested
• Incubation period 5 – 15 days
• Giardia exists as a trophozoite which colonizes the
proximal part of small intestines
• Excystation occurs due to low Ph. (acid) of
pancreatic and duodenal secretions.
• Encystation occurs in high concentration of bile salts
at neutral PH
Pathophysiology
 Infection of the duodenum and jejunum by
trophozoite –> damage to mucosa:-
1. Destruction of microvilli-> deficiency of lactase
dehydrogenase, disaccharides, proteases.
2. Impaired absorption(malabsorption)-especially of :
(i) Carbohydrates ->Diarrhea
(ii) Fats
(iii) Vitamin B12 ->anemia
3. Bacterial growth ->Diarrhea
4. Inhibition of digestive enzymes -> weight loss
5. Bile salt deconjugation.
 Clinical S + S
 Nonspecific Gastro-enteritis with intermittent
exacerbation
 Diarrhea
 Weakness
 Weight loss
 Nausea
 Steotorrhoea
 Flatulence
 Fever
• NB: Many patients are asymptomatic
Diagnosis

1. Stool – o/c – Demonstration of cyst or trophozoite

in approx. 50% of the cases.
- specimens at 3–4 hours interval may yield upto
90%

2. Duodenal or jejunal aspiration.

Treatment
• Metronidazole
• Tinidazole
• Zentel 400mgs odx 5/7

Others
• Mepacrine 100mgs tds x 5-7/7 S/E – Nausea,
Headache, Jaundice
• Furazolidine 100mg od x 7-10/7 S/E – Nausea,
Haemolysis in G6PD
DDX
1. Tropical sprue
2. Celiac disease
3. Strongyloidiasis
4. Cryptosporidiosis
5. Microsporidiosis
NB
1. SSP
– Giardia intestinalis (lamblia, doudenalis)
– Giardia Agilis
– Giardia muris
2. How it looks like:------Drawing
3.Prevention
– Boil drinking water–cysts are susceptible to
heat, but not affected by chlorination
– Good personal hygiene
– Environmental sanitation
 4.LEISHMANIASIS
 Is an infection caused by the parasite of the genus
leishmaniasis
 Zoonotic host are mainly canines and rodents
 Man only interrupts the life cycle when infected

 The main vectors are sand flies i.e phlebotomus –

which transmit the disease between animals and from
animals to man and from man to man

 There are two main types:-

a) Visceral leishmaniasis (Kala-azar)
b) Cutaneous leishmaniasis
a) VISCERAL LEISHMANIASIS (KALAAZAR)
Is a severe chronic systemic infection caused by the
protozoan leishmania donovani

The clinical manifestation and complication result

from infection of the Reticulo-Endothelial system
(RES)
AETIOLOGY / EPIDEMIOLOGY
• Is found in many parts of the world, but in Africa it
is on the Mediterranean coast and in the belt from
L. Chad to Somalia minus high lands of Ethiopia
• In East Africa
- Sudan along Juba River
- Karamoja in Uganda
• Endemic areas in Kenya include:-
–Meru
–Kitui
–Machakos
–Tana River
–Baringo
• Prefers arid and semi-arid climates
• The parasite is carried by Philebotomus (sand
fly) vector
• In sudan it is phlebotomus orientalis
• In Kenya it is phlebotomus maitini
HOST:
• Man – mainly affects male teenagers, solders and
hunters
• Dogs and rodents
 
• NB: the vector lives in termite mound
 LIFE CYCLE
 The parasite exists in 2 forms:

1. AMASTIGOTES
2. PROMASTIGOTES 

1. AMASTIGOTES
 found in the host (vertebrates)
 Oval shaped
 No flagellum
 In macrophages
 Divide by binary fission
• 2. PROMOSTIGOTES
 Found in the vector (sand flies)
 Longitudinally shaped
 Has a flagellum
 Usually stained using Romansky stain
 Measures about 5µm
 PATHOPHYSIOLOGY
A: INFECTION OF THE R.E.S.
• Destruction of the normal architecture of the
spleen –> splenomegaly
• Kupffer cells inflammation ->
– Hepatomegaly
– Cirrhosis
– Low serum albumin -> Oedema
– Ascites
– Oesphageal varices
B: Late Complication Of Untreated Disease -->
inflammation and destruction of BM ->
i) Anaemia
ii) Leucopenia
iii) Secondary Infections
iv) Bleeding tendencies
C: INFECTION OF THE R.E.S. CELLS (PAYER’S PATCHES)
OF THE INTESTINES ->
 Possible necrosis of the intestinal wall
 Malabsorption
a) Diarrhoea
b) Malnutrition

D: INFECTION OF LYMPH NODES ->

 Lymphadenopathy

E: SKIN INFECTIONS ->

 Subcuteneous nodules
 CLINICAL S+S
Incubation period varies from patient to patient
–4/52 – 6/12
–3/52 – 2 years
Cateneous nodules at site of bite by phlebotomus-
often noticed by the patient- Rash called
leishmanioma
Fever
 Intermittent(starting and stopping) or remittent
(abating for a while or at intervals).
 Fever spikes often, highest at noon and midnight.
 Often becomes persistent and of low grade (38oC).
 Left hypochondrial discomfort
 Splenomegally by 4th month after onset of the
illness -----Usually massive and non tender
 Anaemia and leucopenia
 Intercurrent infections ----Dysentery or pneumonia
 Hepatomegally - smooth, non-tender
 Lymphadenopathy
 Dry and rough skin(grey skin)on abdomen, palms
and soles
 Malnutrition / emaciation
 Cancrum oris (vesicle and necrosis) of the buccal
mucosa
 Oedema and ascites – from hypoalbuminaemia
secondary to liver destruction.
 DIAGNOSIS
Clinical S+S in endemic areas are
splenomegaly and fever
Demonstration of leishmania donovani
bodies (LD bodies) in Romansky stain of
spleen, node or marrow aspirate
Immunologic studies i.e complement fixation
tests – antibodies may be detected by
oIndirect immuno fluorescence test
oElisa test and
oHaema agglutination tests
Formal gel Test
oPositive after 2/12 (+ve with 2/12)
oNegative 6/12 later (-ve with 6/12)
 significant because of hyper
globinaeia
Leishmanin skin (Montenegro) test
oThere is delayed hypersensitivity
oIs not reliable as it is negative early in the
disease
 TREATMENT
A: GENERAL Rx
• Nutrition – increase Proteins, enough CHO, and
vitamins
• Good oral hygiene
• Rinse mouth with H2O2 or Betadine
B: SPECIFIC Rx
PENTAVALENT ANTIMONY COMPOUNDS
a) Sodium stibogluconate (pentostam)
-IM or IV 0.1 -0.2 ml/kg daily x 6-30/7 (1ml = 100mg).
(10-20mg/kg) (max. 850mg)
 Three 10 day course as above separated by 10 days
intervals may be given in resistant cases

 In case of nausea and vomiting give on alternated

days, reduce dose or stop the administration
 Drug of choice
b) Pentamidine Isethionate
1ml =40mg
-Deep IM 3-4mg 1-2 weekly until the condition resolves
S/E- vomiting, diarrhea, hypotension, hypoglycaemia,
arrhythmias and pancreatitis

C) Other drugs
- Allopurinol
- Amphotericin B
- Aminosidine (paromomycin) 15mg/kg IM/IV Od x 21/7
- Meglumine antimoniate (glucantine)
D: Treat The Complciations
 Anaemia – iron usually is adequate
 Secondary infection e.g PTB, etc

E: Cure Is Determined By;

 Regression of the spleen
 Resolution of anaemia
 Rise in WBC to 6000 cells / mm3
 Absence of parasite (organisms) in smears
COMPLICATIONS
1. Liver Cirrhosis
 Hypoalbuminaemia
 Ascites
 Bleeding
 Oesophageal varices
2. Secondary infections e.g PTB, pneumonia due to
low WBC
3. Anaemia –> can complicate to CCF
4. Malnutrition ->Failure To Thrive
5. Post Kala-azar dermatitis
PREVENTION 
• Eradication of vectors – spraying homes and
surrounding bushes
–65m perimeter with DDT (Dichloro
Diphenyl Trichloroethane)
–Spray termite mounds
• Proper covering if one stays out
 2. CUTANEOUS LEISHMANIASIS

 Synonym – Oriental sore 

 It is a zoonotic infection characterized by a single or

several chronic cutaneous sores which usually heal
spontaneously.
AETIOLOGY/EPIDEMIOLOGY
• The disease affects people in West Africa. 
• In East Africa affects people in Ethiopia and Kenyan
Highlands
• The zoonotic reservoir is the ROCK HYRAX
• The vectors are sand flies – P. Longipes and P.
Pedifer
• Though cuteneous leishmaniasis is rare, there are
three different forms caused by 3 different species
of Leishmania
1. THE RURAL FORM
• Affects man in unhabited areas and in villages on
the edges of the desert
• It is caused by L. Tropica Major
• The desert Gerbil is the main reservoir
• Transmitted by P. Papatsi

2. THE URBAN FORM

• Is caused by L. Tropica minor
• It is an infection of man and dogs in big cities and
towns
• It is transmitted by P. sergenti
3. Is found in the Ethiopian and Kenyan Highlands
• Is an infection of man and the ROCK HYRAX caused
by L. Aethiopia
• Transmitted by P. Longipes which bites people in
their houses at night
Clinical S+S
• IP 2-8 weeks
• Itchy papule – usually on the face
• Single or multiple ulcers – which may resemble skin
tuberculosis of the face (lupus vulgaris)
• Lymphadenopathy (local)
• Spontaneous healing starts after 2/12
TREATMENT
• Unnecessary usually as spontaneous healing occurs 

• If the lesions are extensive or diffuse – use

pentavalent antimonials e.g sodium
stiboguloconate as in visceral leishmaniasis

• Surgical treatment may be considered

HUMAN AFRICAN TRYPANOSOMIASIS (H.A.T) (SLEEPING SICKNESS)

• An infection by a haemoflagellate genus

trypanosome (gambiense and Rhodesiense) carried
by the tsetse fly Glossina palpitis and glossina
technoides
 AETIOLOGY / EPIDEMIOLOGY

 Common in Sub Saharan Africa

 WHO - appro. 300,000 to 500,000 people are
currently infected

 Caused by two protozoan parasites;

1. Trypanosoma Brucei Gambiense

2. Trypanosoma Brucei Rhodesiense
 1. Trypanosoma Brucei Gambiense
 Tsetsefy – G. Palpalis
 Widely distributed, but less in E .Africa
 Found in Northern Lake Victoria–Uganda– Busoga
 Common also in west and Central Africa
 Causes a much less severe infection than
Rhodesiense
 It is limited to human host
 Causes chronic sleeping sickness
 2. Trypanosoma Brucei Rhodesiense
 Tsetse fly – G. Technoides
 Confined to E. Africa
 Common in South Nyanza – Lambwe valley, Busia,
Alego
 Causes acute sleeping sickness
 Both sexes of the fly carry the infection
 Can cause death in weeks or months (causes a more
severe infection)
 More likely to invade CNS
 Reservior – antelopes, Pigs (Wild animals are main
hosts)
NB: Trypanosomiasis
Debilitation and death can result from CNS
involvement

Affects – Rangers, Hunters, Honey collectors, wood

cutters
 LIFE CYCLE
Man
Tsetse fly Man

Tsetse fly
Man

Wild animals Tsetse fly Game Animals

 PATHOPHYSIOLOGY
1. Lymphadenitis 
• The lymph system is primarily invaded early in the
disease -> Lymphadenitis i.e. organisms can be
found in the LN
• Splenomegaly , hepatomegally 
2. Endarteritis
• Causes inflammation of endothelium of small
arterioles causing:-
-Local ischaemia and gangrene
-Ischaemic injury to heart and brain, which are
susceptible organs
3. CNS involvement (sleeping sickness)
• CNS injury result from endateritis and local
ischaemia
• Trypanosomes invade brain tissue directly from
injured arterioles; -->
-Meningitis
-Encephalitis
-Abscess
 CLINICAL S+S
Local inflammatory reaction at site of fly bite 48-72
hours
Incubation period 3 days–3 weeks
High fever usually at night
Posterior cervical and supraclavicular lymph node
enlargement (Winter bottoms sign)
Splenomegally / hepatomegally
Pruritus
Painful localized oedema (pedal oedema)
Marasmus
CNS – tremous esp. tongue, fingers
-somnolence (sleepiness/drowsiness), apathy
-decreased concentration
-Headache, seizure
-Irritability
-Coma
Impotence
Menstrual disturbance
CCF
NB:
Death is usually from 1o infection, 2o infection or
starvation
 DIAGNOSIS
Depends on demonstration of the
trypanomastigotes in peripheral blood, lymph node
aspirate or CSF
Immunologic tests i.e raised 1gM in blood and CSF
Raised CSF pressure with high mononuclear cells
Reduced Hb and Raised ESR
Monocytosis
Raised proteins
 TREATMENT
1. Good nutrition and good nursing care
2. LP is done initially, then every 3/12 for 3 years after
treatment
3. Chemotherapy

i) Suramin (atrypol)-- IV 200mg stat ,Then 20mg/kg IV

on day 1,3,7,14,21.

NB: -It should be freshly prepared.

-Watch for:-Renal toxicity--proteinuria, haematuria
-Allergic reactions:-collapse , coma or shock may occur.
-Effective against T. Rhodesiense 
ii) Pentamidine Isethionate--Deep IM or IV 4mg/kg in
distilled water Od or every other day (alternate) for
7-10 injections.
NB:--Less effective against T. Rhodesiense
Late Infections / CNS Involvement 

1. Melarsoprol 2-3 mg/kg Iv x 3/7

• Two - three days course
• Each course lasts for three days and are 2 weeks
apart

2. Nitrofurazone 10mg/kg tds x 10/7

 SUMMARY – CURRENT REGIMES
1. Tbg – give :- Pentanidine 4mg/kg 1M x 7/7
2. Tbr – give :-Suramin 20mg/kg/day IV weekly x 5 weeks
3. Melasoprol 3.6 mg/kg/day x 3
• Give two doses of 3.6mgs/kg/day x 3/7
• Rest 8-10 days in between.
• Each course three days 
4. Eflornithine (ornidyl) 400mgs/kg/day for slow
infusions every 6 hours
• in children -150mg/kg per infusion
5. Nifurtimox (Lampit) (for changas disease) 5mg/kg P.O
8hrly x 14-21/7
COMPLICATIONS 
• Reactive encephalopathy – anxiety, hyper
excitability, confusions, idiosyncratic
reactions(bizarre / unusual odd reactions)
 DDX
Fever stage
• Malaria
• Relapsing fever
• Typhoid fever
• Tuberculosis
Visceral stage
• Meningitis
• Leukaemia
• Reticulosis
• Psychosis
• Hookworm anaemia
• Cachexia from other causes (TB, Cancer)
 PREVENTION

• Eliminate vector

• Prevent influx of infected people

 3. BACTERIAL INFECTIONS
1. SHIGELLOSIS
2. ACUTE GASTRONENTERITIS
3. STAPHYLOCOCCAL FOOD POISONING
4. CHOLERA
5. SALMONELLOSIS
a) SALMONELLA GASTRONETERITIS
b) ENTERIC (TYPHOID) FEVER
6. BRUCELLOSIS
7. ANTRHAX
8. PLAQUE
9. LEPTOSPIROSIS
 1. SHIGELLOSIS

• Acute enteritis (acute bacillary dysentery) caused by

shigella species, characterist by; bloody stools,
fever, vomiting and abdominal craps.

• Shigella -Grame –ve

-Non motile
-Non spore forming
 AETIOLOGY / EPIDEMIOLOGY
• Caused by Shigella - especially from food contamination
• Has a world wide distribution
• Man is the sole reservoir
• Is associated with poor hygiene
NB:
Organism spcies:-
• Shigella shigellae
• S. sonnei
• S. boydii
• S. flexeneri
• s. schinitrii
• S. dysenteriae
 TRANSMISSION

• Faeco oral route

• The rule of F
 PATHOPHYSIOLOGY
1. Invasion of the mucosa of the large bowel
• Ulceration
• Abscess
• May cause perforation and peritonitis
2. Bacteraemia
- Rarely causes metastatic infection
3. Immunologic respose can cause
• Reiters syndrome
• Conjunctivitis
• Orchitis
• Arthitis (sterile)
• Haemolytic uraemic syundrome – (Interfere with
erythropoeitin)
 CLINICAL S+S
i. IP – 2-3/7
ii.Abrupt onset of
iii.
Abdominal pain and tenesmus
iv.Small frequent watery diarrhea usually with blood
and mucus
v. Fever usually
 DIAGNOSIS
• Demonstration of the organism on cultures- rectal
swab (mucosa)

• Leucocytosis
 TREATMENT
1. Supportive – fluids and electrolytes

2. Enteric isolations – treat for 5-7/7

 ampicillin will shorten the course of the disease

 Trimethoprim 2 tabs bd 10/7
 Tetracycline caps 500 mgs Qid x 5/7
 Ciprofloxacin 500mgs bd x 5/7

NB:
• Obtain follow up, C/S stool to be certain the patient is
not a carrier.
 PREVENTION
• Maintain high level of personal hygiene

• Proper disposal of faeces

 2. ACUTE GASTRO ENTERITIS (BACTARIAL)
• Acute gastro enteritis caused by enterotoxin
producing strains of E. Coli

AETIOLOGY
• Foecal oral route primarily via contaminated food
• It is the major causes of “Travelers diarrhea”
• Escherichia - Is not invasive – symptoms are
produced by enterotoxin
 PATHOPHYSIOLOGY
• Enterotoxin ( a protein) produces an inflammatory
response in the GIT mucosa which leads to
secretory diarrhea.

• Severe infection can cause dehydration especially in

infants and elderly
 CLINICAL S+S
• Incubation period 24 - 48 hours
• Nausea, vomiting and anorexia
• Abdominal pain and tenesmus
• Diarrhoea (watery)
• Fever, chills
• Total duration 5-7 days if untreated
 DIAGNOSIS
•  Demonstration of enterotoxin in stool

• Exclude other causes of invasive gastroenteritis

(salmonella and shigella, also giardia, E. histolytica)
 TREATMENT
Supportive care
 Fluids and electrolytes

 Tetracycline 500mgs QID x 10/7 PO

 Trimethoprim to children less than 8 years
 Gentamycin
 Ciprofloxacin
 3. STAPHYLOCCAL FOOD POISONING
Acute gastroenteritis caused by enterotoxin produced by strains
of staph. Aureus
AETIOLOGY
A: Contaminated food
Eggs
Milk products
Meat
B: Source of staph.
Infected wound on food handlers
Nasal droplets from food handlers
NB:
• Enterotoxin ABCD is heat stable
• Enterotoxin production is inhibited by refrigeration
 PATHOPHYSIOLOGY

• Same as E. coli
CLINICAL S+S
 Incubation period 4-8 hours
Acute onset of:-
 Nausea, vomiting
 Watery diarrhoea
 Abdominal cramps
NB. All these can cause dehydration
• Afebrile
• Symptoms are self limiting – Resolve in 3-4/7
DIAGNOSIS
• Clinical S+S
• History of ingesting suspected food
• Demonstration of enterotoxin in stool

TREATMENT
• Supportive care
• Replace Fluids and electrolytes
 
PREVENTION
• Careful hygiene and food handling
• Refrigeration
 4. CHOLERA
• An acute enteric infective diarrhoeal disease
caused by vibrio cholerae, and is
characterized by, profuse diarrhea,
dehydration and shock.
 AETIOLOGY / EPIDEMIOLOGY

 Epidemic and endemic in topics

 Epidemic in temperate zones
 Seasons – hot whether in temperate zones
 All ages are affected
 Has no immunity
 Transmission is faeco – oral
 Endemic cholera results form contamination of
water supply and affects children primarily.
 While epidemic cholera results from contamination
of food and affects the whole population.
• Cholara is a gram –ve, small motile curved rods
(comma bacilli)
• It is stained with Carbol Fuchsin
• Original serotypes include – Inaba, Ogawa, and
Hikojima – are dintiguished by “O” antigens
• Current pandemic are caused by el tor Vibrio which
is resistant by cholera bacteriophage (a virus that
attacks bacteria)
• Others e.g. v. parahaemolyticus – are invasive 
NB:
• V. cholera produces enterotoxin while V.
parahaemolyticus is invasive.
• Large infections is as a result of Water
contamination.
PATHOPHYSIOLOGY
Enterotoxin produces secretory diarrhea
(secretion of fluid and electrolytes into the
lumen of the intestines) –> massive (profuse)
loss of sodium appro. 170g in 24 hrs with loss
of extracellular fluid –> dehydration,
haemoconcentration, hypotension –> low
GFR, Oliguria, Anuria, Uraemia and muscular
cramps
Low blood flow to kidneys –> tubular necrosis ->
Renal Failure.
Hypokalaemia due to K+ loss in stool
Metabolic acidosis – shown by marked
hyperventilation and confusion
NB:
when there is loss of fluid to 12% of body weight,
death usually occurs
 CLINICAL S+S

-IP 3-7 days (1-3/7 or 4-7/7)

- Clinical course has 3 stages

1. Stage of evacuation
2. Stage of collapse (Algid)
3. Stage of Recovery
1. STAGE OF EVACUATION
 Abrupt onset
 Vomiting
 Muscle cramps
 Progressive exhaustion
 Extreme thirst
 Stool – Later become white - Rice water stools –
alkaline in nature
 No tenesmus
2. STAGE OF COLLAPSE
 Signs and symptoms associated with volume loss.
 Temperature – sub normal
 Pulse – feeble
 Skin – cold, dry inelastic, clamsy
 Blood pressure - low
 Urine output – Nil
 Conscious although apathetic
 Hypoglycaemia
 Convulsions in children (confusion in adults)
 Hyperventilation
 Collapse due to dehydration
3. STAGE OF RECOVERY 
• Spontaneous or stopped by diarrheal treatment
• Patient takes oral fluids
 DIAGNOSIS
i. S + S
ii. Demonstration of Vibrio cholerae in stools / rectal
swab
iii. Dark field microscopy
iv. Culture / sensitivity
 TREATMENT
 Rest and warmth
 Fluids and electrolyte replacement
 Oral rehydration – mild dehydration
 ORS – 50 -100mls/min till Normal pulse
 IVF – severe dehydration – 2—30ml/kg
 Ringer’s lactate or diarrhoeal Treatment solution (DTS)
DRUGS
 Tetracycline
 Doxcycline
 Septrin
 Chloramphenical
NB:
• Do not wait for C/S to start therapy in suspected
cases.
• Do follow up cultures – carriers are appro. 3-5%
• ORS – contain Nacl 3-5g, NaHco3 – 2.5g or Citrate, Kcl
1.5g, glucose 20g – H2O 1L
• Ringers lactate – contain Na+ / 28mmol/L, K+ mmol/
Ca2+ 3.6mmol/L, Ct – 110.6mmol/L, lactate – 25
mmol/L
• WHO-DTS-IL= Contain;- Sodium 4g, sodium acetate
6.5g, potassium chloride 1g, glucose 10g
• IVF – 2 vol. of isotonic saline mixed with 1 vol. of
isotonic sodium acetate. Acetate to rectify ACIDOSIS
 PREVENTION
 Isolation of patient
 Identify carriers
 Water treatment /boiling
 Good hygiene
– proper excreta disposal
-- Flies
 Doxcycline
 Cholera vaccine – 50% protection for 3 months
 5. BRUCELLOSIS
• Is a systemic infection by brucella abortus,
mellitensis or suis
• Brucella:-
Gram –ve
Cocco bacillus
Non motile
Pleomorphic
AETIOLOGY / EPIDEMIOLOGY
1. Has animal reservoir
• B. abortus – cattle
• B. mellitensis – sheep + goats
• B. suis – pigs, dogs
2. It occurs as an occupational disease to:-
- Vetinarians, Farmers, Butchers
3. The organism is transmitted by;
- Unpasteurized milk and milk products
- Exposure to mucus membrane and blood of infected animals.
4. Portal of entry – Brucella penetrates mucous membrane
and broken skin
5. Endemic areas are North East and Maasai land
PATHOPHYSIOLOGY
 Route and extent of infection;-
 Oropharynx
 Regional LN. ->lymphadenopathy -> moves to
circulation -> distant lesions
 Metastatic infection;
• Bone marrow
• Spleen
• L. Nodes
• Liver
NB:
• These lesions appear as a non specific granuloma
CLINICAL S+S
1: Insidious / gradual non specific onset of:-
 Fever – usually intermittent
 Malaise
 Weakness
 Headaches
 Arthralgia (for weeks or months)
2: Localised symptoms from metastatic infection
 vertebral tenderness – usually lumber -> backache
 Arthralgia – localized swelling, heat over affected joint
 Regional lymphadenopathy
 Splenomegally
COMPLICATIONS
i. Suppurative spondylitis with destruction of lumber
vertebrae
ii. Nephritis
iii. Proteinuria
iv. Haematuria
v. Oliguria
vi. Intraocular infections
vii. CNS – meningoencephalitis
- Myelitis
- 8th C.N palsy
DIAGNOSIS
1.Culture and sensitivity of:-
• Blood
• Node aspirate
• Urine
• Joint aspirate
2. FHG -low WBC
-High Lymphocytes
3. Serum aggulatination tests (Brucellin titre)
-Greater than 1:80 is suggestive
-1:50 – past infection
4. skin tests are available but not accurate
TREATMENT
1st LINE
• Doxcycline 200mg od 45/7
+
• Streptomycin 1mg od x 21/7
or
• IV Gentamycin 240mg od x 21/7
2nd LINE
• Doxcycline 45/7+ Rifampicin 4-6/52
• Surgery = Abscess
• Rifampicin 900mg od x 6/52 – pregnant women
• Less 8 years;
-Rifampicin x 45/7 +
-Gentamycin x 21/7
PREVENTION

 Identify sick animals and destroy

 Treat the sick
 Pasteurize milk
 Vaccine / chemoprophylaxis
 6. TYPHOID FEVER
Definition
• Typhoid fever is an acute febrile disease caused by
salmonella Typhi.
Epidemiology
• Spread-feacal–oral from contaminated water ,
mostly milk, ice creams.
• Food contaminated by food handlers and flies, etc.
• S. Typhi- Is exclusive in human
• Remains viable in water for long periods.
• Infective dose-107 organisms. 
• Organisms are eliminated in feces and urine upto 9
weeks during convalescence (the process of getting
well)-for convalescent carriers.
• Healthy carriers are those who pass S.typhi in feces
(fecal carriers) or urine (Urinary carriers) without
themselves suffering from the disease.
• Fecal carrier state is more likely to follow S.typhi
infection in 10% of cases above the age of 50 years.
• In many cases of fecal carriers, the gall bladder is
the source of persistent S.typhi infection.
 Pathogenesis
NB: Several factors determine the establishment of
infection :-
i. Size of inoculums- The larger the dose the greater
the chance of infection.
ii. Presence of normal gastric acid which rapidly kills
the bacilli.
iii. Virulence of the infecting strain.
iv. The presence of bacterial flora in the jejunum.
 Following ingestion of the Bacilli.
 The bacilli enter through the intestinal epithelial
lining of the jejunum and ileum.
 In the submucosa they are phagocytosed by the
polymorphs and macrophages. The organisms
survive within the phagocytes and they reach the
mesenteric lymph nodes.
 There they multiply and enter the blood stream to
produce a transient bactaraemia. They reach the
spleen, GallBladder, bone marrow, lymph nodes,
lungs and kidneys, where further multiplication of
the organisms occurs.
 Large number of bacilli is discharged from the gall
bladder into the intestines.
 This time they enter the payer’s patches and
lymphoid follicles of the ileum. These lymphoid
structures undergo inflammation, necrosis and
ulceration.
 Clinical manifestation starts when bacteria begin to
re-enter the blood steam from the intracellular
sites. Usually asymptomatic.
 The organism produces endotoxin which accounts
for the fever and many of the systemic effects
 Blood vessels may be eroded->intestinal
haemorrhage.
 Erosion may extend to muscularis mucosa and
serosa->intestinal erosion and perforation.
 Bacteraemia - Fever
 Toxemia - Toxic damage leads to degeneration and
focal necrosis of cardiac muscle.
 Rectus abdominis muscle - Undergo Zenker’s
degeneration(severe hyaline degeneration or
necrosis of skeletal muscles in acute infectious
dses).
 Clinical manifestations

Onset- slow

Prodrome

Anorexia

Malaise

Lethargy

Fever

Headache – Headache may occur from the beginning

Epistaxis

Temp- step-ladder-1st week

Pulse-relatively slow

Non productive cough-in few cases
 Abdominal symptoms
Vague discomfort
Pain
Constipation
Less often diarrhea
 O/E
1st week
 slow pulse
 fever
 Abdominal distension and tenderness
 Erythematous macules i.e. Rose spots.
NB
• *Are 2-3mm in diameter
• *Are due to bacterial embolism
• *lasts for few weeks then they fade
• *Difficult to find in dark skinned individuals
 2nd week
• Temperature is high and remains continuous around
400c with relative bradycardia.
• The patient may become dehydrated, delirious and
exhausted.
• The tongue is coated in the centre and the margins
remain reddish.
• Typhoid state - because of toxaemia.
In this state the patient shows:-
• Subsultus Tendinum. (abnormal twitching or
tremor of muscles due to fever).
• Muttering delirium (i.e. say in a quiet voice which is
difficult to hear)
• Tremulousness of the hands
• Carphology (floccillation) – i.e. Plucking of
bedclothes by a delirious patient- it is a sign of
extreme exhaustion and may be a prelude to death.
• Picking movements of the hands
• Coma vigil
• The patient is comatose but the eye is open
 Abdomen
• Abdomen is moderately distended
(Tumidity/swollen/bulging) with vague tenderness,
especially over the right iliac fossa.
• Palpation may reveal gurgling due to mild
distension of ileal loops.
• Over 75% of the cases show moderate
splenomegaly. (3-4 cm) and is soft.
• Stools are –pea-soup stools- since feaces are loose
and greenish in colour.
• It may contain blood streaks.
 NB:
• Complications such as intestinal perforation and
peritonitis are rare in the 2nd week, but marked
abdominal rigidity and tenderness should suggest
this possibility.
3rd week.
• Fever and toxemia continue
• Complications set in during this period.
• In uncomplicated cases temp starts to fall in lysis, in
the end of 3rd week and touches normal within 7-
10 days.
• Abdominal symptoms subside.
• Gradual improvement begins.
• Convalescence is prolonged.
NB:
• Typhoid shows a wide variation in severity and
duration of illness.

• Overall mortality in hospitals range from 5 to 10 %.

 Complications
(1)General consideration
i. Toxemia and Typhoid state
ii. Hyperpyrexia
iii. Peripheral circulatory collapse
iv. Disseminated intravascular coagulation (DIC)
v. Thrombophlebitis (inflammation of the wall of a
vein –> thrombosis)
vi. Relapse
vii. Drug toxicity especially chloramphenicol
(2) GIT
i. Abdominal distension
ii. Diarrhoea
iii. Perforation of the intestine -> peritonitis
iv. Bleeding from the intestine
v. Toxic Hepatitis
vi. Suppurative paroditis -> (parotid salivary gland)
(3) Neurological
• Coma
• Meningitis
• Peripheral neuritis
• Deafness
(4) Skin and appendages
i. Bed sores
ii. Alopecia

(5)Others
iii. Myocarditis
iv. Pyelonephritis ( i.e. inflammation of the renal
pelvis)
v. Glomerulonephritis
vi. Osteomyelitis

vii. Arthritis
 DDX
1. Hepatic amoebiasis
2. Tuberculosis
3. Infective endocarditis
4. Urinary infections
5. Malaria
6. Rheumatic fever
7. Lymphomas
8. Brucellosis
9. Typhus (spotted) fevers. ( i.e. any one of a group of
infections caused by Rickettsiae)
10. Tularaemia. ( a disease of rodents and rabbits
caused by the bactarium Francisella tularensis)
11. Leptospirosis.
12. Psittacosis. (infection of birds)
13. Viral hepatitis
14. Infectious mononucleosis -infectious disease
caused by Epstein-Bar Virus
15. Mycoplasmal pneumonia (Cause atypical
pneumonia in humans)
 Diagnosis
-clinical suspicion 
• Continuous fever with relative Bradycardia
• Coated tongue
• Tumidity of the abdomen
• Mild Hepatosplenomegaly
• Tenderness and gurgling in the right lower quadrant
of the abdomen.
1. Blood -FHG-low leukocyte count
-Relative lymphocytosis
2. Blood culture-1st week
NB - Culture of blood clot yield better results.
3. Stool-culture/positive in second week and urine-
culture/third week of illness
4. Bone marrow culture-when other methods fail
5. Widal Test- demonstrating rising titers 
-Widal Test- Used to detect and measure the H and
O agglutinins of typhoid and paratyphoid bacilli in
patients’ serum.
-Rising titers demonstrated by repetition of tests at
weekly intervals, IS SUGGESTIVE.
• ‘H’ antibody is non specific, can rise when a person
has received TAB inoculation. ( i.e. a combined
vaccine used to produce immunity against the
disease typhoid, Paratyphoid A, Paratyphoid B).
• ‘O’ Agglutinins are of greater value in diagnosis and
titer of 1:200 or more is very suggestive.
esis (CIE) using
phi may be more

strips- for stool and

 Treatment
1. Bed rest
2. Proper nursing care-to prevent bed sores and oral
sepsis
3. Maintenance of nutrition, fluid and electrolytes
balance.
4. Diet – easily digestible
-low residue type
- 1500-1800 calories/day
- 2-3 liters of fluid/day.
5. Fever and Headache - paracetamol
6. Constipation
• Opened once in 3-4 days with Glycerin enema.
7. Specific drugs
• Chloramphenicol -30-40 mg/kg (1gm) QID x 14/7
• Ciprofloxacin 500mg bd x 14/7
• Ceftriaxone 1-2g IV or IM od or bd x 7-10/7
• Ofloxacin 400mg bd x 10-12/7
• Pefloxacin 400mg bd x 7-12/7
Other drugs
• Ampicillin 1g/day QID x 2/52
• Amoxicillin 1gm tds X 2/52
• Cotrimoxazole
• Furazolidone 100mg Tab Q/D
Treatment of complications 
1. Typhoid state
• Correct fluid and electrolytes
• Adequate antibiotic therapy
• Short course of corticosteroids. 
(2) Intestinal perforation
• Surgical
• Antibiotics
(3) Intestinal haemorrhage
• Transfusion
• Parenteral antibiotics
• Manage Toxaemia
(4)Relapse
• similar to primary attack

(5)Treatment of carriers
• Ampicillin and cotrimoxazole given in repeated
courses
• Add probenecid to improve eradication rate
• Ciprofloxacin x 4/52
• Cholecystectomy is curative in over 85% of the
cases with Gall bladder disease
General preventive measures/prophylaxis
1. Avoid food contamination
2. Good personal hygiene
3. Provision of protected water supply.
4. Personal prophylaxis
5. TAB vaccine
• Dose 0.5mls -Two doses
-1 to 2 weeks apart
• Booster dose every year.
 7. ATHRAX
• An infection caused by bacillus anthracis
• It is a gram +ve spore forming bacillus
Of three clinical types
i. Anthrax of skin
ii. Anthrax of the lung – wool sorters disease
iii. Intestinal anthrax

• Cuteneous anthrax is the most common form

• Severe sequelae can result form anthrax pnemonitis
and septicaemia
 AETIOLOGY / EPIDEMIOLOGY
•  Animal reservoir – cows, goats, sheep
• Spores can survive for years in soil.
• Is endemic in Africa, Asia, India and South America
• Infections occurs when spores enter a break in the
skin (cuteneous) or when spores are inhaled (wool
sorters disease) –> anthrax pneumonitis

special characteristics of anthrax 

• Capsule prevents phagocytosis; resistant to heat
and gastric juice
• Toxin –> Haemorrhage and oedema
 PATHOPHYSIOLOGY
1. Primary cuteneous infection ->
• Local necrosis –Non suppurative
• Oedema – Jelly like
 
2. Spread to regional LN and to circulation ->
• Bactaraemia
• Meningitis
• Pneumonia

3. wool sorters disease

• Diffuse haemorrhagic pneumonitis –> haemoptysis
 CLINCIAL S+S
• IP – 3-5 days
1. Cuteneous anthrax
• Early pruritic papule at site of scratch on skin surface
• Vesicle formation –> haemorrhage and rupture
• Non tender ulcer covered with black escar, surrounded
by marked, non tender pitting oedema
• Regional lymphadenopathy –> bactaraemia->
-Pneumonia
-Meningitis 
NB:
• Generally in uncomplicated cuteneous anthrax, there
are very few systemic symptoms  
2. Wool sorters disease
• High fever, malaise
• Dry cough – haemoptysis
• Severe chest pain
• Dyspnoea
• Cyanosis
• Haemorrhagic mediastinitis
3. CNS
• Meningitis – fever
• Bloody CSF
4. Intestinal anthrax
•  Follows ingestion of organism, through meat eating
• Abdominal pain
• Vomiting and diarrhoea – bloody
• High fever
 DIAGNOSIS
1. Cuteneous anthrax
• Typical clinical presentation and Hx
• Gram stain – large gram positive rods (Facultative,
anaerobic, encapsulated)
• C/S
2. Septicaemia
• Blood for C/S 
3. Pneumonia
• Sputum - gram stain , C/S
• Typical history – occupational exposure
• Blood cultures
 DDX
• Staphylococcus skin infection.
-Pus
-Tender
 TREATMENT
1. Cutaneous
• X-pen or PPF
(a) lm PPF 4mls Od x 7/7
(b) lm/lv xpen 4mu Qid 7/7
- Incase of allergy to penicillin
- Tetracycline 500mgs Qid 10/7
- Others; Doxycycline, CAF, Streptomycin
2. Bactaraemia / meningitis/ penumonia
• Iv X-pen 3-8 mu Qid x 7/7
 PREVENTION
• Proper disposal of dead animals
• Meat inspection
• Careful wound care
• Strict rules for disinfecting skins and hides in
leather processing industry
• Vaccine - people at risk
 8. PLAQUE
 Is an infectious disease of animals mainly wild and
domestic rodents 
 It has two major clinical forms:-
1. BUBONIC
• Characterized by high fever, lymphadenopathy,
suppuration of regional lymphnodes, bacteraemia
and prostration.
2. PNEUMONIC
• Can be a direct respiratory transmission or
secondary to pneumonia. It is highly fatal.
 AETIOLOGY / EPIDEMIOLOGY
• Plague is endemic in rodents. Transmission is
through the flea mainly. It is also possible through
ticks, lice, bed bugs. 

• These vectors acquire the disease through ingestion

of blood from a bacteraemic animal.

• Can also get infected by direct contact with infected

tissues, animal bite, dry scratching of infected
material into the skin. 
• Droplet spread causes plaque pneumonia i.e man to
man spread. Incidence increases when the
population of rats increase

• Organism- Yersinia pestis – gram –ve, non motile,

non sporing cocco bacillus
• Grown both aerobically and anaerobically

• Small out breaks – Kenya, Uganda, Tanzania, Eastern

Zaire, and Namibia
 PATHOLOGY
• Following introduction the organism into the body
by the flea, there is regional LN inflammation

• The LNs become haemorhagic and oedematous

• Haemorrhagic septicaemia may occur with sub

pericardial and meningeal haemorhages – also in
liver, lungs, spleen, kidneys
 CLINICAL S+S
A: BUBONIC
• IP 1-12 days (average – 2-4 days)
• Sudden onset of chills and fever (T 39oc – 40oc)
• Tachycardia, HA, vomiting
• Marked prostration, and delirium
• Palpable spleen +/- ( firm and tender)
• Swollen, tender haemorhagic inquinal glands (60-
75%) -BUBOES
• Petechial haemorrhages
B: SEPTICAEMIC
• Is a severe variant of pneumonic plaque 
• Is severe disease with chills, fever tachycardia, H/A,
Nausea, Vomiting, Delirium 
• Death occurs within a few days before lesions
become apparent
C: PNEUMONIC 
• 5% of bubonic plaque develops pneumonia. Then
there is man to man transmission. It is a
fulminating infection with prostration, cough,
dyspnoea and cyanosis
 
• The sputum is copious and blood stained, full of Y.
Pestis.

• Usually there are no obvious pulmonary signs –

there could be scattered crepitations and areas of
dullness.
 LABORATORY DIAGNOSIS.
• FH – Raised wbc 12000-15000 / mm3
- Raised ESR
• Urine – Proteinuria + haematuria
• Culture
– Bubo aspirate - Thick with rounded ends
- Blood - Gram –ve
- Sputum - Bipolar appearance
 DDX
• Malaria
• Influenza
• Enteric fever
• Pneumonia
• LGV
 TREATMENT
• Highly effective drugs are Tetracycline,
Chloramphenicol and Streptomycin
A. DRUGS
• Streptomycin
-1gm Bd x 72hrs (lm)
-Then 1gm Od x 7-10/7
• Chloramphenicol or Tetracycline
500mgs Qid x 5/7 (PO)
• Kanamycin and Cotrimoxazole are also effective
• Plaque meningitis – Chloramphenicol +
Streptomycin
B: SUPPORTIVE
• Support peripheral circulation
• O2 + Tracheostomy
• Isolate patient
• Postural drainage
 PREVENTION
1. Extermination of rats
2. Extermination of ectoparasites vectors e.g. Fleas
with insecticides
3. Immunization
• Killed vaccines – 2 or 3 days
• Live attenuated– one dose – booster 3-6/12
4. Outbreak – actinomycin / streptomycin
5. Protective wear – gloves, masks
 PROGNOSIS

• In the past mortality was as high as - 50-90% , and

100% in pneumonia, septicaemic and meningitis.

• Now with treatment it is 5-10% mortality

 9. LEPTOSPIROSIS
• Is infection of man to animals by organism of the
genus leptospira.

• There are over 200 serotypes e.g.:-

 Leptospira interrogans Icterohaemorrhagicae
- Rodents / wild
 Leptospira interrogans canicola
- Pigs and dogs
 Leptospira interrogans hardjo and L. I. Pamona
- Cattle
• The organisms – colonize renal tubules of animals
and are excreted in the urine of animals. 

NB:
• L. Interrogans – pathogenic strains
• L. Biflexa – consists of saprophytic strains
 AETIOLOGY / EPIDEMIOLOGY
• The disease is endemic in domestic and wild
animals e.g. cattle, pigs, sheep, dogs etc

• Human infection is an incidental occurrence.

• The organisms are excreted in urine and can live

outside the body i.e. in water, soil or vegetations for
upto 2 weeks.
TRANSMISSION TO MAN IS BY:-
• Direct contact with urine or tissue of infected
animals.
• Indirect contact with contaminated water, soil or
vegetations.
 
PORTAL OF ENTRY INCLUDE:-
• Exposed conjunctiva, nasal or oral mucous
membrane
• Abraded skin – particularly around the feet
AFFECTS ALL AGES ESPECIALLY:-
 Abattoir (Slaughterhouse) and farm workers e.g. can
cutters
 Veterinarians (animal specialist, Vet, animal Doctor)
 Vagrants (A person who wanders from place to
place or lives a wondering Live)
 Sewer workers
 Mines and fish cleaners
 
NB: Sex incidence – same
 PATHOPHYSIOLOGY
1: LIVER
• Proliferation of hepatocytes –> tender enlargement,
Hypoplasia, and mild focal necrosis of kupffer cells

• Centrilobular biliary stasis

• Jaundice (conjugated hyper bilirubinaemia)

• Raised transaminases greater than 230 i.u.

2: KIDNEY
• Usually enlarged, with small haemorrhages
throughout
• Variable degenerative changes of the convulated
tubule and loop of henle
• Glomeruli – less affecfed
• S+S
o Proteinuria
o Dysuria
o Haematuria
o Uraemia – renal failure
3: LYMPHNODES + SPLEEN
- Enlarge
4: VOLUNTARY MUSCLES
• Especially in gastrocnemius, there is non
inflammatory degeneration, with loss of striate and
hyaline change
5: BLOOD
• FHG
o Anaemia
o Raised ESR
o Raised WBC – 20 – 30,000 PMNL
 CLINICAL S+S
• IP 2-20 days – average 10/7
• Leptospirosis occurs in 3 phases;

A. Leptospiramic phase
B. Immune phase
C. Convalescent phase
A: LEPTOSPIRAMIC PHASE
- 1st Phase
• 4-9 days – blood + CSF • Lymphadenopathy
• abrupt onset of severe • Skin rashes
frontal Headache. • Photophobia
• Fever 39oc • Disturbed sensorium
• Malaise • Relative bradycardia
• Anorexia • The leptospira disappear
• Myalgia from blood or CSF
• Conjunctival oedema • Asymptomatic phase –
• Arthralgias lasts 1-3 days
• Hepatosplenomegaly
B: IMMUNE PHASE - 2nd Phase
• 50% of patients have meningismus
• 1/3 have high CSF lymphocytes and increase in CSF protein
• Appearance of IgM antibodies 
NB: Majority recover at this stage, however a small
proportion progress to Weils disease i.e ->
• Fever and earlier symptoms recur
• Meningismus may develop
• Hepatomegaly
• Jaundice
• Haemolytic anaemia
• Haematuria (microscopic)
• Oliguria – renal failure
• CCF – due to atrial and ventricular dysrythmias
• Iridocyclits
• Optic neuritis
• Encephalitis
• Myelitis
• Peripheral neuropathy
• Epistaxis, haemoptysis
• Pneumonitis 
NB:
Weils disease means severe leptospirosis accompanied
by, jaundice, azotaemia, haemorrhages, anaemia,
disturbed consciousness and continued fever
C: CONVALESCENT PHASE – 3rd Phase

• Fever and aches may recur

• In pregnancy there is increased risk of foetal loss
 DIAGNOSIS
1. BLOOD – FH
• Blood count – mild elevation in an icteric (relating to or having
jaundice) patient
• With jaundice – 50 000 cells/mm3
• Neutrophilia less than 70% (20-30,000)
• Thrombocytopenia
-Rare
-Can be a cause of bleeding
• ESR raised 
2: URINALYSIS 
• Proteinuria
• Casts
• Pus cells 
* jaundice is associated with Ureamia 
3: CULTURE
• Blood culture – 1st week
• Fletcher’s or castanelas medium
• - for Pre-icteric stage
• Urine culture 2nd week - C/s
• CSF 2nd week 
4. SEROLOGY - 2nd week
• IgM antibodies +ve (Agglutination reaction) 
5: BIOPSY – Muscle
• Characteristic histological changes
 DDX
1. Meningitis
2. Hepatitis
3. Nephritis
4. Malaria – cerebral malaria
5. Influenza
6. Fever of unknown origin (FUO)
 COMPLICATIONS
 
1. Renal failure
2. Liver failure
3. CCF
4. Meningitis (aseptic)
5. Bleeding tendencies
 TREATMENT
1. Treat renal or liver problems/disease appropriately
2. Specific
- Penicillin 1-2 mu QID x 1/52
- Streptomycin 500 -750mgs Od x 1/52
- Tetracycline – 500mg QID x 1/52
- Chloramphenicol
- Erythromycin
 
NB:
• Many drugs are given at any stage
PROGNOSIS
• Death in appro. 40%
• Higher in old patient
• Worse in those with jaundice
• ARF – Good
 
PREVENTION
• Avoid direct contact with rats
• Avoid emersions in natural waters
 4. VIRAL INFECTIONS

1. RIFT VALLEY FEVER

2. YELLOW FEVER
3. EBOLA
4. DENGUE FEVER
 1. EBOLA
• EBOLA VIRUS DISEASE also known as EBOLA
HEMORRHAGIC FEVER (EHF)
• Is a viral hemorrhagic fever of humans and other
primates cased by ebolaviruses