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Ricketisial Diseases

Epidemic And Endemic Typhus

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Definition
Rickettisiae are small intracellular bacteria that are spread to man
vectors namely human body lice, fleas, ticks & larval
by arthropod vectors,
mites.

The organisms inhabit the gastrointestinal tract of these arthropods &

spread to human host by the direct bite of the vector or the inoculation
of the organism contained in the feces of the vector by bite
induced body itching.

These infections are characterized by persistence in the body, widespread

vasculitis (invading endothelial cells of small blood vessels) & multi-system
involvement.

Except in louse borne typhus humans are accidental hosts in most

rickettisial diseases.

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Classification
Major rickettsial diseases

Tick and mite borne spotted fever group

Flea and louse borne typhus group

Scrub typhus:
typhus free-living mite that feeds on the skin and other
tissues of mammals, including humans, causing irritation and
swelling.

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Etiology and Epidemiology of Epidemic and Endemic

Typhus
Epidemic Typhus (Louse born ):
Is caused by R.prowazekii and transmitted by human body louse
(Pediculus humanus corporis).
Lice acquire the rickettsia while ingesting a blood meal from an
infected patient, the rickettsia multiply in the midgut epithelial cells of
the louse and are excreted via louse faeces.
The infected louse defecates during a blood meal and the patient auto
inoculates the organisms by scratching.
It is commonly associated with poverty, cold weather, war and natural
disasters.
The disease is prevalent in mountainous areas of Africa, South America,
and Asia.

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Endemic Typhus (Flea born) / Murine Typhus:

Is cause by R. thyphi which is transmitted by fleas.

R. typhi is maintained in mammalian host/flea cycles, with rats.

Fleas acquire R.thyphi from rikettsemic rats and carry the

organism throughout the rest of their life span.

Humans and rats are infected when rickettsia –laden fleas are
scratched in to pruritic bite lesions.

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Clinical Features
Epidemic typhus (Louse borne typhus)
Incubation period of 1 week

Abrupt onset of illness with prostration, severe headache and rapidly

rising fever of 38.8 to 40.0 °C

Cough is seen in 70 % of patients , myalgia may also occur which may

be severe

Rash, begins on upper trunk around 5th day and then becomes
generalized, involving the entire body except face, palms and soles;

at first, rash is macular, becoming maculopapular, petechial and

confluent without treatment, although in black people, rash may be
absent (spotless epidemic typhus)

Photophobia,
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with
MeU
conjunctival injection and eye pain; frequent
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Tongue may be dry, brown, furred

The signs of central nervous system involvement, commonly as
meningo-encephalitis, appear towards the end of the 1st week
progressing to seizure and coma.
Brill-Zinsser disease (recrudescent
Brill- recrudescent typhus):
typhus This is a mild form of
epidemic typhus caused by reactivation of dormant R. prowazekii in the
body (in the lymph nodes) as a result of immuno-suppression or old
age.
Occurs after several years of acute infection.
The manifestation of the disease is similar to acute epidemic typhus but
milder.
The organisms may infect other people in the presence of vectors (body
lice).

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Clinical Features
Endemic typhus (Flea borne typhus)
Endemic typhus (also known as murine typhus) is a relatively milder.
The incubation period is 1 - 3 weeks and followed by sudden onset of
fever, rigors, frontal headache, pain in the back and limbs, constipation
and cough (due to bronchitis).
The fever becomes constant after the third day and associated with
conjunctivitis and orbital pain.
Rash appears on the fifth day initially as blanching macules at the anterior
axillary folds, which subsequently spread to involve other parts of the
body (sparing the face & the neck) and become purpuric.
During the second week symptoms worsen and additional manifestations,
such as sore lips, dry brown tremulous [unsteady] tongue, feeble pulse,
enlarged spleen & delirium appear.

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Complications of Endemic and Epidemic Typhus

Skin necrosis, gangrene of digits, Venous thrombosis
Interstitial pneumonia in severe cases Myocarditis
Oliguric renal failure
Parotitis
Diagnosis of rickettsial diseases is based on
History, clinical course of the disease and epidemiologic of the disease
may give a clue for diagnosis.
Laboratory investigations;
Serologic tests:
Indirect fluorescent antibody test
Weil-Felix agglutination test: This is widely used by many of the
hospitals and the private clinics in this country, is not specific or sensitive.
Isolation of the organism by inoculation into laboratory animals is
possible, it is time consuming and technically demanding.

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Treatment of rickettsial diseases

Endemic Typhus
Doxycycline 100mg bid PO for 7-15 days
Chloramphenicol 500mg QID PO for7-15 days
Epidemic typhus
Doxycycline 200mg as single dose PO until the patient is afebrile for 24 hours.
Delousing louse borne typhus
Supportive Therapy
Attention to fluid balance, prevention of bed sores,
Treat agitation with diazepam
Steroid treatment (prednisolone 20 mg daily for adults) in severe cases
Prognosis: Untreated disease is fatal in 7 to 40 % of cases, depending on
condition of host. In untreated survivors, renal insufficiency,
insufficiency multiorgan
involvement and neurologic manifestations (12 %) are common.
However, endemic typhus has better prognosis with a mortality of only 1 – 2%.
Serious neurological, renal and other complications are unusual.
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Prevention
For flea borne typhus
Elimination of fleas on clothing & bedding using insecticides like 1%
Malathion powder.
Apply residual insecticide powder on the floor & bedding to kill hatching
fleas.
Rodent control using chemicals (e.g. warfarin)
For louse borne typhus
Eradicate all lice on clothing & bedding using insecticides (1% Malathion
powder) including all family contacts.
DDT is not useful as the lice are often resistant to it .
Wash the patient with soap and water & apply insecticides all over &
disinfect clothing with insecticides in a bag or sterilize by autoclaving.
Protective wearing smeared with insect repellents is recommended for
nurses and other attendants
Chemoprophylaxis: Doxycycline 100mg weekly will protect those at
risk
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Spirochetal disease (relapsing fever)

Definition
Relapsing fever is an acute febrile illness caused by Borrelia species,
presenting with recurrence of characteristic febrile periods lasting for days
alternating with afebrile periods.
Relapsing fever describes two distinct diseases:
Louse borne (Endemic) relapsing fever (LBRF):- transmitted by body
louse Pediculus humanis var corporis
Tick borne (Epidemic) relapsing fever (TBRF)- transmitted by tick
(Ornithodoros)
Etiology
Relapsing fever is caused by Borrelia species, which are spirochetal gram
negative helical [spiral] bacteria.
B. recurrentis is the only species that cause LBRF
B. duttoni is the commonest causes of TBRF in sub-Saharan Africa.
Borrelia demonstrates remarkable antigenic variation and strain
heterogeneity which help the parasite to escape the immune response of
the host and result in recurrence of febrile episodes.
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Transmission
LBRF: Body lice become infected by B. recurrentis while feeding on
spirochetemic human blood, the only reservoir of infection.

Humans acquire infection when infected body lice are crushed and their
fluids contaminate mucous membrane or breaks in the skin (such
as abrasions caused by scratching of pruritic louse bites)

LBRF is now an important disease only in the north eastern Africa,

specially the highlands of Ethiopia where an estimated 10,000 case occur
annually.

In Ethiopia the disease affects mostly homeless men living crowded

together in very unhygienic circumstances especially during rainy seasons.

Some of the risk factors for LBRF are overcrowding like in military
camps, civilian population disrupted by war and other disasters.

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Transmission
TBRF: Rodents are the primary hosts and vector ticks become
infected when they feed spirochetemic rodents.

Ticks transmit the borreliae vertically over several generations.

TBRF is most highly endemic in sub-Saharan Africa but also is

found in Mediterranean and Middle eastern countries.

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Clinical Features
The manifestation of both LBRF and TBRF are similar.
Incubation period is 7 days (ranging from 2-18 days).
The onset is sudden with high grade irregular fever, fever headache, chills,
myalgias, arthralgias, and insomnia.
Patient will be withdrawn, disinterested to food and other stimuli and
thirsty.
Patient will have delirium associated with high grade fever, tachycardia and
dry tongue, injected conjunctiva and photophobia
Summation gallop , occasionally resulting from myocardial involvement
Upper abdominal tenderness with hepatosplenomegally,
Scattered petechiae over the trunk, extremities and mucous membrane in
1/3 LBRF and fewerTBRF
Symptoms and signs of meningial irritation may be seen in some patients.
Icteric sclera may be found in late stage of the disease.

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Complications
Life threatening complications are unusual in otherwise healthy persons
if the disease is diagnosed and treated early.
Complications are common in late disease in untreated patients.

Epistaxis,, blood streaked sputum other bleeding tendencies

Epistaxis

Neurologic manifestations like iridocyclitis, meningitis, coma, isolated

cranial nerve palsies, Pneumonitis, Myocarditis Spleenic rupture etc.

Without treatment, symptoms intensify over 2-7 days period and

subside with spontaneous crisis during which borrelia disappear from
the circulation.

Such cycles of febrile periods alternating with afebrile periods may

recur several times.

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Diagnosis
Diagnosis of relapsing fever is made based on demonstration of the
organisms in blood, bone marrow, CSF etc
Blood Film:
Giemsa or Wright stained peripheral blood smear is the most
commonly done laboratory test in Ethiopia, and an ideal test in the
resource limited setting.
Spiral organisms can be demonstrated on peripheral blood taken during
febrile period preceding the crisis.
This is positive in more than 70% of LBRF and in lower percentage of
patients withTBRF.
Other Tests
Dark field microscopy of unstained blood/CSF
Serologic tests

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Treatment
Relapsing fever is treated with antibiotics.
In LBRF single dose of erythromycin, tetracycline, doxycycline or
chloramphenical, produces rapid clearance of borrelia from the blood &
remission of symptoms.
TBRF is less sensitive to these antibiotics and requires a 7 days course of
treatment.
Adult Dosage
Medication LBRF (single dose) TBRF (7 day schedule) Oral
Erythromycin 500mg 500mg every 6 hrs
Tetracycline 500mg 500mg every 6 hrs
Doxycycline 100mg 100mg every 12 hrs
Chloramphenicol 500mg 500mg every 6 hrs
Parenteral
Penicillin G (procaine) 600,000 I.M stat 600,000 IM daily
Delousing of patients with Relapsing fever is important to prevent
transmission and recurrence
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Prevention and Control of Relapsing Fever

Avoiding over crowding
Apply hygienic practices that reduce the number of body lice
(washing clothes)
Elimination of ticks
Health education
Early case detection and treatment of infected persons and close
contacts
In out breaks of LBRF, empirical single dose treatment with
doxycycline
Eradication of Rodents to control TBRF: ( Rodenticides )

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Schistosomiasis (Biliharziasis
(Biliharziasis))

Schistosomiasis (Biliharziasis) is a group of diseases

caused by the genus Schistosoma affecting mainly the

gastrointestinal &

genitourinary organs.

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Etiology
Schistosomiasis in man is caused by five species of
Schistosoma
S. mansoni
S. haematobium
S. japonicum- in southeast Asia
S. makongi- in southeast Asia (makongi valley Laos, Cambodia)
S. intercalatum - endemic in Congo basin

The first three are common causes of schistosomiasis.

S. haematobium is the cause of urinary schistosomiasis and

all the rest cause intestinal schistosomiasis.

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Epidemiology
Endemic in 74 developing countries

Infecting more than 200 million people in rural agricultural

and per-urban areas and 500- 600 million being at risk.

Irrigation is favors the transmission of the disease

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Schistosomiasis in Ethiopia
It occurs in many parts of Ethiopia with more prevalence in the northern
part of the country.

Both S. mansoni and S. haematobium are endemic in Ethiopia

Increasing evidence for continued spread of both diseases

Small streams and irrigation canals are most important transmission

sites

Morbidities resulting from both infections are poorly appreciated

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Typical transmission site (Worke river, Kemisse)

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Life cycle
Man is the definitive host where sexual reproduction takes
place after cercarial entry by skin penetration and snails
are intermediate hosts in which asexual regeneration
continues.

Each species of Schistosoma has a specific snail host i.e.

S. mansoni -Biomphalaria species

S. haematobium - Bulinus species

S. japonicum - Onchomelania species

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Reservoir
The principal reservoir is man
Fresh water snail serves as intermediate host

Mode of transmission
Eggs leave - urine (S. haematobium) and feces others - eggs hatch
larvae (miracidia
miracidia) - penetrate into a suitable freshwater snail hosts -
circariae emerge from the snail - penetrate the human skin.

Incubation period - infections 2-6 weeks after exposure

Susceptibility and resistance

Susceptibility is universal. Resistance is poorly defined

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Clinical Manifestation
Itching at sites of circariae

Fever, eosinophilia, abdominal pain and transient generalized

urticaria (known as katayama syndrome
syndrome)

Headache, malaise, arthralgias, cough, bloody diarrhea,

Hepatospleenomegally, right upper quadrant pain on the

abdomen and tenderness

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Chronic Schistosomiasis

Patient with chronic may present months to several years

Symptoms includes bloody diarrhea, abdominal pain, cramping

hematemesis (with portal hypertension), ascites (with portal
hypertension) and so on

Dribbling, incontinence, frequency, dysuria and hematuria

Diagnosis
Based on history of contacts with running water, clinical
manifestation
Demonstration of ova in urine or feces,

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Pictural overview of morbidity in schistosomiasis

mansoni
Normal liver

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Nodular appearance in advanced schistosomal liver

disease

Silva et al 2007
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Cut--surface of normal liver

Cut

Portal vein Hepatic vein

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Gross pathology in schistosomal PPF

Cut surface showing severe PPF

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Schistosomal PPF

b) Portal vein cast in schistosomal PPF

a) Portal veins cast of healthy liver
“dry tree appearance
Silva et al 2007
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Patient with advanced schistosomal PPF and portal hypertension

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Prevention and control

Treatment of cases
Intermittent irrigation
Drainage of water bodies
Clearing of vegetation
Treating water with molluscicides
Educating the public
Proper disposal of human feces and urine
Avoid swimming in water bodies known to have the infection
Use rubber boots
Report
Treatment
Praziquantel
Metrifonate
Oxaminoquine
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Guinea Worm Infection

Definition
An infection of the subcutaneous and deeper tissues by large
nematode.
Infections agent
Dracunculus medinensis, a nematode
Epidemiology
Occurrence-
In Africa (16 countries south of the Sahara) and in Asia (India and
Yemen) especially in regions with dry climates.
Local prevalence varies greatly. In some locales, nearly all inhabitants
are infected, in others, few, mainly young adults.

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Reservoir- Humans
Mode of transmission
Larvae discharged by the female worm into stagnant fresh water are
ingested by minute crustacean copepods (Cyclops species).
In about 2 weeks, the larvae develop into the infective stage.
People swallow the infected copepods in drinking water from infested
step wells and ponds.
The larvae are liberated in the stomach, cross the duodenal wall,
migrate through the viscera and become adults.
The female, after mating, grows and develops to full maturity, then
migrates to the subcutaneous tissues (most frequently of the legs).

Incubation period- About 12 months

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Period of communicability-
From rupture of vesicle until larvae have been completely
evacuated from the uterus of the gravid worm, usually 2-3
weeks.
In water, the larvae are infective for the copepods for about 5
days.
After ingestion by copepods, the larvae become infective for
people after 12-14 days at temperatures >25c0 and remain
infective in the copepods for about 3 weeks.
Susceptibility and resistance- Susceptibility is universal.
No acquired immunity; multiple and repeated infections may
occur in the same person.

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Clinical Manifestation
Few or no clinical manifestations are evident until just before
the blister forms.
Fever and generalized allergic symptoms, including periorbital
edema, wheezing, and urticaria.
The emergence of the worm is associated with local pain and
swelling.
When the blister ruptures, the adult worm releases larvarich
fluid and this is associated with a relief of symptoms.
The shallow ulcer surrounding the emerging adult worm heals
over weeks to months.
Diagnosis
Based on clinical and epidemiological grounds

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Treatment
Gradual extraction of the worm by winding of a few centimeters on a
stick each day remains the common and effective practice.
Worms may be excised surgically.
Administration of thiabendazole or metronidazol may relive symptoms
but has no proven activity against the worm.
Prevention and control
Provide health education programs in endemic communities to covey
three messages:
The guinea-worm infection comes from their drinking water
Villagers with blisters or ulcers should not enter any source of
drinking water and
That drinking water should be filtered through fine mesh cloth to
remove copepods
Provision of safe drinking water

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NURSING RESPONSIBILITIES IN THE MANAGEMENT: for

vector-borne diseases
Draining water or ditches, and any accumulation of water around the
village or filling in holes and ditches so that water will not accumulate.
Clearing bush and grass along water banks and in the village.
All containers likely to hold water are to be collected and disposed.
No water container should have water in it longer than one week.
Snails can be controlled by disturbing their habitant through changes in
water level, filling or damming habitant, and clearing habitat.
Mosquito net should be used at night.
Appropriate treatment of cases and provision of chemoprophylaxis.

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