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Third stage
Medicine
Lec-2
د
.
حسين
1/1/2014
Rickettsial infections
Pathogenesis
Intracellular Gram-negative, parasitise the intestine of arthropods, conveyed to humans
skin from the excreta of arthropods.
Multiply in capillary endothelial cells, producing skin, CNS, heart, lungs, kidneys and skeletal
muscles lesions. Endothelial proliferation, associated with a perivascular reaction,
thrombosis and purpura.
In epidemic typhus the brain is the target organ.
In scrub typhus the cardiovascular system and lungs are attacked.
Eschar is often found in tick- and mite-borne typhus, which is crusted necrotic sore at the
site of the bite due to vasculitis. Regional lymph nodes often enlarge.
Classification of rickettsial diseases
Spotted fever group
1. Rocky Mountain spotted fever
2. Other tick borne typhus fevers
Typhus group
1. Epidemic typhus (louse borne typhus)
2. Endemic typhus (flea borne typhus)
3. Scrub typhus (mite borne)
Rocky Mountain spotted fever
Caused by Rickettsia rickettsii,
Transmitted by tick bites,distributed in USA.
Incubation period: 7 days
Clinical features:
fever , maculopapular measles-like
Rash bleeding , peripheral gangrene
hepatosplenomegaly.
Mortality is 2-12%.
Epidemic (louse-borne) typhus
Causative agent: R. prowazekii
Vector: Human body louse through its excreta by scratching.
Endemic in Africa and South America.
Patients infect the lice, which leave when the patient is febrile. In conditions of
overcrowding the disease spreads rapidly.
Incubation period: 10 – 14 days
Clinical features:
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First Week
High fever, rigor, congested eyes,confusion, rash (erythematous, then petecheal) on the
trunk, then spreads.The neck and face are seldom affected.
Second Week
worsening symptoms,,stupor ,palpable spleen. The temperature falls rapidly at the end of
the second week and the patient recovers gradually.
In fatal cases , patient usually dies in the second week from toxaemia, cardiac or renal
failure, or pneumonia.
Endemic (flea-borne) typhus
Caused by R. mooseri is endemic world-wide. Humans are infected when the faeces or
contents of a crushed flea which has fed on an infected rat are introduced into the skin. The
incubation period is 8-14 days. The symptoms resemble those of a mild louse-borne typhus.
The rash may be scanty and transient .
Scrub typhus fever
Caused by R. tsutsugamushi ,transmitted by mites. It occurs in the Far East, Pakistan,
Bangladesh, India, Indonesia .one or more eschar develops, surrounded by cellulitis and
enlargement of regional lymph nodes.
Mild or subclinical cases are common. The onset is usually sudden with headache, fever,
malaise, cough. Maculo-papular rash often appears on about the 5th-7th day and spreads
to the trunk, face and limbs including the palms and soles ,fades by the 14th day, with
generalised painless lymphadenopathy. temperature falls by lysis on about the 12th-18th
day.In severe infection Cardiac, renal failure and haemorrhage may develop.
Investigation of rickettsial infection
Diagnosis is made on clinical grounds and response to treatment.
Differential diagnoses include malaria, typhoid, meningococcal sepsis and
leptospirosis.
The Weil-Felix reaction is the agglutination of the somatic antigens of non-motile
Proteus species by the patient's serum. It is now seldom used due to its lack of
specificity and sensitivity.
Species-specific antibodies may be detected in specialised laboratories.
Management of the rickettsial diseases
all respond to tetracycline or chloramphenicol 500 mg 6-hourly for 7 days.
Louse-borne and scrub typhus can be treated with a single dose of 200 mg doxycycline,
for 2-3 days to prevent relapse.
Resistant strains of R. tsutsugamushi may need treatment with rifampicin .
Nursing care is important, especially in epidemic typhus.
Sedation may be required for delirium and blood transfusion for haemorrhage.
Prevention of rickettsial infections
Vector and reservoir control , Lice, fleas, ticks and mites need to be controlled with
insecticides.
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Q FEVER
World-wide,caused by rickettsia-like organism Coxiella burnetii an obligate intracellular
organism.
Cattle, sheep and goats are important reservoirs .
Transmitted by inhalation of aerosolised particles .
An important characteristic of C. burnetii
is its antigenic variation, called phase variation, due to a change of lipopolysaccharide (LPS).
When isolated from animals or humans, C. burnetii express phase I antigen and are very
infectious (a single bacterium is sufficient to infect a human). In culture there is an antigenic
shift to the phase II form, which is not infectious.
Clinical features
The incubation period is 3-4 weeks. Fever, headache and chills; maculo-papular rash .
Other presentations include pneumonia and hepatitis.
Chronic Q fever may present with osteomyelitis, encephalitis and endocarditis .
Investigations
Diagnosis is usually serological.
stage of the infection can be distinguished by isotype tests and phase-specific
antigens. The antigenic shift can be measured and is valuable for the differentiation
of acute and chronic Q fever.
Phase I and II IgM titres peak at 4-6 weeks.
In chronic infections IgG titres to phase I and II antigens may be raised.
Management
Prompt treatment of acute Q fever with doxycycline reduces fever duration.
Treatment of Q fever endocarditis is problematic, requiring prolonged therapy with
doxycycline and rifampicin or ciprofloxacin; even then, organisms are not always
eradicated.
Valve surgery is often required.