1. RICKETTSIAL INFECTIONS
For Third- Year Medical Students
Dr: Hussein Mohammed Jumaah
CABM
Mosul College of Medicine
16/3/2014

2. RICKETTSIAL INFECTIONS
Spotted fever group
Rocky Mountain spotted fever
Other tick borne typhus fevers
Typhus group
Epidemic typhus (louse borne typhus)
Endemic typhus (flea borne typhus)
Scrub typhus (mite borne)
The rickettsial fevers are the most common tick-borne infections.
There are two main groups : spotted fevers and typhus group.

3. Pathogenesis
Rickettsia are 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.

4. 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.

5. 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%.

6. Rocky Mountain spotted fever

7. 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.

8. Epidemic (louse borne typhus)
Incubation period: 10 – 14 days
Clinical features:
First Week
High fever, rigor, congested eyes, confusion, rash (erythematous, then petecheal) on the trunk, then spreads.
Second Week
worsening symptoms, stupor , palpable spleen. The temperature falls rapidly and the patient recovers gradually.
In fatal cases , patient usually dies in the second week from toxaemia, cardiac or renal failure, or pneumonia.

9. 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.

10. 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.
Enlargement of regional lymph nodes.

11. Scrub typhus fever Mild or subclinical cases are common.
Onset is usually sudden , headache, fever, malaise,
cough. Maculo-papular rash often appears on
about the 5th-7th day and spreads to the trunk,
face and limbs, fades by the 14th day,
generalised painless lymphadenopathy.
temperature falls by lysis on about the 12thday.
In severe infection Cardiac, renal failure and
haemorrhage may develop.

12. Diagnosis of rickettsial infection
Diagnosis is made on clinical grounds and response to treatment.
The Weil-Felix reaction is the agglutination of the somatic antigens of 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.
Differential diagnoses
include malaria, typhoid, meningococcal sepsis
and leptospirosis.

13. 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
asingle 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.

14. Prevention of rickettsial infections
Vector and reservoir control , Lice, fleas, ticks and mites need to be controlled with insecticides.

15. Q FEVER
World-wide, caused by rickettsia-like organism Coxiella burnetii an obligate Gram negative 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.

16. 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.

17. 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.

18. Management
Prompt treatment of acute Q fever with doxycycline (100 mg twice daily for 14 days)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.