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

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 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)

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%.

Rocky Mountain spotted fever

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.

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.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.

Scrub typhus fever 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.

Investigation of rickettsial infection 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 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.

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

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.