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Tick bite fever and arthritis associated with travel to Africa
  1. T Ding1,
  2. G Lloyd2,
  3. H Tolley2,
  4. A Bradlow3
  1. 1Department of Rheumatology, Nuffield Orthopaedic Centre, Windmill Road, Headington, Oxford OX3, 7LD, UK
  2. 2CAMR, Porton Down, Salisbury, Wiltshire SP4 0JG, UK
  3. 3Department of Rheumatology, Battle Hospital, Oxford Road, Reading RG30 1AG, UK
  1. Correspondence to:
    Dr T Ding
    tina.dingdoctors.org.uk

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CASE REPORT

A 52 year old woman was admitted with fever and acute polyarthritis. She had visited a game reserve in Northern Province, South Africa 5 weeks before admission. Two weeks before admission she developed fever and flu-like symptoms, then mouth ulcers, and a non-itchy, maculopapular rash that covered her whole body and her scalp. Three days after the start of the rash she developed painful and swollen joints—notably, the hands, elbows, wrists, knees, and feet.

On examination at admission she was apyrexial with no visible rash and no lymphadenopathy. She had florid synovitis at elbows, wrists, knees, and dactylitis affecting the right index finger (fig 1A), left thumb, and left 4th toe. Spinal movement was normal. Examination was otherwise unremarkable.

Figure 1

 Dactylitis affecting the right index finger (A) and 99mTc-MDP bone scan showing increased uptake over both wrists, left 1st interphalangeal joint and 4th proximal interphalangeal joints and right 2nd and 3rd metacarpophalangeal joints (B).

The full blood count and renal function were normal, erythrocyte sedimentation rate 131 mm/1st h and C reactive protein (CRP) 324 mg/l (normal <6 mg/l). A chest radiograph, and x ray examination of hands, feet, and sacroiliac joints were normal. A 99mTc-MDP bone scan showed increased uptake over the elbows, wrists, tarsi, left 1st interphalangeal joint and 4th proximal interphalangeal joints, and right 2nd and 3rd metacarpophalangeal joints (fig 1B). Antinuclear antibodies, rheumatoid factor, HLA-B27, hepatitis A and B, brucella, coxiella, chlamydia, parvovirus, and arbovirus serology were all negative, as was stool culture for salmonella, shigella, and campylobacter. It was confirmed that the patient’s serum contained anti-rickettsia “spotted fever group” antibody, titre 1/640, by screening using sheep red blood cells sensitised with spotted fever group specific antigen in an immune-haemagglutination assay.1

Doxycline was started empirically before the rickettsial serology result was known, and continued for 3 weeks. Intramuscular depomedrone 120 mg produced little improvement in joint symptoms and CRP. After 2 weeks sulfasalazine and oral prednisolone 15 mg daily were started; marked and continuing improvement followed despite rapid tapering of the steroid dosage.

The incubation period of rickettsial disease is 1 to 2 weeks, followed by abrupt onset of malaise, headache, and fever. An eschar is sometimes visible at the site of tick bite. A maculopapular or petechial rash is present usually on days 7 to 10 after the bite.

DISCUSSION

African tick bite fever has been recognised since the beginning of the 20th century as a rural disease, contracted from ticks of cattle and game. Initially, the condition was thought to be exclusively due to Rickettsia conorii. The first human infection with R africae was reported from Zimbabwe only in 1992. Recently R africae has also been identified in Amblyomma ticks from Niger, Mali, Burundi, and Sudan.2

Arthralgias occur commonly during rickettsial infections, but arthritis is rare and is usually acute aseptic monarthritis of a large joint. However, pauci- and polyarthritis have also been described.3 There have been 12 previous reports of arthritis with Mediterranean spotted fever,2 caused by R conorii, and there has been only a single case report of arthritis associated with Rocky Mountain spotted fever.4 As far as we know, this is the first reported case of arthritis in association with spotted fever (R africae and R conorii) originating from South Africa.

Between 1998 and 2002 spotted fever predominately due to R africae was detected in 131 cases (four with arthralgia) returning from southern Africa to the UK. More cases may be seen world wide if southern Africa continues to develop as a tourist destination.

In conclusion, we have described a patient who developed polyarthritis owing to rickettsial disease acquired in South Africa. Diagnosis was made based on the clinical history and the presence of anti-spotted fever group antibodies. Rickettsial infection should be included in the differential diagnosis of acute aseptic arthritis in travellers returning from sub-Saharan Africa5; effective treatment with tetracycline may otherwise be overlooked.

REFERENCES

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Footnotes

  • We have no conflict of interest to declare. Dr Ding as corresponding author had full access to all the data in this case report and had final responsibility for the decision to submit for publication.

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