Spotted Fever Rickettsiosis Infection in a Traveler From Sri Lanka

Philip H. Stokes MBBS, Barry J. Walters FRACP, FRANZCOG
DOI: 436-438 First published online: 1 November 2009


A case is reported of travel‐acquired tick‐borne spotted fever rickettsiosis from Sri Lanka. Little is known about rickettsial disease in Sri Lanka and this case may be the first documented instance of travel‐acquired spotted fever group rickettsiosis from that origin.

Spotted fever group (SFG) rickettsioses are found in many parts of the world. They are zoonoses caused by Rickettsia, small obligate intracellular bacteria. 1 Spotted fever group rickettsioses are transmitted by many species of ticks 1 with humans being incidental hosts. Rickettsial infections are being diagnosed more frequently in travelers. 2 Very little is known about the prevalence and distribution of rickettsial disease in Sri Lanka with very few studies having been published. 3

Case Presentation

A 40‐year‐old woman of Sri Lankan descent presented with fever for 8 days, commencing 6 days after spending 2 weeks visiting relatives in Sri Lanka. She took no malaria prophylaxis, recalled no mosquito bites, and reported no illness while traveling. She was using only the oral contraceptive pill, and there was no history of medical problems. She had no un‐well contacts.

Her symptoms began with fever, chill, myalgias, polyarthralgia, headache, nausea, and vomiting. She presented to her family doctor on day 2 of her illness (6 days before presenting to Royal Perth Hospital) and was prescribed cephalexin. Two days later she developed a rash that she attributed to the antibiotic, which she ceased.

Fever and other symptoms continued unabated and she subsequently developed abdominal pain. On presentation to the Emergency Department she was febrile at 40.0°C, with a heart rate of 120 beats per minute, respiratory rate of 20 per minute, blood pressure of 120/70, and oxygen saturation of 98% on room air. She had suffused conjunctivae, a maculo‐papular rash on the arms, legs, palms, soles and trunk, and tender hepatomegaly extending 3 cm below the costal margin. The spleen was not palpable and there was no jaundice. Auscultation of her heart and chest revealed no abnormal findings. There was no palpable lymphadenopathy. Significantly no eschar was identified. Results from the Mycoplasma and Ebstein Bar Virus serology taken earlier were available and both were negative.

Initial investigations revealed only a mild thrombocytopenia, raised C‐reactive protein (CRP), and mildly elevated liver function tests. Hemoglobin and white cell count were within normal limits. A midstream urine examination was normal, as was chest radiography. Serological studies for dengue and hepatitis B were advised as were thin and thick films for malaria. Malaria was not confirmed.

After admission, the management was initially supportive with nonsteroidal anti‐inflammatories and intravenous hydration. Further investigations included typhoid, leptospirosis, and rickettsial serology.

The constellation of symptoms was considered consistent with a rickettsial illness with other possibilities including dengue fever, malaria, leptospirosis, or typhoid. A total of 100‐mg doxycycline twice daily was commenced orally. Fever continued for a further 24 hours with improvement over the following days. Liver enzymes and CRP returned to normal. Blood and urine cultures remained negative as were repeat malarial blood films. Typhoid fever, dengue fever, and leptospirosis serology were negative. Rickettsia serology, using the Inverness test kit at the Pathwest laboratory in Nedlands, revealed an indirect fluorescent antibody (IFA) of 128, eventually rising to 1,024 more than 7 days after the acute phase of the illness, for Rickettsia conorii IgM. Other rickettsial (R. typhi, Orientia tsutsugamushi) serology was negative. The diagnosis was a spotted fever rickettsiosis infection acquired in Sri Lanka, testing positive for R. conorii. The patient was discharged asymptomatic on the sixth day after presentation.


SFG rickettsioses are prevalent in many parts of the world with the agents and vectors responsible varying from region to region. Among these are Rickettsia rickettsii, the agent of Rocky mountain spotted fever (RMSF) in North and South America, 1 the subspecies of R. conorii which causes illness in Southern Europe, Africa, Russia, and India, and Rickettsia africae in sub‐Saharan Africa responsible for African tick bite fever. 2

SFG rickettsiosis typically presents with fever, a maculopapular rash, and a black eschar. The presence of eschar varies between species being absent in RMSF, 2 uncommon in Indian tick typhus (R. conorii indica) 4 and Israeli spotted fever (R. conorii israelensis) 5 but is present in > 80% of cases of Mediterranean spotted fever (R. conorii conorii) 6,7 and is common in Queensland tick typhus (Rickettsia australis) and African tick bite fever, where eschars are often multiple. 2,6 Other features of SFG rickettsiosis can include arthralgias, myalgias, headache, and less commonly gastrointestinal symptoms, hepatomegaly, and cough. The rash can be petechial or vesicular depending on the organism and typically appears on day 5 to 7. 6,7

SFG rickettsiosis can be severe and even fatal particularly due to R. rickettsii or R. conorii. 2,8 Either can cause death in otherwise healthy adults. 5,8 Death often results from multiorgan failure. SFG rickettsiosis can cause severe respiratory, hepatic, renal, and neurological complications. 8,9

The diagnosis of SFG rickettsiosis is complicated by the fact that antibodies are not usually detectable in serum until late in the infection, 2 as in this case where a serological diagnosis was not made until after the acute period. Clinical diagnosis is therefore vital if prompt treatment is to be initiated. The treatment of SFG infections utilizes doxycycline 100 mg twice daily for 5 to 7 days with supportive therapy as required depending on disease severity. Oral therapy is appropriate in all but the most severe cases. 9 It should also be remembered that there is significant cross reactivity between Rickettsial species on serology. 1 Positive results for one agent based on serology alone are not definitive. In our case, it is impossible to be certain if the causative agent was indeed R. conorii or another spotted fever group agent. Given Sri Lanka's close proximity to India, the home of R. conorii indica, it is certainly possible that R. conorii is found in Sri Lanka.

Spotted fever group rickettsioses are of increasing importance in travel medicine being diagnosed more frequently as more people travel to exotic locations. 2 The Rickettsial species most often isolated from travelers is R. africae 10 acquired in sub‐Saharan Africa. Rickettsia conorii is also commonly reported in travelers. 2 One case of Indian tick typhus in a traveler from France was reported in 2001. 11 In a patient recently returned from an endemic area with fever and a rash, particularly one involving the palms, clinicians should consider Rickettsia as a possible diagnosis. Rickettsial infections generally respond well to the treatment and can have potentially fatal sequelae and as such therefore physicians should have a low threshold for commencing treatment if it is in the differential diagnosis in a returned traveler. 6 Travelers should be advised to wear protective clothing and avoid direct contact with local animals to minimize the exposure to potentially infective ticks. 9

There is little published information about rickettsial infections in Sri Lanka and no documentation of travel‐acquired cases. In a study by Kuluratne and colleagues, serology was performed on suspected cases of typhus, 16% of acute cases were found to be reactive to SFG antigens, including R. conorii antigen but also Rickettsia honei and Rickettsia japonica. Thirteen percent of acute cases were reactive to O. tsutsugamushi, the agent responsible for scrub typhus. 3 In the study, the spotted fever group infections were more severe with high fever and a maculopapular rash with occasional skin necrosis. Only one case was found to have an inoculation eschar. This study suggests that there is a significant morbidity from Rickettsia in Sri Lanka from multiple agents. The authors commented that the diversity of reactive serum among the spotted fever group may be due to hitherto unknown species or strains cross reacting with several antigens. 3 Another similar study carried out in the Western Province of Sri Lanka also detected infections with both R. conorii and O. tsutsugamushi species. 12

We have described a case of travel‐acquired SFG rickettsiosis (reacting to R. conorii antigen) infection from Sri Lanka presenting in Australia. The clinical and laboratory features were consistent with those reported from SFG infections in Sri Lanka with high fever, rash, severe disease, and lack of inoculation eschar being shared characteristics. 3 It does appear that the clinical and laboratory features described herein may characterize a distinct clinical entity and with further characterization a tick typhus unique to Sri Lanka may emerge as clinical entity.

Declaration of interests

The authors state that they have no conflicts of interest to declare.


The authors would like to acknowledge the assistance of and advice of Dr Jjante Taljaard and Mr Anthony Jones.


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