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Flinders Island Spotted Fever Rickettsioses Caused by “Marmionii” Strain of Rickettsia Honei, Eastern Australia Nathan B

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Flinders Island Spotted Fever Rickettsioses Caused by “Marmionii” Strain of Rickettsia Honei, Eastern Australia Nathan B RESEARCH Flinders Island Spotted Fever Rickettsioses Caused by “marmionii” Strain of Rickettsia honei, Eastern Australia Nathan B. Unsworth,* John Stenos,* Stephen R. Graves,* Antony G. Faa,† G. Erika Cox,‡ John R. Dyer,§ Craig S. Boutlis,¶ Amanda M. Lane,# Matthew D. Shaw,# Jennifer Robson,** and Michael D. Nissen†† Australia has 4 rickettsial diseases: murine typhus, murine typhus (Rickettsia typhi), scrub typhus (Orientia Queensland tick typhus, Flinders Island spotted fever, and tsutsugamushi), and the spotted fever group (SFG) dis- scrub typhus. We describe 7 cases of a rickettsiosis with an eases—Queensland tick typhus (QTT; R. australis) and acute onset and symptoms of fever (100%), headache Flinders Island spotted fever (FISF; R. honei) (2). (71%), arthralgia (43%), myalgia (43%), cough (43%), mac- QTT, first described in 1946, was characterized as a ulopapular/petechial rash (43%), nausea (29%), pharyngi- tis (29%), lymphadenopathy (29%), and eschar (29%). relatively mild disease with symptoms of fever, headache, Cases were most prevalent in autumn and from eastern malaise, enlarged lymph nodes, and a maculopapular Australia, including Queensland, Tasmania, and South (sometimes vesicular) rash. Most patients have an eschar Australia. One patient had a history of tick bite and some have a slight cough, myalgia, and chills (3,4). (Haemaphysalis novaeguineae). An isolate shared 99.2%, Cases of QTT have been detected only on the eastern 99.8%, 99.8%, 99.9%, and 100% homology with the 17 seaboard of mainland Australia, with most originating in kDa, ompA, gltA, 16S rRNA, and Sca4 genes, respective- late winter (5). FISF was described in Australia, in 1991. It ly, of Rickettsia honei. This Australian rickettsiosis has sim- is found in southeastern Australia and is characterized by ilar symptoms to Flinders Island spotted fever, and the fever, headache, myalgia, transient arthralgia, macu- strain is genetically related to R. honei. It has been desig- nated the “marmionii” strain of R. honei, in honor of lopapular rash, and cough in some cases (6,7). Most cases Australian physician and scientist Barrie Marmion. occur in summer. Both QTT and FISF are transmitted to humans by tick bites. Ticks of the genus Ixodes, especially I. holocyclus, are the main arthropod hosts of QTT and ustralia has several endemic rickettsial diseases. In Bothriocroton hydrosauri (formerly Aponomma hydro- Aaddition, epidemic typhus arrived with the first fleet sauri) are the main hosts of FISF (8–10). in 1788 (1), but the disease did not become established in We describe 7 cases of a rickettsial disease similar to Australia. The current endemic rickettsial diseases are FISF, which occurred in the eastern half of Australia. The etiologic agent of this disease is an SFG rickettsia, geneti- *Australian Rickettsial Reference Laboratory, Geelong, Victoria, cally related to R. honei and less closely related to R. aus- Australia; †Warwick Hospital (Southern Downs Health Services tralis. The etiologic agent of the rickettsiosis has been District), Warwick, Queensland, Australia; ‡Launceston General designated the “marmionii” strain of R. honei. Hospital, Launceston, Tasmania, Australia; §Fremantle Hospital, Fremantle, Western Australia, Australia; ¶Menzies School of Case Reports Health Research, Darwin, Northern Territory, Australia; #University of Queensland, Brisbane, Queensland, Australia; **Sullivan Patient 1 Nicolaides Pathology, Brisbane, Queensland, Australia; and A 37-year-old woman from Port Willunga, South ††Royal Brisbane Hospital, Brisbane, Queensland, Australia Australia, sought treatment in February 2003, with a 2- 566 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 13, No. 4, April 2007 "marmionii" Strain of Rickettsia honei week history of headache, fever, and sweats. No rash or were negative. Antibiotics were not given because the ill- eschar was seen, and she had no recollection of arthropod ness was thought to be viral. His symptoms resolved with- exposure. She had traveled to Kangaroo Island 2–3 weeks in the following 2 weeks. Antirickettsial antimicrobial before the onset of illness. Laboratory tests showed elevat- agents were not given at any stage during the illness. Day ed levels of liver function test enzymes, mild leukopenia, 3 serum and follow-up serum specimens obtained 6 and thrombocytopenia. Her health improved after receiv- months later were both negative for rickettsial antibodies; ing oral doxycycline for 5 days. Rickettsial serology later however, results of PCR and culture on the day 3 blood showed an increase in antibody titer. Both PCR and culture specimen were positive for SFG rickettsiae (Table 1). results were positive for an SFG rickettsia (Table 1). Patient 4 Patient 2 A 10-year-old boy was brought to the Yam Island A 9-year-old girl sought treatment at the Darnley Health Clinic, Torres Strait, Queensland, in May 2003, five Island Health Clinic, Torres Strait, Queensland, in days into an illness with manifestations of fever (38.1°C), February 2003. She was febrile (38.5°C) and reported headache, and cough. Diagnostic tests for scrub typhus, headache, nausea, and abdominal pain. She had no eschar malaria and leptospirosis were initiated but he was given or rash. She was initially thought to have a viral illness; no specific antimicrobial therapy. Two days later, he however, after 3 days she was still febrile (39.0°C), and the seemed improved, and a provisional diagnosis of viral provisional diagnosis was changed to scrub typhus; a reg- upper respiratory tract infection was made. However, imen of oral doxycycline, 100 mg per day, was begun. She when he was seen on day 14, some symptoms remained was not seen by medical or nursing staff between day 3 (cough and headache), and treatment with amoxicillin was and 8 of the illness, but was afebrile and well by day 8. Her begun. He was well when examined on day 22. At no stage SFG title increased, despite a 6-month delay in obtaining was he given antirickettsial therapy. His day 5 blood sam- the convalescent-phase serum. Results of culture and PCR ple was negative for SFG/typhus group (TG) rickettsial of the blood sample taken on day 8 were positive for an antibodies, but results of PCR and culture were positive for SFG rickettsia (Table 1). a SFG rickettsia. Follow-up serum taken 14 months later was negative for rickettsial antibody (Table 1). Patient 3 A 27-year-old man sought treatment at the Darnley Patient 5 Island Health Clinic in March 2003. His temperature was A 50-year-old man was admitted to Innisfail Hospital, 37.4°C, and he reported headache, arthralgia, and cough. Innisfail, Queensland, in June 2003. He reported a 7-day He exhibited no eschar or rash. The provisional diagnosis history of fever and rigors and a 4-day history of macu- was of viral upper respiratory tract infection. He was seen lopapular rash. He also reported myalgia, arthralgia, con- again on days 3 and 4 with persisting symptoms and a sore junctivitis, swollen hands, dry cough, and constipation. An throat. On the latter visit his condition was diagnosed as eschar was found on the right side of his neck. His temper- tonsillitis, and treatment with penicillin V was begun. ature was 38.5°C and blood pressure 95/60 mm Hg. Serum Blood tests for malaria and scrub typhus were initiated. He chemistry showed elevated levels of total bilirubin (23; returned on day 29 with fever (37.6°C), cough, pharyngi- normal range 2–20 µmol/L), alkaline phosphatase (276; tis, and arthralgia. Results of serologic investigations for normal range 30–115 units/L), gamma-glutamyl transpep- Plasmodium falciparum and rickettsia (taken on day 3) tidase (199; normal range 0–70 units/L), aspartate Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 13, No. 4, April 2007 567 RESEARCH transaminase (AST) (301; normal range 5–40 units/L), ala- A widespread maculopapular/petechial rash also appeared nine transaminase (ALT) (129; normal range 5–40 over his body. High fever, severe lethargy, and myalgias units/L), and lactate dehydrogenase (LDH) (701, normal continued. On day 9, he visited his doctor in Brisbane range 100–225 units/L). Further investigation showed pro- where the examination confirmed a widespread macu- teinuria, moderate thrombocytopenia (59; normal range lopapular/petechial rash with generalized lymphadenopa- 150–400×109/L), mild neutrophilia with left shift (7.9; thy and myalgias affecting large muscle groups. A large normal range 2.0–7.5 × 109/L), and lymphopenia (0.7; nor- eschar was found on his left lower abdomen. An SFG ill- mal range 1.0–4.0 × 109/L). Examination of convalescent- ness was suspected, and treatment with doxycycline, 100 phase serum showed seroconversion to SFG rickettsia. mg twice per day, was begun His doctor reexamined him Results of rickettsial PCR and culture were positive for a on day 20, and his condition had improved. His myalgia member of the SFG (Table 1). He recovered after treatment had decreased, and the rash faded over 5 weeks. with oral doxycycline (100 mg twice per day) for 5 days. Laboratory testing on day 10 showed lymphopenia (0.8; normal range 1.0–4.0 × 109/L) and mild thrombocy- Patient 6 topenia (146; normal range 150–400 × 109/L). Liver func- A 33-year-old man from Lilydale, a small town in tion tests showed slightly elevated AST (48; normal range northeastern Tasmania, sought treatment from his general 5–40 units/L) and ALT (44, normal range 5–40 units/L) practitioner in May 2003 (day 1) after a recent fishing trip. and mildly elevated LDH (325; normal range 100–225 His symptoms included fever (38.3°C) and headache. On units/L). Rickettsial serology was negative on day 10 but day 6 the patient was improving but had developed cervi- convalescent-phase serology on day 23 showed an SFG cal lymphadenopathy. His illness was thought to be viral in seroconversion.
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