Seroepidemiology of Q fever in Nova Scotia and Prince Edward Island

1984 ◽  
Vol 30 (1) ◽  
pp. 129-134 ◽  
Author(s):  
Thomas J. Marrie ◽  
John Van Buren ◽  
Ruth S. Faulkner ◽  
E. Vanora Haldane ◽  
James C. Williams ◽  
...  

The prevalence of Coxiella burnetti infection (Q fever) was determined among Nova Scotia (N.S.) and Prince Edward Island (P.E.I.) blood donors by using the complement fixation and microimmunofluorescence (IF) test. The complement fixation and IF antibody tests measured antibody prevalence for the phase II or phase I and II antigens, respectively. Complement-fixing antibodies to phase II antigen were detected in 4.1% of 997 N.S. and 5.0% of 219 P.E.I. blood donors. Anti-phase II antibodies were detected by microimmunofluorescence in 11.8 and 14.6% of the blood donors in the two provinces, respectively. Anti-phase I antibodies were detected among 2.8% of the N.S. blood donors and 6.3% of the P.E.I. blood donors. Comparison of rates of anti-phase II IF by counties in N.S. revealed that there was at least one county where infection by C. burnetti is hyperendemic. Rates of antibody prevalence were similar in all three areas of P.E.I. examined. We conclude that "Q fever" is endemic in N.S. and P.E.I. and that the microimmunofluorescence test is more suitable than the complement fixation test for seroepidemiologic studies.

1988 ◽  
Vol 34 (9) ◽  
pp. 1043-1045 ◽  
Author(s):  
Thomas J. Marrie

A seroepidemiological survey, using an indirect immunofluorescence test, was carried out on serum samples obtained from New Brunswick and Manitoba blood donors during 1986. The antigens were Coxiella burnetii phase I and phase II from strain Nine Mile. Eighty of the 503 (15.9%) Manitoba blood donors had a phase II antibody titer of ≥ 1:8, while 41 (4.2%) of the 966 New Brunswick blood donors had such antibodies. We have recently diagnosed three cases of Q fever in New Brunswick but none have been diagnosed in Manitoba. Our data suggest that Q fever may be increasing in New Brunswick and repeated seroepidemiological studies are indicated. It is likely that undetected cases of Q fever are occurring in Manitoba.


Author(s):  
Paulo Sérgio Gonçalves da Costa ◽  
Marco Emilio Brigatte ◽  
Dirceu Bartolomeu Greco

Q fever has been considered non-existing in Brazil where reports of clinical cases still cannot be found. This case-series of 16 patients is a result of a systematic search for such illness by means of clinical and serologic criteria. Serologic testing was performed by the indirect microimmunofluorescence technique using phase I/II C. burnetii antigens. Influenza-like syndrome was the most frequent clinical form (eight cases - 50%), followed by pneumonia, FUO (fever of unknown origin), mono-like syndrome (two cases - 12.5% each), lymphadenitis (one case - 6.3%) and spondylodiscitis associated with osteomyelitis (one case - 6.3%). The ages varied from four to 67 years old with a median of 43.5. All but one patient had positive serologic tests for phase II IgG whether or not associated with IgM positivity compatible with acute infection. One patient had both phase I and phase II IgG antibodies compatible with chronic Q fever. Seroconvertion was detected in 10 patients. Despite the known limitations of serologic diagnosis, the cases here reported should encourage Brazilian doctors to include Q fever as an indigenous cause of febrile illness.


1996 ◽  
Vol 7 (1) ◽  
pp. 45-48
Author(s):  
TJ Marrie ◽  
Linda Yates

Western immunoblotting was used to compare the immune response toCoxiella burnetiiphase I and phase II antigens of humans with acute and chronic Q fever with that of infected cats, rabbits, cows and raccoons. The cats, rabbits, cows and raccoons had an immunoblot profile similar to that of the human with chronic Q fever.


1989 ◽  
Vol 102 (1) ◽  
pp. 119-127 ◽  
Author(s):  
Thomas J. Marrie ◽  
Donald Langille ◽  
Vasilia Papukna ◽  
Linda Yates

SUMMARYWe describe an outbreak of Q fever affecting 16 of 32 employees at a truck repair plant. None of the cases were exposed to cattle, sheep or goats. the traditional reservoirs of Q fever. The cases did not work, live on, or visit farms or attend livestock auctions. One of the employees had a cat which gave birth to kittens 2 weeks prior to the first case of Q fever in the plant. The cat owner fed the kittens every day before coming to work as the cat would not let the kittens suckle. Serum from the cat had high antibody titres to phase I and phase IICoxiella burnetiiantigens. The attack rate among the employees where the cat owner worked. 13 of 19 (68%), was higher than that of employees elsewhere, 3 of 13 (28%) [P <0·01]. The cat owner's wife and son also developed Q fever. None of the family members of the other employees with Q fever was so affected.We conclude that this outbreak of Q fever probably resulted from exposure to the contaminated clothing of the cat owner.


2008 ◽  
Vol 137 (5) ◽  
pp. 744-751 ◽  
Author(s):  
D. WEBSTER ◽  
D. HAASE ◽  
T. J. MARRIE ◽  
N. CAMPBELL ◽  
J. PETTIPAS ◽  
...  

SUMMARYIn Atlantic Canada, the traditional risk factor for acquisition of Q fever infection has been exposure to infected parturient cats or newborn kittens. In this study we describe the first case of Q fever in Nova Scotia acquired as a result of direct exposure to sheep. A serosurvey of the associated flock was undertaken using an indirect immunofluorescence assay (IFA) testing for antibodies to phase I and phase IICoxiella burnetiiantigens. This serosurvey revealed that 23 of 46 sheep (50%) were seropositive for the phase II antibody. Four of these sheep had titres of 1:64 including three nursing ewes, one of which had delivered two lambs that died shortly after delivery. Only one ewe had phase I antibodies but had the study's highest phase II antibody titre (1:128). Molecular studies using polymerase chain reaction (PCR) failed to detectC. burnetiiDNA in any of the milk specimens.


2015 ◽  
Vol 179 (1-2) ◽  
pp. 102-108 ◽  
Author(s):  
Laura Lucchese ◽  
Katia Capello ◽  
Antonio Barberio ◽  
Federica Zuliani ◽  
Arjan Stegeman ◽  
...  
Keyword(s):  
Phase I ◽  
Phase Ii ◽  

2012 ◽  
Vol 19 (10) ◽  
pp. 1661-1666 ◽  
Author(s):  
C. C. H. Wielders ◽  
L. M. Kampschreur ◽  
P. M. Schneeberger ◽  
M. M. Jager ◽  
A. I. M. Hoepelman ◽  
...  

ABSTRACTLittle is known about the effect of timing of antibiotic treatment on development of IgG antibodies following acute Q fever. We studied IgG antibody responses in symptomatic patients diagnosed either before or during development of the serologic response toCoxiella burnetii. Between 15 and 31 May 2009, 186 patients presented with acute Q fever, of which 181 were included in this retrospective study: 91 early-diagnosed (ED) acute Q fever patients, defined as negative IgM phase II enzyme-linked immunosorbent assay (ELISA) and positive PCR, and 90 late-diagnosed (LD) acute Q fever patients, defined as positive/dubious IgM phase II ELISA and positive immunofluorescence assay (IFA). Follow-up serology at 3, 6, and 12 months was performed using IFA (IgG phase I and II). High IgG antibody titers were defined as IgG phase II titers of ≥1:1,024 together with IgG phase I titers of ≥1:256. At 12 months, 28.6% of ED patients and 19.5% of LD patients had high IgG antibody titers (P= 0.17). No statistically significant differences were found in frequencies of IgG phase I and IgG phase II antibody titers at all follow-up appointments for adequately and inadequately treated patients overall, as well as for ED and LD patients analyzed separately. Additionally, no significant difference was found in frequencies of high antibody titers and between early (treatment started within 7 days after seeking medical attention) and late timing of treatment. This study indicates that early diagnosis and antibiotic treatment of acute Q fever do not prohibit development of the IgG antibody response.


2019 ◽  
Author(s):  
Shengdong Luo ◽  
Zemin He ◽  
Zhihui Sun ◽  
Yonghui Yu ◽  
Yongqiang Jiang ◽  
...  

AbstractCoxiella burnetii is a Gram-negative, facultative intracellular microorganism that can cause acute or chronic Q fever in human. It was recognized as an obligate intracellular organism until the revolutionary design of an axenic cystine culture medium (ACCM). Present axenic culture of C. burnetii strictly requires a hypoxic condition (<10% oxygen). Here we investigated the normoxic growth of C. burnetii strains in ACCM-2 with or without tryptophan supplementation. Three C. burnetii strains - Henzerling phase I, Nine Mile phase II and a Nine Mile phase II transformant, were included. The transformant contains a pMMGK plasmid that is composed of a RSF1010 ori, a repABC operon, an eGFP gene and a kanamycin resistance cassette. We found that, under normoxia if staring from an appropriate concentration of fresh age inocula, Nine Mile phase II can grow significantly in ACCM-2 with tryptophan, while the transformant can grow robustly in ACCM-2 with or without tryptophan. In contrast, long-term frozen stocks of phase II and its transformant, and Henzerling phase I of different ages had no growth capability under normoxia under any circumstances. Furthermore, frozen stocks of the transformant consistently caused large splenomegaly in SCID mice, while wild type Nine Mile phase II induced a lesser extent of splenomegaly. Taken together, our data show that normoxic cultivation of phase II C. burnetii can be achieved under certain conditions. Our data suggests that tryptophan and an unknown temperature sensitive signal are involved in the expression of genes for normoxic growth regulated by quorum sensing in C. burnetii.


1980 ◽  
Vol 26 (7) ◽  
pp. 819-826 ◽  
Author(s):  
Oswald G. Baca ◽  
Irene L. Martinez ◽  
Adam S. Aragón ◽  
David Klassen

A lipopolysaccharide (LPS) was isolated by hot phenol–water extraction from phase II Coxiella burnetii. The LPS was isolated from organisms that had a history of 95 serial yolk sac passages and others that were cloned. The chemical composition of the LPS was partially determined and compared with that of LPS previously isolated from phase I organisms. Most of the sugars present in phase I LPS were detected in phase II LPS; however, there were some quantitative and qualitative differences. The fatty acid profiles of phase I and II LPS were identical. The amount of LPS extracted from phase II organisms was about [Formula: see text] the amount extracted from phase I C. burnetii. Limulus lysate gelation was observed with subnanogram amounts of both phase I and II LPS. In complement fixation tests, both LPSs reacted only with antisera containing antibodies versus phase I antigen. Ouchterlony immunodiffusion tests demonstrated immunological identity of the two LPSs.


1999 ◽  
Vol 6 (2) ◽  
pp. 173-177 ◽  
Author(s):  
Pierre-Edouard Fournier ◽  
Didier Raoult

ABSTRACT Diagnosis of acute Q fever is usually confirmed by serology, on the basis of anti-phase II antigen immunoglobulin M (IgM) titers of ≥1:50 and IgG titers of ≥1:200. Phase I antibodies, especially IgG and IgA, are predominant in chronic forms of the disease. However, between January 1982 and June 1998, we observed anti-phase II antigen IgA titers of ≥1:200 as the sole or main antibody response in 10 of 1,034 (0.96%) patients with acute Q fever for whom information was available. In order to determine whether specific epidemiological or clinical factors were associated with these serological profiles, we conducted a retrospective case-control study that included completion of a standardized questionnaire, which was given to 40 matched controls who also suffered from acute Q fever. The mean age of patients with elevated phase II IgA titers was significantly higher than that usually observed for patients with acute Q fever (P = 0.026); the patients were also more likely than controls to live in rural areas (P = 0.026) and to have increased levels of transaminase in blood (P = 0.03). Elevated IgA titers are usually associated with chronic Q fever and are directed mainly at phase I antigens. Although the significance of our findings is unexplained, we herein emphasize the fact that IgA antibodies are not specific for chronic forms of Q fever and that they may occasionally be observed in patients with acute disease. Moreover, as such antibody profiles may not be determined by most laboratories, which test only for total antibody titers to phase I and II antigens, the three isotype-specific Ig titers should be determined as the first step in diagnosing Q fever.


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