Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide

Datasheet

Coxiella burnetii

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Datasheet

Coxiella burnetii

Summary

  • Last modified
  • 19 November 2019
  • Datasheet Type(s)
  • Invasive Species
  • Preferred Scientific Name
  • Coxiella burnetii
  • Taxonomic Tree
  • Domain: Bacteria
  •   Phylum: Proteobacteria
  •     Class: Alphaproteobacteria
  •       Order: Legionellales
  •         Family: Coxiellaceae

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Pictures

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PictureTitleCaptionCopyright
Coxiella burnetii. Transmission electron micrograph showing a Gram-negative-like cell wall. Original magnification, x75,000. (From Journal of Clinical Microbiology, 36:(7):1823-1834. 1998.)
TitleHistopathology
CaptionCoxiella burnetii. Transmission electron micrograph showing a Gram-negative-like cell wall. Original magnification, x75,000. (From Journal of Clinical Microbiology, 36:(7):1823-1834. 1998.)
CopyrightDidier Raoult/Universite de la Mediterranee, France
Coxiella burnetii. Transmission electron micrograph showing a Gram-negative-like cell wall. Original magnification, x75,000. (From Journal of Clinical Microbiology, 36:(7):1823-1834. 1998.)
HistopathologyCoxiella burnetii. Transmission electron micrograph showing a Gram-negative-like cell wall. Original magnification, x75,000. (From Journal of Clinical Microbiology, 36:(7):1823-1834. 1998.)Didier Raoult/Universite de la Mediterranee, France

Identity

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Preferred Scientific Name

  • Coxiella burnetii (Derrick) Philip

Taxonomic Tree

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  • Domain: Bacteria
  •     Phylum: Proteobacteria
  •         Class: Alphaproteobacteria
  •             Order: Legionellales
  •                 Family: Coxiellaceae
  •                     Genus: Coxiella
  •                         Species: Coxiella burnetii

Diseases Table

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Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Last updated: 10 Jan 2020
Continent/Country/Region Distribution Last Reported Origin First Reported Invasive Reference Notes

Africa

BotswanaAbsent, No presence record(s)
BurundiAbsent, No presence record(s)
Cabo VerdeAbsent, No presence record(s)
CameroonAbsent, No presence record(s)
Central African RepublicAbsent, No presence record(s)
Congo, Democratic Republic of theAbsent, No presence record(s)
Côte d'IvoireAbsent, No presence record(s)
DjiboutiPresent
EgyptAbsent, No presence record(s)
EritreaAbsent, No presence record(s)
EthiopiaAbsent, No presence record(s)
GuineaAbsent, No presence record(s)
KenyaAbsent, No presence record(s)
LibyaAbsent, No presence record(s)
MadagascarAbsent, No presence record(s)
MauritiusAbsent, No presence record(s)
MoroccoAbsent, No presence record(s)
NigeriaAbsent, No presence record(s)
São Tomé and PríncipeAbsent, No presence record(s)
SeychellesAbsent, No presence record(s)
South AfricaPresent
SudanAbsent, No presence record(s)
TogoAbsent, No presence record(s)
ZambiaAbsent, No presence record(s)

Asia

AfghanistanAbsent, No presence record(s)
BhutanAbsent, No presence record(s)
GeorgiaAbsent, No presence record(s)
IndonesiaAbsent, No presence record(s)
IsraelPresent
JordanPresent
KazakhstanAbsent, No presence record(s)
KuwaitAbsent, No presence record(s)
LebanonAbsent, No presence record(s)
Malaysia
-Peninsular MalaysiaAbsent, No presence record(s)
-SabahAbsent, No presence record(s)
-SarawakAbsent, No presence record(s)
North KoreaAbsent, No presence record(s)
OmanPresent, Serological evidence and/or isolation of the agent
PhilippinesAbsent, No presence record(s)
QatarAbsent, No presence record(s)
SingaporeAbsent, No presence record(s)
South KoreaAbsent, No presence record(s)
Sri LankaAbsent, No presence record(s)
SyriaAbsent, No presence record(s)
TaiwanAbsent, No presence record(s)
ThailandAbsent, No presence record(s)
TurkmenistanAbsent, No presence record(s)
United Arab EmiratesAbsent, No presence record(s)
UzbekistanAbsent, No presence record(s)

Europe

AndorraPresent, Serological evidence and/or isolation of the agent
BelarusAbsent, No presence record(s)
Bosnia and HerzegovinaPresent
BulgariaPresent
CroatiaPresent
DenmarkPresentCAB Abstracts Data Mining
EstoniaAbsent, No presence record(s)
FinlandAbsent, No presence record(s)
FrancePresent
GermanyPresent
IcelandAbsent, No presence record(s)
IrelandPresentCAB Abstracts Data Mining
JerseyAbsent, No presence record(s)
LatviaAbsent, No presence record(s)
LiechtensteinAbsent, No presence record(s)
LithuaniaAbsent, No presence record(s)
LuxembourgAbsent, No presence record(s)
MaltaAbsent, No presence record(s)
NetherlandsPresent
North MacedoniaPresent
NorwayAbsent, No presence record(s)
PolandPresent
PortugalPresent
RomaniaAbsent, No presence record(s)
RussiaAbsent, No presence record(s)
SlovakiaPresent
SloveniaPresentCAB Abstracts Data Mining
SwedenPresent, Serological evidence and/or isolation of the agent
SwitzerlandPresent
UkraineAbsent, No presence record(s)
United KingdomPresent
-Northern IrelandPresentCAB Abstracts Data Mining

North America

BarbadosAbsent, No presence record(s)
BelizeAbsent, No presence record(s)
BermudaAbsent, No presence record(s)
British Virgin IslandsAbsent, No presence record(s)
CanadaPresent
Cayman IslandsAbsent, No presence record(s)
Costa RicaAbsent, No presence record(s)
CubaAbsent, No presence record(s)
CuraçaoAbsent, No presence record(s)
DominicaAbsent, No presence record(s)
Dominican RepublicAbsent, No presence record(s)
El SalvadorAbsent, No presence record(s)
GuadeloupeAbsent, No presence record(s)
GuatemalaAbsent, No presence record(s)
HaitiAbsent, No presence record(s)
HondurasAbsent, No presence record(s)
JamaicaAbsent, No presence record(s)
MartiniqueAbsent, No presence record(s)
MexicoAbsent, No presence record(s)
NicaraguaAbsent, No presence record(s)
PanamaAbsent, No presence record(s)
Saint Kitts and NevisAbsent, No presence record(s)
Saint Vincent and the GrenadinesAbsent, No presence record(s)
Trinidad and TobagoAbsent, No presence record(s)
United StatesPresent

Oceania

AustraliaPresent, Serological evidence and/or isolation of the agent
French PolynesiaAbsent, No presence record(s)
New CaledoniaAbsent, No presence record(s)
New ZealandAbsent, No presence record(s)
SamoaAbsent, No presence record(s)
VanuatuAbsent, No presence record(s)

South America

BoliviaAbsent, No presence record(s)
ChilePresent, Serological evidence and/or isolation of the agent
ColombiaPresent, Serological evidence and/or isolation of the agent
EcuadorAbsent, No presence record(s)
Falkland IslandsAbsent, No presence record(s)
GuyanaAbsent, No presence record(s)
ParaguayAbsent, No presence record(s)
PeruAbsent, No presence record(s)
UruguayPresent
VenezuelaAbsent, No presence record(s)

Pathogen Characteristics

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Morphology


Coxiellaburnetii, the aetiological agent of Q fever, is an obligate intracellular, Gram-negative rickettsia (0.2 to 0.4 µm wide, 0.4 to 1 µm long) that replicates within the phagolysosome of the eukaryotic phagocyte. It is highly infective to both humans and livestock. In humans, the disease manifests as an acute flu-like illness. C.burnetii is able to survive outside the host for a long time. The clinical specimens or laboratory cultures of C. burnetii are stained best by Gimenez stain (Gimenez, 1964) and stain poorly with Gram’s stain.


Genetic variability, virulence and resistance


The genome size is highly variable among different C. burnetii strains, ranging from 1.5 to 2.4 Mb. It is 2.1 Mb in C. burnetii Nine Mile strain (Willems et al., 1998). A physical macrorestriction map of C.burnetii Nine Mile Phase I has also been constructed, and 25 DNA fragments distinguished by pulsed-field gel electrophoresis (PFGE) after restriction of total DNA with NotI. (Willems et al., 1996; Willems et al., 1998).

Eleven chromosomal genes of C. burnetii that have been cloned and expressed in E. coli include gltA, the citrate synthase gene; sodB, the superoxide dismutase gene; htpA, the 14-kDa heat shock protein gene; htpB, the 62-kDa heat shock protein gene; omp, a 27-kDa surface antigen gene; pyrB, the aspartate carbamoyl transferase gene; qrsA, a sensor protein gene; dnaJ, a heat shock protein gene; mucZ, the capsule induction protein gene; serS, the seryl-tRNA synthase gene; and algC, the phosphomannomutase gene.

The C. burnetii genome comprises facultatively a 36- to 42-kb plasmid, whose function remains undetermined. G+C content is 43%. C.burnetii displays antigenic variations similar to the smooth-rough variation in the family, Enterobacteriaceae. Phase variation is related mainly to mutational variation in the lipopolysaccharide (LPS) (Hackstadt et al., 1985; Hackstadt, 1988). Phase I is the natural phase found in infected animals, arthropods or humans. It is highly infectious and corresponds to smooth LPS. In contrast, Phase II is not very infectious and is obtained only in laboratories after serial passages in cell cultures or embryonated egg cultures. It corresponds to rough LPS. Compared with Phase I, Phase II displays a truncated LPS and lacks some protein cell surface determinants (Amano and Williams, 1984). LPS seems to be the only antigen and immunogen differing between Phases I and II in C.burnetii.

C.burnetii expresses a low degree of genetic heterogeneity among strains by DNA-DNA hybridization (Vodkin and Williams, 1988). However, when DNA samples from 38 C. burnetii isolates were examined by restriction fragment length polymorphism (RFLP) analysis, six genomic groups (I to VI) were described (Hendrix et al., 1991). Analysis of NotI and SfiI C.burnetii DNA restriction fragments by pulsed-field gel electrophoresis (PFGE) resulted in the characterization of four different DNA fragment patterns representing isolates from genomic groups I, IV, V and VI (Heinzen et al., 1990). Genetic variability among different C. burnetii strains, as demonstrated by different RFLP-based genomic groups (Hendrix et al., 1991), specific plasmid regions (Samuel et al., 1985), and LPS variations (Hackstadt, 1986) has been tentatively related to the virulence. Genomic Groups I, II and III have been found associated with the animal, tick, or acute Q fever human isolates, referred to as ‘acute strains’; Groups IV and V associated with the human Q fever endocarditis isolates, referred to as ‘chronic strains’; whereas, Group VI isolates from the feral rodents in Dugway (Utah, USA) were of unknown pathogenicity. However, there is also data that indicates that genetic variation in isolates is more closely associated with geographical origin than with clinical presentation.

C.burnetii demonstrates a sporulation-like process conferring resistance to harsh environmental conditions (Gaburro and Campo, 1956). It survives in phagolysosomes where a low pH (pH 4.5) is necessary for its metabolism (Cottalorda et al., 1995; Cowley et al., 1992). The extracellular forms of C. burnetii resist environmental conditions such as desiccation, low or high pH, chemical products such as ammonium chloride, disinfectants such as 0.5% sodium hypochlorite, 1 % phenol, and UV radiation (Babudieri,1959; Scott and Williams, 1990). Organisms survive for at least 586 days in dried tick faeces and for three months in the moist soil of lambing pens (Stoenner et al., 1959a,b). They are very resistant to drying, and remain stable under a variety of environmental conditions. The pathogens survive for months and even years in the environment, and in biological material like dried sputum (30 days), dust (up to 120 days), dried guinea pig urine (49 days), tick faeces (586 days), milk (42 months at 4-6°C), wool (12-16 months at 4-6°C). The agents survives in milk at 62°C but does not survive after 30 min at 63°C (Enright et al., 1957). They are inactivated by ether, chloroform, gamma irradiation, and by heating at 130°C for 60 min.

Disease(s) associated with this pathogen is/are on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's Handistatus database on disease occurrence. Please see the AHPC library for further information from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.

Vectors and Intermediate Hosts

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VectorSourceReferenceGroupDistribution
AmblyommaTickWidespread where hosts occur
Amblyomma americanumMINED DATA; 16/11/01 14:00:0Tick
ArgasTickWidespread where hosts occur
BoophilusTickWidespread where hosts occur
DermacentorTickWidespread where hosts occur
Dermacentor pictusMINED DATA; 16/11/01 14:00:0Tick
Euryparasitus emarginatusMiteRussian Federation
HaemaphysalisTickWidespread where hosts occur
Haemaphysalis cuspidataMINED DATA; 16/11/01 14:00:0
Haemaphysalis spinigeraMINED DATA; 16/11/01 14:00:0
Haemogamasus mandschuricusMiteRussian Federation
HyalommaTickWidespread where hosts occur
IxodesTickWidespread where hosts occur
Ixodes ricinusMINED DATA; 16/11/01 14:00:0Tick
OrnithodorosTickWidespread where hosts occur
Ornithodoros moubata moubataMINED DATA; 16/11/01 14:00:0Tick
Otobius megniniTickWidespread where hosts occur
Phlebotomus argentipesMINED DATA; 16/11/01 14:00:0
Phlebotomus papatasiMINED DATA; 16/11/01 14:00:0
RhipicephalusTickWidespread where hosts occur
Sergentomyia babu babuMINED DATA; 16/11/01 14:00:0

References

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Amano K-I; Williams JC, 1984. Chemical and immunological characterization of lipopolysaccharides from phase I and phase II Coxiella burnetii. Journal of Bacteriology, 160(3):994-1002; 44 ref.

Babudieri B, 1959. Q fever: a zoonosis. Advances in Veterinary Science, 5:81.

Cottalorda J; Jouve JL; Bollini G; Touzet P; Poujol A; Kelberine F; Raoult D, 1995. Osteoarticular infection due to Coxiella burnetii in children. Journal of Pediatric Orthopedics, 4:219-221.

Cowley R; Fernandez F; Freemantle W; Rutter D, 1992. Enzyme immunoassay for Q fever: comparison with complement fixation and immunofluorescence tests and dot immunoblotting. Journal of Clinical Microbiology, 30(9):2451-2455; 27 ref.

Enright JB; Sadler WW; Thomas RC, 1957. Thermal inactivation of Coxiella burnetii and its relation to pasteurization of milk. Washington, DC, USA: US Government Printing Office. Public Health Service Monograph 47.

Gaburro D; Campo del A, 1956. Considerazioni epidemiologiche e cliniche su un’infezione da Coxiella burnetii in tre gemelle immature. Mal Infections Parsitologie, 8:384.

Gimenez DF, 1964. Staining rickettsiae in yolk sac cultures. Stain Technology, 30:135-137.

Hackstadt T, 1986. Antigenic variation in the phase I lipopolysaccharide of Coxiella burnetii isolates. Infection and Immunity, 52(1):337-340; 31 ref.

Hackstadt T, 1988. Steric hindrance of antibody binding to surface proteins of Coxiella burnetii by phase I lipopolysaccharide. Infection and Immunity, 56(4):802-807; 33 ref.

Hackstadt T; Peacock MG; Hitchcock PJ; Cole RL, 1985. Lipopolysaccharide variation in Coxiella burnetii: intrastrain heterogeneity in structure and antigenicity. Infection and Immunity, 48(2):359-365; 50 ref.

Heinzen RA; Stiegler GL; Whiting LL; Schmitt SA; Mallavia LP; Frazier ME, 1990. Use of pulsed field gel electrophoresis to differentiate Coxiella burnetii strains. Annals New York Academy of Sciences, 590:504-513.

Hendrix LR; Samuel JE; Mallavia LP, 1991. Differentiation of Coxiella burnetii isolates by analysis of restriction-endonuclease-digested DNA separated by SDS-PAGE. Journal of General Microbiology, 137(2):269-276; 19 ref.

OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.

OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.

OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.

Samuel JE; Frazier ME; Mallavia LP, 1985. Correlation of plasmid type and disease caused by Coxiella burnetii. Infection and Immunity, 49(3):775-779; 14 ref.

Scott GH; Williams JC, 1990. Susceptibility of Coxiella burnetii to chemical disinfectants. Annals of New York Academy of Sciences, 590:291-296.

Stoenner HG; Holdenreid R; Lackman DB; Orsborn JS Jr, 1959. The occurrence of Coxiella burnetii, Brucella and other pathogens among fauna of the Great Salt Lake in Utah. American Journal of Tropical Medicine and Hygiene, 8:590.

Stoenner HG; Jelison WL; Lackman DB; Brock D; Casey M, 1959. Q fever in Idaho. American Journal of Hygiene, 69:202.

Vodkin MH; Williams JC, 1988. A heat shock operon in Coxiella burnetii produces a major antigen homologous to a protein in both mycobacteria and Escherichia coli.. Journal of Bacteriology, 170(3):1227-1234; 37 ref.

Willems H; Jäger C; Baljer G, 1998. Physical and genetic map of the obligate intracellular bacterium Coxiella burnetii. Journal of Bacteriology, 180(15):3816-3822; 60 ref.

Willems H; Thiele D; Burger C; Ritter M; Oswald W; Krauss H, 1996. Molecular biology of Coxiella burnetii. In: Kazar J, Toman R, eds. Rickettsiae and Rickettsial Diseases. Bratislava, Slovakia: Slovak Academy of Sciences, 363-378.

Distribution References

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004)., Paris, France: Office International des Epizooties.

Distribution Maps

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