| Bartonella | |
|---|---|
| Scientific classification | |
| Kingdom: | Bacteria |
| Phylum: | Proteobacteria |
| Class: | Alpha Proteobacteria |
| Order: | Rhizobiales |
| Family: | Bartonellaceae |
| Genus: | Bartonella |
| Species: | quintana |
Bartonella quintana, originally known as Rochalimaea quintana,[1] and "Rickettsia quintana",[2] is a microorganism that is transmitted by the human body louse.[3] This microorganism is the caustative agent of trench fever.[3] This bacteria resulted in over 1 million soldiers in Europe during World War I being infected with Trench Fever.[4]
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Bartonella quintana has an estimated genome size of 1,700 to 2,174 kb.[5]
Bartonella quintana is a fastidious aerobic Gram-negative (bacillus). The infection caused by this microorganism, trench fever, was first documented in soldiers during World War I, but has now been seen Europre, Asia and North Africa. It's primary vector is known to be "Pediculus humanus" variety corporis, also known as the human body louse.[6] It was first isolated in axenic culture by J.W. Vinson in 1960, from a patient in Mexico City. He then followed Koch's postulates, infecting volunteers with the bacteria, showing consistent symptoms and clinical manifestations of Trench Fever. The media best for growing this bacteria are blood-enriched media in an atmosphere containing 5% carbon dioxide.[2]
Humans are the only known animal host for this bacteria in vivo. The bacteria infects endothelial cells and can infect erythrocytes by binding and entering with a large vacuole. Once inside they begin to proliferate and cause nuclear atypia(this is known as intraerythrocytic B.quintana colonization).[7] This leads to apoptosis being suppressed, pro-inflammatory cytokines are released and vascular proliferation increases. All of these processes result in patients possessing systemic symptoms (chills, fever, diaphoresis), bacteremia and lymphatic enlargement. A major role in B.quintana infection is it's lipopolysaccharide (LPS) covering which is an antagonist of the Toll-like receptor 4 (TLR-4).[8] The reason why this infection might persist is because this organism also results in monocytes over-producing interleukin-10 (IL-10), thus weakening the immune response. B.quintana also induces lesions seen in bacillary angiomatosis that protrude into vascular lumina, often occluding blood flow. The enhanced growth of these cells is believed to be due to the secretion of angiogenic factors, thus inducing neovascularization. Release of a icosahedral particle, 40 nm in length, has been detected in cultures of quintana's close relative, henselae. This particle contains a 14-kb linear DNA segment, however it's function in Bartonella pathophysiology is still unknown.[9] In Trench Fever or B.quintana-induced endocarditis patients, Bacillary Angiomatosis lesions are also seen. Notably, endocarditis is a new manifestation of the infection, not seen in WWI troops.
Bartonella quintana infection has subsequently been seen in every continent except Antartica. Local infections have been associated with risk factors such as poverty, alcoholism and homelessness. Serological evidence of B.quintana infection showed that of hospitalized homeless patients, 16% were infected, as opposed to 1.8% of non-hospitalized homeless persons, and 0% blood donors at large.[10] Lice have been demonstrated, as of recently, to be the key componetent in trasmitting B.quintana, as several epidemiological studies have demonstrated.[11][12] This has been attributed to living in unsanitary conditions and crowded areas, where there is the increased risk of coming into contact with other individuals carrying B. quintana and ectoparasites (body louse). Also noteworthy, the increasing migration worldwide may also play a role in spreading Trench Fever, from area's where it is endemic to susceptible populations in urban areas. Recent concern is the possibility of the emergence of new strains of B. quintana through horizontal gene transfer, which could result in the acquisition of other virulence factors. This is the theory for the recent increase in prevalence of Trench Fever that has been seen.[6]
The clinical manifestations of B.quintana infection are highly variable. The incubation period is now known to be 5-20 days, as opposed to original thought which was 3-38 days. The infection can start out as an acute onset of a febrile episode, relapsing febrile episodes, or as a persistent typhoidal illness. Commonly seen are maculopapular rashes, conjunctivitis, headache and myalgias, with splenomegaly being less common. Most patients present with pain in the lower legs (shins), sore muscles of the legs and back, and hyperaesthesia of the shins. Rarely is B.quintana infection fatal, unless endocarditis develops and goes untreated. Weightloss, and thrombocytopenia are sometimes also seen. Recovery can take up to a month long.
To have a definite diagnosis of infection with Bartonella quintana, requires specific tests either serological, cultures, or nucleic acid amplification techniques. To differentiate between different species, immunofluorescence assays that use mouse antisera are used, as well as DNA hybridization and restriction fragment length polymorphisms, or citrate synthase gene sequencing.[13] Treatment usually consists of a 4-6 week course of doxycycline, erythromycin or azithromycin.[14][15]
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