Bartonellosis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

Humans acquire it through flea or tick bites from infected dogs, cats, coyotes, foxes, and humans.[1] Once bitten the victim develops a localized infection. The first sign of infection is a raised skin papule which resolves on its own. As the illness progresses, symptoms including fatigue, headaches, memory loss, disorientation, insomnia, and loss of coordination develop. The bacteria blocks the normal immune response by suppressing the NF-κB apoptosis pathway.[2] Disease progression will be accelerated if the host is subsequently infected by an immunesuppressing virus such as Epstein Barr or XMRV and likewise, as the host's infectious load increases the immune system will be more prone to infection due to the weakening response.

In mammals, each Bartonella species is highly adapted to its reservoir host as the result of intracellular parasitism and can persist in the bloodstream of the host. Intraerythrocytic parasitism is only observed in the acute phase of Carrión´s disease. Bartonella also have a tropism for endothelial cells, observed in the chronic phase of Carrión´s disease (also known as Verruga Peruana) and bacillary angiomatosis. Pathological response can vary with the immune status of the host. Infection with Bartonella henselae can result in a focal suppurative reaction (CSD in immunocompetent patients), a multifocal angioproliferative response (bacillary angiomatosis in immunocompromised patients), endocarditis or meningitis.

Some of the diseases can resolve spontaneously without treatment.[3]

Carrion's Disease

The clinical symptoms of Carrion's disease are pleomorphic and some patients from endemic areas may be asymptomatic.

The two classical clinical presentations are the acute phase and the chronic phase, corresponding to the two different host cell types invaded by the bacterium (red blood cells and endothelial cells).

  • Acute phase: (Carrion's disease) the most common findings are fever (usually sustained, but with temperature no greater than 102°F (39°C)), malaise. This phase is characterized by severe hemolytic anemia and transient immunosuppression. The case fatality ratios of untreated patients exceeded 40% but reach around 90% when opportunistic infection with Salmonella species occurs. In a recent study the attack rate was 13.8% (123 cases) and the case-fatality rate was 0.7%.
  • Chronic phase: (Verruga Peruana or Peruvian Wart) it is characterized by an eruptive phase, in which the patients develop a cutaneous rash produced by a proliferation of endothelial cells and is known as "Peruvian warts" or "verruga peruana".

The most common findings are bleeding of verrugas, fever, malaise, arthralgias, anorexia, myalgias.

Peliosis Hepatis

The condition is typically asymptomatic and is discovered following evaluation of abnormal liver function test. However, when severe it can manifest as jaundice, hepatomegaly, liver failure and haemoperitoneum.

Trench Fever

The disease is classically a five-day fever of the relapsing type, rarely with a continuous course instead. Latent period is relatively long (about two weeks). The onset of symptoms is usually sudden with high fever, severe headache, pain on moving the eyeballs, soreness of the muscles of the legs and back, and frequently hyperaesthesia of the shins. The initial fever is usually followed in a few days by a single short rise but there may be many relapses between periods without fever. The most constant symptom is pain in the legs. Recovery takes a month or more. Lethal cases are rare, but in a few cases "the persistent fever might lead to heart failure". After effects may include neurasthenia, cardiac disturbances and myalgia.

References

  1. Breitschwerdt, EB. Bartonella sp. Bacteremia in Patients with Neurological and Neurocognitive Dysfunction. JOURNAL OF CLINICAL MICROBIOLOGY. Sept. 2008. 46(9): 2856–2861
  2. Faherty, CS. Staying alive: bacterial inhibition of apoptosis during infection. Trends in Microbiology (16:4). 175.
  3. Resto-Ruiz S, Burgess A, Anderson BE (2003). "The role of the host immune response in pathogenesis of Bartonella henselae". DNA Cell Biol. 22 (6): 431–40. doi:10.1089/104454903767650694. PMID 12906736. Unknown parameter |month= ignored (help)




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