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Rickettsiae and related rickettsia-like bacteria such as Ehrlichia , Anaplasma , and Coxiella burnetii bacteria are an unusual type of bacteria that cause several similar diseases, including the following:. Rocky Mountain spotted fever. Epidemic typhus. Q fever. These bacteria differ from most other bacteria in that they can live and multiply only inside the cells of another organism host and cannot survive on their own in the environment.

Many species of these bacteria live in small animals such as rats and mice , which are called the host. Cattle, sheep, or goats are the hosts for Coxiella burnetii , which causes Q fever. Humans are the usual host for Rickettsia prowazekii , which causes epidemic typhus.

The Challenge Of Rickettsial Pathogens

Host animals may or may not be ill from the infection. Rickettsiae and rickettsia-like bacteria are usually spread to people through the bites of ticks, mites, fleas, or lice that previously fed on an infected animal. Ticks, mites, fleas, and lice are called vectors because they spread transmit organisms that cause disease from one host to another. Q fever, caused by Coxiella burnetii , can be spread through the air or in contaminated food and water and do not require a vector. Some of these bacteria and the diseases they cause occur worldwide.

Others occur only in certain geographic regions. Some of these bacteria infect the cells lining small blood vessels, causing the blood vessels to become inflamed or blocked or to bleed into the surrounding tissue. Other bacteria Ehrlichia and Anaplasma enter white blood cells.

Rickettsia pathogenesis

Infecting Organism. Areas Where Infection Occurs. Epidemic typhus lice-borne typhus. Brill-Zinsser disease a recurrence of epidemic typhus, sometimes years after the first infection. Rickettsia prowazekii , transmitted by lice or by unknown methods when the hosts are flying squirrels. Throughout the world uncommon in the United States, but occasionally occurs in people who have had contact with flying squirrels.

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About 7 to 14 days after the bacteria enter the body, symptoms begin suddenly, with fever, headache, and extreme fatigue prostration. A rash appears on the 4th to 6th day. Untreated, the infection may be fatal, especially in people older than About 8 to 16 days after the bacteria enter the body, symptoms begin and are similar to those of epidemic typhus but are less severe. Scrub typhus. Orientia tsutsugamushi formerly, Rickettsia tsutsugamushi , transmitted by mite larvae chiggers.

About 6 to 21 days after the bacteria enter the body, symptoms begin suddenly, with fever, chills, headache, and swollen lymph nodes. A black scab may develop at the site of the chigger bite. A rash appears on the 5th to 8th day.


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Spotted fever. African tick-bite fever. About 4 to 10 days after the bacteria enter the body, symptoms begin. A black scab usually develops at the site of the tick bite. Mediterranean spotted fever boutonneuse fever. About 5 to 7 days after the bacteria enter the body, symptoms begin. A black scab may develop at the site of the tick bite. North Asian tick-borne rickettsiosis. Queensland tick typhus. Rickettsia parkeri rickettsiosis.

About 2 to 10 days after the bacteria enter the body, symptoms begin. A small black scab appears at the site of the mite bite. It develops into a small sore that leaves a scar when it heals. About 1 week later, fever, headache, muscle pains, and a widespread rash develop. Ehrlichiosis and anaplasmosis. About 12 days after a tick bite, symptoms usually begin. A rash may develop on the torso, arms, and legs. Coxiella burnetii , transmitted by inhaling infected airborne droplets containing the bacteria or by consuming contaminated raw milk.

About 9 to 28 days after bacteria enter the body, symptoms begin suddenly. They include fever, severe headache, chills, extreme weakness, muscle aches, loss of appetite, sweating, an unproductive cough, chest pain, and shortness of breath caused by pneumonia , but no rash. A sore covered by a black scab eschar may form at the site of the bite. Because the rash often does not appear for several days, early rickettsial infection is often mistaken for a common viral infection, such as influenza.

People may have swollen lymph nodes. As the infection progresses, people typically experience confusion and severe weakness—often with cough, difficulty breathing, and sometimes vomiting. When the infection is advanced, gangrene may develop, the liver or spleen may enlarge, the kidneys may malfunction, and blood pressure may fall dangerously low causing shock.

Death can result. Because rickettsiae and rickettsia-like bacteria are transmitted by ticks, mites, fleas, and lice, doctors ask people. Being bitten is a helpful clue—particularly in geographic areas where rickettsial or a related infection is common. However, many people do not recall such a bite.

If doctors suspect Q fever, they may also ask whether people were at or near a farm because cattle, sheep, and goats are the host for the bacteria that cause this infection. A physical examination is done to determine which parts of the body are affected and what the rash looks like. Doctors also look for an eschar that people may not have noticed and for swollen lymph nodes.

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Testing is usually needed to confirm the diagnosis. Often, doctors cannot confirm an infection with rickettsiae or rickettsia-like bacteria quickly because these bacteria cannot be identified using commonly available laboratory tests. Special blood tests for these bacteria are not routinely available and take so long to process that people usually need to be treated before test results are available. Doctors base their decision to treat on the person's symptoms and the likelihood of possible exposure. In immunofluorescence assays, foreign substances produced by the bacteria antigens are labeled with a fluorescent dye.

Thus, although many of these infections are thought to cause tissue damage by direct bacteria-mediated cell injury, an open question is to what degree host inflammation and immunity contribute to overall disease pathogenesis. Although much study of the histopathology of both HME and RMSF has been conducted, little correlation of these findings with potential pathogenetic mechanisms has been attempted; for example, the occurrence of hemophagocytosis in both entities is well described [ 5 , 13 — 15 ], but the potential importance of this feature in immunopathologic reactions is not well addressed.

Tissue injury seen in RMSF is most likely a combination of direct rickettsia-mediated endothelial cell injury, manifested by vasculitis and increased vascular permeability [ 16 , 17 ], as well as by immune-mediated injury, demonstrated here by hemophagocytosis. Animal studies have shown that in balance, the potentially detrimental effects of Th1 immunity, local macrophage activation, and generation of cytotoxicity associated with CD8 or NK cells in rickettsial infection are beneficial to the host, owing to effective pathogen control [ 16 , 18 ].

However, this process could also cause bystander tissue injury as suggested by the detection of hemophagocytosis [ 17 , 19 ]. Given the differences in bacterial load between RMSF and HME, tissue damage in HME is more likely a result of poorly controlled macrophage activation and release of effector molecules, including nitric oxide and reactive oxygen species [ 3 , 17 , 20 ].

The excessive cytokine production induced with E. As demonstrated in this study, hemophagocytosis and evidence of inflammation-mediated tissue injury is observed in HME and RMSF to an extent greater than that in the selected infectious and non-infectious control cases. This further indicates that CD8 cells and possibly cellular cytotoxicity likely play a significant role in HME pathogenesis.


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  • Whether a similar role for CD8 cells exists for RMSF, as suggested by studies in animal models, could not be adequately assessed here and needs further investigation. Unlike the situation for the vasculotropic rickettsioses, evidence for direct ehrlichia-mediated cell injury in vivo has not been found, but the frequent presence of hemophagocytosis implicates inflammatory- and immune-mediated injury as possible major contributors. The relative lack of infected cells in HME compared to RMSF, despite similar degrees of hemophagocytosis, and the marked CD8 T cell expansion that could drive such responses, suggests that Ehrlichia chaffeensis infection often leads to macrophage activation, generation of inflammatory effectors, mediators, and cytokines, non-specific phagocytic activity, and consequent immune-mediated injury [ 22 ].

    Hematologic data were not available for these cases, which in general reflect the more severe end of the disease spectrum. However, it is well recognized that patients with HME and RMSF, especially when severe, demonstrate leukopenia, thrombocytopenia, and anemia, although the disease process and degree of cytopenias differ from those observed in severe acquired or hereditary hemophagocytic syndromes [ 23 ].

    The precise mechanism by which E. Potential pitfalls of this study include the biased selection of patients that represent the most severe spectrum of HME or RMSF — fatal cases — and the relatively small number of cases examined. Both of these situations result from the relatively rare access to pathologically-examined cases of both HME and RMSF, limiting the power of this study.

    Similarly, the small number of infectious controls could equally under-represent immunopathologic responses among these entities. Despite these limitations, the small number of cases allowed at least partial study, and provides evidence of rickettsial immunopathogenicity in humans that should provide impetus for further study in both HME and RMSF, even among mild to moderately severe infections. HME and RMSF are both caused by related obligate intracellular bacteria, and both induce hemophagocytosis in lymph nodes to a degree greater than a cohort of randomly selected normal and infectious disease controls.

    Animal models clearly show a direct role for pathogen-induced cytotoxic injury in vivo with R. However, the relatively low quantities of E. Much more study will be required to dissect the immunopathogenesis of Ehrlichia infections, and the studies here provide additional evidence that infection may involve cytotoxic T cell activation and proliferation that could drive excessive macrophage activation as a mechanism for generating tissue-damaging effectors in HME.

    Int J Syst Evol Microbiol. Clin Microbiol Rev. Ann N Y Acad Sci. Med Clin North Am. Discovery and diagnosis of emerging tick-borne infections and the critical role of the pathologist. Arch Pathol Lab Med. Hum Pathol. J Infect Dis. Martin ME, Caspersen K, Dumler JS: Immunopathology and ehrlichial propagation are regulated by interferon-gamma and interleukin in a murine model of human granulocytic ehrlichiosis.

    Am J Pathol. Clin Diagn Lab Immunol. Comp Med. J Clin Microbiol. Am J Clin Pathol. Am J Hematol. Case report and pathological correlation. Hematologic and lymphoreticular observations. Feng HM, Walker DH: Mechanisms of intracellular killing of Rickettsia conorii in infected human endothelial cells, hepatocytes, and macrophages. Infect Immun.

    Overview of Rickettsial Infections

    New perspectives and opportunities offered by unusual intracellular parasites. Microbes Infect. Fisman DN: Hemophagocytic syndromes and infection. Emerg Infect Dis. J Immunol. Mosser DM: The many faces of macrophage activation. J Leukoc Biol. Grom AA: Natural killer cell dysfunction: A common pathway in systemic-onset juvenile rheumatoid arthritis, macrophage activation syndrome, and hemophagocytic lymphohistiocytosis?. Arthritis Rheum. Download references. The authors would like to thank the immunohistochemistry laboratory at The Johns Hopkins Hospital for assistance in preparation of the immunophenotyping stains.

    Correspondence to J Stephen Dumler. KD participated in the design of the study, examination of specimens, and analysis of data and drafted the manuscript.