eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Rickettsial Infection

Author: Mobeen H Rathore, MD, CPE, FAAP, FIDSA, Chief of Division of Pediatric Infectious Diseases/Immunology, Associate Chairman of Department of Pediatrics, University of Florida College of Medicine at Jacksonville; Hospital Epidemiologist and Section Chief of Infectious Disease and Immunology, Wolfson Children's Hospital; Director of University of Florida Center for HIV/AIDS Research, Education and Service (UF CARES)
Coauthor(s): Nizar F Maraqa, MD, Assistant Professor of Pediatrics, Pediatric Infectious Diseases, University of Florida at Jacksonville
Contributor Information and Disclosures

Updated: May 11, 2009

Introduction

Background

Rickettsiae comprise a group of microorganisms that phylogenetically occupy a position between bacteria and viruses. The genus Rickettsia is included in the bacterial tribe Rickettsiae, family Rickettsiaceae, and order Rickettsiales. They are obligate intracellular gram-negative coccobacillary forms that multiply within eukaryotic cells. Rickettsiae do not stain well with Gram stain, but they take on a characteristic red color when stained by the Giemsa or Gimenez stain. They have typical gram-negative cell walls and lack flagella. Their genome is very small, composed of 1-1.5 million bases.^1,2

Rickettsiae are a rather diverse collection of organisms with several differences; this prohibits their description as a single homogenous group. A general characteristic of rickettsiae is that mammals and arthropods are natural hosts. Rickettsioses are usually transmitted to humans by arthropods. Q fever, traditionally described among the rickettsial illnesses until recently, is primarily acquired by inhalation of contaminated airborne droplets.^3,4,5

The epidemiology of human diseases caused by rickettsiae is intimately related to the biology of the vector that transmits it. Rickettsial diseases widely vary in severity from self-limited mild illnesses to fulminating life-threatening infections.⁴

Rickettsial illnesses, caused by organisms within the genus of rickettsiae, are recognized and can be divided into the following 3 biogroups:^2,6

• Spotted fever biogroup (15 rickettsioses)
  • Rocky Mountain spotted fever (RMSF), caused by Rickettsia rickettsii
  • Rickettsialpox, caused by Rickettsia akari
  • Boutonneuse fever (ie, Kenya tick-bite fever, African tick typhus, Mediterranean spotted fever, Israeli spotted fever, Indian tick typhus, Marseilles fever)
• Typhus group: These are similar diseases that differ epidemiologically. The causative organisms (Rickettsia prowazekii and Rickettsia typhi) are similar to those of the spotted fever group but are antigenically distinct.
  • Louse-borne (epidemic) typhus
  • Brill-Zinsser disease (ie, relapsing louse-borne typhus)
  • Murine (endemic or flea-borne) typhus
• Scrub typhus biogroup (Tsutsugamushi disease): The rickettsial agents of scrub typhus have a single taxonomic name: Orientia tsutsugamushi. However, these organisms represent a heterogeneous group that strikingly differs from Rickettsial species of the spotted fever and typhus groups. The 3 major serotypes are Karp, Gilliam, and Kato.
• Other rickettsioses and closely related illnesses
  • New or reemerging rickettsioses have been described in the last few decades, including tickborne lymphadenopathy (TIBOLA) and Dermacentor -borne-necrosis-eschar-lymphadenopathy (DEBONEL) related to Rickettsia slovaca infection, as well as lymphangitis-associated rickettsiosis attributed to Rickettsia sibricia infection.¹
  • Ehrlichia organisms (the cause of human monocytic ehrlichiosis and Ehrlichia ewingii infection), Anaplasma phagocytophilum (the cause of human granulocytic anaplasmosis), and Bartonella species (the cause of Catscratch disease, relapsing fever, and Trench fever) are organisms related to the rickettsiae. They are discussed in separate articles.
  • Q fever is a disease caused by Coxiella burnetii, which has recently been removed from the Rickettsiales.⁵ The disease is described here for comparison with other rickettsioses.
• The environmental stability, small size, aerosol transmission, persistence in infected hosts, low infectious dose and high associated morbidity and mortality have made pathogenic rickettsiae desirable bioterrorism agents. In fact, R prowazekii and C burnetii have been weaponized. However, developing rickettsial pathogens as biological weapons has many drawbacks, such as the lack of direct host-to-host transmission and availability of therapeutic countermeasures against them.⁷

Pathophysiology

Rickettsiae microorganisms appear to exert their pathologic effects by adhering to and then invading the endothelial lining of the vasculature within the various organs affected. The adhesins appear to be outer membrane proteins that allow the rickettsia to be phagocytosed into the host cell. Once inside, the rickettsial organisms either multiply and accumulate in large numbers before lysing the host cell (typhus group) or they escape from the cell, damaging its membrane and causing the influx of water (spotted fever group).⁴

Rickettsiae rely on the cytosol of the host cells for growth. To avoid phagocytosis within the cells, they secrete phospholipase D and hemolysin C, which disrupt the phagosomal membrane, allowing for rapid escape.

The most important pathophysiologic effect is increased vascular permeability with consequent edema, loss of blood volume, hypoalbuminemia, decreased osmotic pressure, and hypotension. On the other hand, disseminated intravascular coagulation is rare and does not seem to contribute to the pathophysiology of rickettsiae.

Studies of murine models have demonstrated that rickettsiae are cleared by cytotoxic CD8 cells and by cytokine-activated rickettsicidal nitrogen and oxygen species. In fact, antibodies do not play an important role in immunity against pathogenic rickettsia upon fist exposure. Walker provided an excellent review of this topic.¹

• RMSF: In RMSF, rickettsiae multiply within the endothelial cells of small blood vessels and then gain access to the bloodstream after skin inoculation. Focal areas of endothelial proliferation and perivascular mononuclear cell infiltration cause leakage of intravascular fluid into tissue space. These vascular lesions can affect all organs; however, they most readily are found in the skin and adrenals. In the CNS and heart, a damaging host response (primarily cell-mediated) accompanies the vasculitis. The liver is usually affected with portal triaditis. Vascular wall destruction consumes platelets, causing thrombocytopenia. Multiple factors lead to hypoalbuminemia (eg, renal loss, decreased intake, hepatic involvement) and hyponatremia (eg, renal loss, extracellular fluid shifts, cellular exchange of sodium for potassium).
• Rickettsialpox: The organism that causes this illness is known to cause angiitis similar to other rickettsiae. Biopsies, which are rarely needed to establish the diagnosis of rickettsialpox, show evidence of thrombosis and necrosis of capillaries, as well as perivascular mononuclear cell infiltration.
• Boutonneuse fever: Features of this illness are related to involvement of the vascular structures of the dermis in a manner similar to that observed in RMSF. Endothelial cells of the capillaries, venules, and arterioles (ie, small-to-medium sized vessels) in various organs may also become involved as the organism disseminates.⁸ Additionally, a few cases of leukocytoclastic vasculitis have been reported with this infection.
• Louse-borne (epidemic) typhus: The pathology is similar to that described for the spotted fever group of rickettsial diseases. However, typhus group rickettsiae do not stimulate actin-based mobility and rather extensively multiply and accumulate intracellularly until they burst the endothelial cell and disseminate into the bloodstream.
• Brill-Zinsser disease (ie, relapsing louse-borne typhus): The pathology is similar to that described for the spotted fever group of rickettsial diseases. However, the organisms appear to lie dormant, most likely in the cells of the reticuloendothelial system, until they are reactivated by an unknown stressor, multiply and cause another acute but milder infection.
• Murine (endemic or flea-borne) typhus: Pathology is similar to that described for epidemic typhus.
• Tsutsugamushi disease (ie, scrub typhus): After invading the host cell and replicating in its cytoplasm, the Orientia tsutsugamushi exits by budding enveloped by part of the host cell membrane as it invades adjacent cells. Perivasculitis of small blood vessels occurs similarly to other rickettsial diseases. Usually, a necrotic inflammatory skin lesion occurs at the mite-bite site, and regional and generalized lymphadenopathy is associated with this infection.
• Q fever: In Q fever, the Coxiella organism directly causes disease in various organs. It has been demonstrated in macrophages in the lungs and in vegetations of the heart valves. Host-mediated pathogenic mechanisms also appear to play an important role in disease pathogenesis; the disease causes granulomatous changes in reticuloendothelial organs (granulomatous hepatitis).

Frequency

United States

• RMSF: RMSF is caused by R rickettsii. Now reported in all geographic areas of the United States, RMSF was first recognized in and thought to be limited to the Rocky Mountain area. Its incidence sharply declined with the introduction of broad-spectrum antibiotics in the 1950s; the incidence soared again in the 1960s and peaked in 1981. Incidence has declined since that time. The average annual incidence from 1997-2002, based on passive surveillance, was 2.2 cases per million population. The major endemic areas in the United States today include North Carolina, Oklahoma, South Carolina, Tennessee and Arkansas. More than 90% of patients with RMSF are infected from April through September. Individuals with frequent exposure to dogs and who reside near wooded areas or areas with high grass are at an increased risk of infection.^3,9,10
• Rickettsialpox: In the United States, rickettsialpox most commonly occurs in the Northeast, especially in New York city. Despite sporadic periodic outbreaks, incidence appears to be declining. The natural host is the common house mouse (Mus musculus).
• Boutonneuse fever: This disease is very rare outside a limited geographical area in the Mediterranean, Africa, and India. With increased travel and ecotourism in endemic areas, more imported cases of the disease are described in travelers returning to the United States from Mediterranean regions.⁸
• Louse-borne (epidemic) typhus: This is rare in the United States, but sporadic cases have been reported. The presumed source of infection is the southern flying squirrel.
• Brill-Zinsser disease (ie, relapsing louse-borne typhus): The distribution of this disease is analogous to louse-borne epidemic typhus. Recently, it has been rarely reported in the United States, and all cases had acquired the primary infection elsewhere.^11,2,12
• Endemic murine (flea-borne) typhus: This type of typhus is prevalent in urban cities and costal ports where rats are abundant. This is because it is transmitted rat-to-rat by a rat flea (Xenopsylla cheopis) and transmitted accidentally to humans by the feces of infected fleas. The cat flea (Ctenocephalides felis) may also serve as a vector for transmission of this disease to humans. These may be important vectors in Texas and southern California. Incidence has declined coincident with increased use of insecticides. Cases occur throughout the year, with peak prevalence from April through June in Texas and during the warm months of summer and early fall elsewhere.^11,13
• Tsutsugamushi disease (ie, scrub typhus): This is extremely rare outside the southwest Pacific and Southeast Asia.
• Q fever: Outbreaks are most common in slaughterhouses, research facilities, and plants, where handling of animals or their birth products is a source of exposure. Prevalence of Q fever in the United States is underestimated. Since Q fever became a nationally reportable disease in 1999 in the United States, a linear increase has been observed in the number of human cases identified (21 cases in 2000 compared with 110 cases in 2005).⁵

International

The spotted fever rickettsiae have been found in every continent except Antarctica.²

• RMSF: This primarily occurs in the continental United States but has been reported in southern Canada, Central America, Mexico, and parts of South America. It is rarely seen elsewhere.⁹
• Rickettsialpox: This may be more prevalent worldwide than is reported. It has been identified in large cities in Russia, South Africa, and Korea.
• Boutonneuse fever has demonstrated an increased incidence in Mediterranean countries, such as Spain, Italy, and Israel. Along with African tick–bite fever, these infections have been identified in Algeria, Malta, Cyprus, Slovenia, Croatia, Kenya, Somalia, South Africa, Ethiopia, India, and Pakistan, as well as rural Sub-Saharan Africa, the eastern Caribbean, and around the Black Sea.^4,8
• Louse-borne (epidemic) typhus: Epidemics have occurred in Europe, Asia, and Africa. African countries, especially Ethiopia and Nigeria, have reported most of the cases in the last 2 decades.
• Brill-Zinsser disease (ie, relapsing louse-borne typhus): This disease follows the epidemiology of louse-borne epidemic typhus and rarely, if ever, occurs in children because the reactivation usually occurs decades after primary infection.
• Murine (endemic or flea-borne) typhus: This is prevalent in large cities around the world where rats abound. It has been reported in travelers returning from ports and beach resorts in Asia, Africa and Europe.²
• Tsutsugamushi disease (ie, scrub typhus): Cases are usually seen in rural south and southeast Asia, limited to the geographical area bound by Japan, the Solomon Islands, and Pakistan. It is estimated that 1 million cases occur each year.
• Q fever: This zoonotic disease is observed in humans who come in contact with infected animals in Australia and Canada, as well as other areas of the world. Incidence figures widely vary.⁵

Mortality/Morbidity

Rickettsial diseases vary in clinical severity according to the virulence of the Rickettsia and host factors, such as age, male gender, and other underlying diseases. The most virulent rickettsiae are R rickettsii and R prowazekii, which kill a significant portion of infected persons unless the diseases are sufficiently treated early with an effective antimicrobial agent.^4,7

• RMSF: The overall mortality rate is 4%, despite effective antibiotic therapy. This most likely is caused by delay in the diagnosis and initiation of proper treatment. Patients treated during the first week of illness have the highest chance of complete recovery; however, if the disease is allowed to progress to the second week untreated, even optimal therapy progressively becomes less effective.¹⁴ Deficiency of glucose-6-phosphate dehydrogenase (G-6-PD) enzyme is associated with a high proportion of severe cases of RMSF. This is a rare clinical course that is often fatal within 5 days of onset of illness.
• Rickettsialpox: No mortality has occurred from this infection. Morbidity is minimal, as noted in Clinical.
• Boutonneuse fever: This infection generally runs a benign course. Severe forms of the disease have been described and fatalities are rare.⁸
• Louse-borne (epidemic) typhus: Mortality rates in untreated cases correlate with the patient's age. The mortality rate is approximately 10% in young adults but approaches 60-70% in patients older than 50 years.
• Brill-Zinsser disease (ie, relapsing louse-borne typhus): These relapses tend to be milder, shorter, and less debilitating.
• Murine (endemic or flea-borne) typhus: Complications and mortality (1% mortality rate in the United States) are uncommon.
• Tsutsugamushi disease (ie, scrub typhus): The illness usually is mild and self-limited. However, if left without treatment complications may include pneumonitis, meningoencephalitis, disseminated intravascular coagulation and renal failure. Fatality rate ranges from 1-35%, depending on the virulence of the infecting strain, host factors, and institution of proper treatment.
• Q fever: Uncomplicated disease is self-limited, lasting for 10-90 days. The mortality rate is approximately 1%. Complications are rare but may increase the mortality rate to 30-60%.⁵

Race

No specific racial predilection is observed.

Sex

Males appear to be at higher risk for infection with tick-borne rickettsioses. This is likely because of greater recreational or occupational exposures to tick habitats. However, in some spotted fever illnesses (eg, Q fever), females seem to be less susceptible to the infection possibly due to a protective role of female hormones.⁸

Age

• Two thirds of patients with RMSF are aged 15 years or younger.⁴
• Rickettsialpox, boutonneuse fever, epidemic and endemic typhus, and Tsutsugamushi disease affect all ages.
• Q fever occurs in all age group but is more prevalent between age 30-70 years.⁵

Clinical

History

Early signs and symptoms of these infections are notoriously nonspecific and may mimic benign viral illnesses, making the diagnosis more difficult. Certain features that aid in making the early diagnosis of rickettsial diseases include (1) a history of tick bite or exposure, (2) recent travel to endemic areas, and (3) similar illness in family members, coworkers, or family pets (especially dogs).

• Rocky Mountain spotted fever (RMSF)¹⁵
  • Fever, headache, rash, confusion, and myalgia are cardinal features.
  • Onset may be gradual or abrupt, beginning approximately 1 week (range, 2-14 d) following a bite from an infected tick. As many as 40% of patients may be unaware of the tick bite, which is usually painless and may go unnoticed or be easily forgotten.
  • Headache is usually persistent, intense, and intractable.
  • Patients may appear toxic, and this usually progresses to mental confusion and delirium.
  • GI symptoms (eg, abdominal pain and diarrhea) commonly occur during early stages of illness.
  • Conjunctival injection may also be seen.
• Rickettsialpox⁴
  • After an incubation period of 9-14 days, a red papule develops at the site of the mite bite. The papule subsequently develops an eschar. The appearance of the latter roughly coincides with the appearance of fever.
  • Irregular fluctuating fever (38-41°C) occurs and lasts for less than a week. Fever is accompanied by headache, chills, rigors, profuse sweating, myalgias, and occasionally by rhinorrhea, cough, sore throat, nausea, vomiting, and abdominal pain.
• Boutonneuse fever
  • Incubation period is usually 6 days (ranges from 1-16 d).
  • An eschar or cutaneous necrosis caused by rickettsial vasculitis at the tick-bite site of inoculation, known as tache noire ("black spot"), is pathognomonic. However, it may not be seen in 14-40% of cases. This lesion heals slowly over 10-20 days without leaving a scar.
  • The disease has an acute onset with high fever (above 39°C), headache,  malaise and arthromyalgias. Headaches are less frequent in children.⁸
  • African tick bite fever is similar but has a more timid presentation. It differs from other similar rickettsioses in that it produces a painful lymphadenopathy, multiple eschars, nuchal myalgia, and, occasionally, a sparse vesicular rash.^1,16
• Louse-borne (epidemic) typhus
  • The illness has an abrupt onset occurring 1-2 weeks following the bite of an infected louse.
  • Patients develop fever, intractable headache, and rash. The rash appears on days 4-7 of illness and spreads from the trunk to the extremities, sparing the face, palms, and soles. The lesions progress from macules to maculopapules to petechiae.
  • Conjunctival injection, rales, and delirium commonly occur.
• Brill-Zinsser disease (relapsing louse-borne typhus): Presentation is analogous to primary louse-borne epidemic typhus but is milder.
• Murine (endemic or flea-borne) typhus¹¹
  • Murine typhus is similar to louse-borne typhus but tends to have a milder and shorter course.
  • Fever is less pronounced and remittent, headache is less severe, and rash is less extensive. The latter may be absent in approximately 50% of patients.
• Tsutsugamushi disease (ie, scrub typhus)¹¹
  • The incubation period is approximately 1-2 weeks.
  • In fewer than half of patients, the site of the mite bite develops a necrotic eschar with enlargement of regional lymph nodes similar to rickettsialpox.
  • Inquiring about history of travel to the Southwest Pacific or Southeast Asia, where patients almost exclusively contract this disease is also helpful.
• Q fever^17,5
  • Primary infection is usually asymptomatic. Adults and men are more likely to have symptomatic infection compared with children and women, respectively.
  • Incubation period ranges from 2-6 weeks.
  • Acute Q fever infection usually has an abrupt onset, with fever, intractable headache, chills, myalgia, cough, and chest pain. The three clinical presentations more commonly observed are flulike illness, pneumonia, and hepatitis.
  • Rash is absent in over 90% of cases.
  • Chronic Q fever infection is less common (1-5%). It may be manifested as endocarditis, chronic or relapsing multifocal osteomyelitis, chronic hepatitis, chronic vascular infection, endocarditis, pericarditis, or myocarditis.¹⁸ The infection may be insidious, developing months to years following the acute infection.
  • Humans contract the disease by inhaling contaminated aerosols when they come in contact with infected animals or materials contaminated by them. Workers who handle livestock (eg, cattle, sheep, goats), especially at the time of slaughter or parturition, are at an increased risk of infection. Human infection also occurs after ingestion of contaminated raw milk.⁵
• Tickborne lymphadenopathy (TIBOLA) and Dermacentor -borne-necrosis-eschar-lymphadenopathy (DEBONEL)¹
  • An eschar associated with painful cervical lymphadenopathy appears 1 week after a tick bite to the occipital scalp.
  • Fever and rash are seldom present.
  • Patients may develop persistent asthenia and alopecia at the site of the eschar.

Physical

• RMSF
  • Fever reaches 40-41°C and, more commonly, has a persistent pattern rather than an oscillating one.^15,4
  • Rash starts on the second or third day of the illness. It usually appears peripherally on the wrists and ankles and spreads to involve the extremities and trunk. Rarely, the rash may be evanescent or localized to a particular region of the body.¹⁹
  • Typically, the lesions are small (1-5 mm), blanching, erythematous macules that may progress to maculopapules and petechiae.  
  • Skin necrosis is rare. In as many as 20% of cases, patients may not develop a rash (spotless RMSF), but this should not delay institution of proper therapy based on historical and clinical data.
  • Signs of meningoencephalitis and coma may follow delirium.
  • Meningismus may accompany the disease but is not necessarily associated with abnormal cerebrospinal fluid (CSF) findings (eg, minor elevation of CSF lymphocyte count). Other neurologic findings may include cortical blindness, seizures, central deafness, ataxia, paralysis, and cranial palsies.
  • Cardiac involvement frequently occurs. Adequate monitoring and workup are necessary to exclude arrhythmias and congestive cardiac failure.
  • Pulmonary manifestations may range from atelectasis to infiltrates or pulmonary edema.
  • Myalgia is a common feature and usually manifests as thigh or calf tenderness.
  • Retinal disease (i.e., edema, papilledema, cotton wool exudates, hemorrhages, retinal artery occlusion) occurs more commonly than uveitis or iritis.
  • Enlargement of the liver or spleen is infrequent.
• Rickettsialpox
  • Regional lymph nodes at the area of the primary eschar typically become enlarged.
  • A macular rash develops within several days of the onset of fever. The lesions then develop into vesicular maculopapules over a few days. The rash is distributed on the face, neck, trunk, and extremities and easily may be confused with the rash of varicella, especially in adult patients (hence, the name). In addition to the exanthem, the disease also may involve the mucus membranes, causing an enanthem. The pox usually heals within 2-3 weeks without scarring.
  • In addition to the exanthem, the disease also may involve the mucus membranes, causing an enanthem.
• Boutonneuse fever
  • Generalized myalgia occurs, and even myositis can be demonstrated.
  • Eschars can be often found in the trunk, arms and legs of cases. In young children they are frequently found on the scalp in a retroauricular area.
  • A rash appears on days 3-5 after the fever onset. It spreads from the extremities to the trunk, neck, palms, and soles within 36 hours. It usually spares the face.⁸
  • The lesions progress from macular to maculopapular and may persist for 2-3 weeks.
  • Atypical cutaneous findings may occur in a few patients and 1-4% of cases never develop a rash.
  • Cervical adenopathy may be found in 33-75% of affected children.
  • Patients with African tick–bite fever usually have a lower incidence of rash. It is usually vesicular and sparser than in Boutonneuse fever. Also, multiple eschars and prominent regional lymphadenopathy are present.¹⁶
  • Other manifestations and complications are similar to those seen in patients with RMSF.
• Louse-borne (epidemic) typhus¹¹
  • A rash appears on days 4-7 of illness and spreads from the trunk to the extremities, sparing the face, palms, and soles. Initially the rash may be concentrated in the axilla.
  • The lesions progress from macules to maculopapules to petechiae.
  • Uncommonly, complications such as gangrene, pericarditis, myocarditis, pleural effusion, and pneumonia may occur.
  • In severe cases, meningoencephalitis and delirium with fatal cardiac and renal failure may ensue.
• Brill-Zinsser disease (ie, relapsing louse-borne typhus): This is analogous to primary louse-borne epidemic typhus. The rash is usually milder and resolves faster.
• Murine (endemic or flea-borne) typhus
  • It is similar to louse-borne typhus but tends to have a milder and shorter course.
  • The rash is less extensive. Unlike RMSF, the rash usually spreads from the trunk to the extremities.
• Tsutsugamushi disease (ie, scrub typhus)
  • Unlike in other rickettsial diseases, generalized lymphadenopathy is a common feature (80%) of scrub typhus. It develops concomitantly with other manifestations, such as fever, headache, and rash.¹¹
  • The rash, which occurs 1-3 weeks following exposure to the vector, is frequently truncal and has a short duration. In 50% of cases, patients have an inoculation eschar.
  • Hepatosplenomegaly, ocular pain, and conjunctival injection are relatively common.
  • Other less common manifestations include deafness, tinnitus, myocarditis, atypical pneumonia, and adult respiratory distress syndrome.
• Q fever¹⁷
  • Pneumonitis occurs in more than half of patients. Cough is usually nonproductive and physical findings may not be pronounced.
  • Radiography may reveal a wide variety of pathologic findings, ranging from multiple segmental opacities to pleural effusion, lobar consolidation, or linear atelectasis.
  • Hepatitis presents with a fever and silent elevation of liver enzymes (transaminases). Hepatosplenomegaly may be present.⁵
  • Chronic Q fever infection must be excluded in patients with multifocal osteomyelitis, especially if a history of exposure to farm animals is noted.¹⁸

Causes

• RMSF
  • This disease is caused by R rickettsii.^1,6
  • Tick vectors of RMSF include the Rocky Mountain wood tick (Dermacentor andersoni) in the Western United States and Canada, the American dog tick (Dermacentor variabilis) in the East along the Pacific coast and central United States, and the Lone Star tick (Amblyomma americanum) in some southern areas.³
    
    

    

    This photo shows the relative sizes of the adult forms of Ixodes scapularis (right) and Dermacentor variabilis (left). These ticks are shown next to a common match for scale. I scapularis is also referred to as Ixodes dammini. Photo by Darlyne Murawski; reproduced with permission.

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    This photo shows the relative sizes of the adult forms of Ixodes scapularis (right) and Dermacentor variabilis (left). These ticks are shown next to a common match for scale. I scapularis is also referred to as Ixodes dammini. Photo by Darlyne Murawski; reproduced with permission.

    
    

    

    This photo is of an adult female, Amblyomma americanum, and a nymphal form of the same species (shown next to a common match for scale). Photo by Darlyne Murawski; reproduced with permission.

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    This photo is of an adult female, Amblyomma americanum, and a nymphal form of the same species (shown next to a common match for scale). Photo by Darlyne Murawski; reproduced with permission.

  • From 2002-2004, cases of RMSF reported from rural Arizona by Demma and colleagues were attributed to exposure to the common brown dog tick (Rhipicephalus sanguineus).²⁰ This represents a change from the typical vectors for this disease.
  • Rickettsiae multiply within ticks and pass to the next generation transovarially.
  • Rickettsiae are transmitted to a vertebrate host through saliva while a tick is feeding. It usually takes several hours of attachment and feeding before the rickettsiae are transmitted to the host. The risk of exposure to a tick carrying R rickettsii is low. Generally, about 1-3% of the tick population carries R rickettsii, even in areas where the majority of human cases are reported.
  • Recognized or potential tick-borne spotted fever group rickettsial pathogens in the United States, other than R rickettsii include R akari, Rickettsia felis, Rickettsia parkeri, Rickettsia amblyomii, Rickettsia rhipicephali, and various unnamed serotypes (eg, Tillmook, 364-D).²¹
• Rickettsialpox
  • It is caused by R akari, a member of the spotted fever group of Rickettsiae.
  • The disease is distinguishable from other rickettsial infections by the presence of an eschar at the site of the mouse mite (Liponyssoides sanguineus) bite, a vesiculopustular eruption, and the absence of Weil-Felix agglutinins.
  • The house mouse (Mus musculus) is the natural host of the mite transmitting rickettsialpox in the United States. Other rodents have been associated with the disease in other parts of the world.⁶
• Boutonneuse fever
  • This disease is a tick-borne infection caused by various subspecies of Rickettsia conorii complex (R conorii conorii is the cause of Mediterranean spotted fever; R conorii israelensis is the cause of Israeli spotted fever; R conorii caspica is the cause of Astrakhan spotted fever; and R conorii indica is the cause of Indian tick typhus) , Rickettsia africae (the cause of African tick–bite fever) , or R slovaca, which are obligate intracellular organisms transmitted to humans by various ticks, depending on the geographical location.⁸
  • Contact with dogs carrying infected ticks appears to be the important risk factor for human infection.
• Louse-borne (epidemic) typhus
  • This disease is caused by R prowazekii.
  • It is transmitted to humans by lice (ie, Pediculus humanus). Humans are the primary reservoir for R prowazekii.
• Brill-Zinsser disease (ie, relapsing louse-borne typhus): The rickettsial cause is the same but is related to the reactivation of the organism from a poorly defined latent state.
• Murine (endemic or flea-borne) typhus
  • This disease is primarily caused by R typhi (Rickettsia mooseri) and R felis, which share a large antigenic moiety with R prowazekii.
  • It is transmitted from rat-to-rat by a rat flea (X cheopis) and accidentally to humans by the feces of infected fleas.
  • The cat flea (C felis) may also transmit the disease.
• Tsutsugamushi disease (ie, scrub typhus)
  • This disease is caused by O tsutsugamushi, which has a remarkable antigenic heterogeneity.
  • It is transmitted to humans by the larval form of trombiculid mites (ie, chiggers) that live and breed in the soil and scrub vegetation. The mite is both the reservoir and the vector that passes the bacteria transovarially. Rodents are also reservoirs. Humans are accidentally infected.
• Q fever
  • The name derives from "Query Fever," given in 1935 following an outbreak of febrile illness in an abattoir in Australia. The disease is caused by C burnetii, a short, Gram negative, strictly intracellular bacterium.
  • Originally classified in the order Rickettsiales, C burnetii has since been placed (with Legionella and Francisella) into the gamma subdivision of the Proteobacteria on the basis of sequences of the 16SrDNA encoding genes.⁵
  • Unlike human rickettsial infections, it is a zoonosis transmitted from diseased animals to humans by the aerosol route or ingestion of raw milk.
  • Animals commonly infected include domestic livestock, especially cattle, sheep, and goats, as well as rodents, marsupials (in Australia), and cats (in Canada).
  • Ticks play a very minor role, if any, in transmission of the disease to humans; however, they transmit the disease to rodents and domestic animals.
  • C burnetii is a resilient organism that remains latent in infected hosts (eg, domestic livestock) until it is activated by a physiologic stressor, such as parturition. It then multiplies and contaminates the animals' surroundings, where it remains a potential source of infection for months. It is considered by the Center for Disease Control and Prevention (CDC) a potential agent of bioterrorism (class B).^6,5

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