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 INFECTIOUS DISEASE

BACTERIOLOGY IMMUNOLOGY MYCOLOGY PARASITOLOGY VIROLOGY

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BACTERIOLOGY - CHAPTER   TWENTY ONE  

RICKETTSIA, ORIENTIA, EHRLICHIA, ANAPLASMA, COXIELLA AND BARTONELLA

Dr. Gene Mayer

 

    
 
 
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READING: Murray et al. Medical Microbiology, 6th Ed., Chapter 44

Most images on this page come from the Centers for Disease Control

 

 

TEACHING OBJECTIVES
To describe the interactions of the Rickettsia, Ehrlichia, Coxiella and Bartonella with the host cell
To describe the pathogenesis, epidemiology and clinical syndromes associated with Rickettsia, Ehrlichia, Coxiella and Bartonella
To discuss the methods for treatment, prevention and control of rickettsial diseases

 

KEY WORDS
Reservoir
Vector
Rocky Mountain spotted fever
Ehrlichiosis
Rickettsialpox
Scrub typhus
Epidemic typhus
Murine typhus
Q fever
Trench fever
Cat-scratch disease
Transovarian passage
Weil-Felix test
Brill-Zinsser disease
Morula

 

Rickettsial infections have played a significant role in the history of Western civilization. Epidemic typhus has been known since the 16th century and it has long been associated with famine and war. The outcome of several wars was influenced by epidemic typhus. Typhus killed or caused great suffering to over 100,000 people in the two World Wars. In spite of its long history, it was not until the early part of the 20th century that the causative agent was determined. Howard Ricketts described the causative agent of Rocky Mountain Spotted Fever and was able to culture it in laboratory animals. Others then realized that the causative agent of epidemic typhus was related to the organism that Ricketts described. After the discovery of the importance of arthropod vectors in the spread of typhus, vector control measures were instituted to control the disease. However, as Hans Zinsser has pointed out, typhus is not dead.

The Rickettsia, Ehrlichia, Anaplasma and Coxiella are all small obligate intracellular parasites which were once thought to be part of the same family. Now, however, they are considered to be distinct unrelated bacteria. Like the Chlamydia these bacteria were once thought to be viruses because of their small size and intracellular life cycle. However, they are true bacteria, structurally similar to Gram negative bacteria. They are small Gram negative coccobacilli that are normally stained with Giemsa since they stain poorly with the Gram stain. Although these bacteria are able to make all the metabolites necessary for growth, they have an ATP transport system that allows them to use host ATP. Thus, they are energy parasites as long as ATP is available from the host.

All of these organisms are maintained in animal and arthropod reservoirs and, with the exception of Coxiella, are transmitted by arthropod vectors ( e.g., ticks, mites, lice or fleas). Humans are accidentally infected with these organisms. The reservoirs, vectors and major diseases caused by these organisms are summarized in Table 1 (Adapted from: Murray,et al. Medical Microbiology).

 

Table 1

Disease

Organism

Vector

Reservoir

Rocky Mountain spotted fever

R. rickettsii

Tick

Ticks, wild rodents

Ehrlichiosis

E. chaffeensis
E. ewingii
 

Tick

Deer
Deer
Small mammals

Anaplasmosis A. phagocytophilum Tick Deer
Deer
Small mammals

Rickettsialpox

R. akari

Mite

Mites, wild rodents

Scrub typhus

R. tsutsugamushi

Mite

Mites, wild rodents

Epidemic typhus

R. prowazekii

Louse

Humans, squirrel fleas, flying squirrels

Murine typhus

R. typhi

Flea

Wild rodents

Q fever

C. burnetii

None

Cattle, sheep, goats, cats

 

 

rick1.jpg (37437 bytes) Figure 1
Rickettsial and Orientia infection of endothelial cells

Rickettsia and Orientia

Orientia were formerly called Rickettsia

Replication

The Rickettsia preferentially infect endothelial cells lining the small blood vessels by parasite-induced phagocytosis (figure 1). Once in the host cell, the bacteria lyse the phagosome membrane with a phospholipase and get into the cytoplasm where they replicate. The mode of exit from the host cell varies depending upon the species. R. prowazekii exits by cell lysis while R. rickettsii get extruded from the cell through local projections (filopodia). F actin in the host cell associates with R. rickettsii and the actin helps to "push" the bacteria through the filopdia (figure 2). O. tsutsugamushi exits by budding through the cell membrane and remains enveloped in the host cell membrane as it infects other cells.

Antigenic structure

Based on their antigenic composition, the Rickettsia are divided into several groups. The organisms in each group, the diseases caused by the organisms and their geological distribution are summarized in Table 2 (Adapted from: Murray, et al., Medical Microbiology).

 

Table 2

Spotted fever group

Organism Disease Distribution

R. rickettsii

Rocky Mountain spotted fever

Western hemisphere

R. akari

Rickettsialpox

USA, former Soviet Union

R. conorii

Boutonneuse fever

Mediterranean countries, Africa, India, Southwest Asia

R. sibirica

Siberian tick typhus

Siberia, Mongolia, northern China

R. australis

Australian tick typhus

Australia

R. japonica

Oriental spotted fever

Japan

Typhus group

Organism Disease Distribution

R. prowazekii

Epidemic typhus

Recrudescent typhus

Sporadic typhus

South America and Africa

Worldwide

United States

R. typhi

Murine typhus

Worldwide

Scrub typhus group

Organism Disease Distribution

O. tsutsugamushi

Scrub typhus

Asia, northern Australia, Pacific Islands

 

Pathogenesis and Immunity

Pathogenesis is primarily due to destruction of the infected cells by the replicating bacteria. Destruction of endothelial cells results in leakage of blood and subsequent organ and tissue damage due to loss of blood into the tissue spaces. No evidence for immunopathological damage has been obtained. Both humoral and cell mediated immunity are important in recovery from infection. Antibody-opsonized Rickettsia are phagocytosed and killed by macrophages and delayed type hypersensitivity develops following rickettsial infections.

Figure 2

rick1ml.jpg (85044 bytes)  Attachment of rickettsiae to the surface of an endothelial cell is followed by their entry into the cell via rickettsia- induced phagocytosis. Following phagocytosis, the phagosome membrane (arrow) is lost and the rickettsiae escape into the host cell cytoplasm.
Vsevolod Popov and David H. Walker, University of Texas Medical Branch at Galveston, Galveston, Texas  USA and The MicrobeLibrary

rick2ml.jpg (91737 bytes) Following release from the phagosomes, rickettsiae grow free in the cytoplasm of cultured cells, dividing by binary fission (seen at arrows). The inset photo highlights the outer and inner membranes of rickettsia. Vsevolod Popov and David H. Walker, University of Texas Medical Branch at Galveston, Galveston, Texas  USA and The MicrobeLibrary

rick3ml.jpg (102260 bytes) Rickettsiae are propelled through the host cell cytoplasm by stimulating the polymerization of host cell F-actin, seen in the comet-like 'tail' (arrow). Vsevolod Popov and David H. Walker, University of Texas Medical Branch at Galveston, Galveston, Texas  USA and The MicrobeLibrary

rick4ml.jpg (62820 bytes) Propulsion by F-actin into long host cell projections known as filopodia precedes the release of rickettsiae from the cell surface or their spread to adjacent endothelial cells. Vsevolod Popov and David H. Walker, University of Texas Medical Branch at Galveston, Galveston, Texas  USA and The MicrobeLibrary

rick5ml.jpg (105012 bytes)  Growth of rickettsiae (arrows) in the endothelium results in damage to vascular integrity and thus the leakage of fluid into a vital organ such as the brain. The accumulation of fluid (edema) in the perivascular space (asterisks) may result in clinical encephalitis.  Vsevolod Popov and David H. Walker, University of Texas Medical Branch at Galveston, Galveston, Texas  USA and The MicrobeLibrary

rick6ml.jpg (94916 bytes)  Gamma interferon and tumor necrosis factor alpha, substances secreted by host immune cells, "activate" the infected endothelial cell to kill intracellular rickettsiae via the creation of autophagosomes. Later, fusion of lysosomes with autophagosomes results in the digestion of dying rickettsia (arrow).  Vsevolod Popov and David H. Walker, University of Texas Medical Branch at Galveston, Galveston, Texas  USA and The MicrobeLibrary

 

 

WEB RESOURCES
CDC Rocky Mountain Spotted Fever Site

 

Rickettsia rickettsii (Rocky Mountain Spotted Fever)

Epidemiology

Rocky Mountain Spotted Fever is the most common rickettsial disease in the United States with 400 - 700 cases occurring annually.

While the disease was originally described in the Rocky Mountain states, it is now most common in the South Central states, including South Carolina (figure 4). 

The organism is transmitted by the bite of an infected tick with most infections occurring from April through September because of more frequent human contact with ticks at this time of the year. The Rickettsia in the tick are in a dormant state and must be activated by the warm blood meal. They are then released into the saliva of the tick. Thus, prolonged exposure (24 - 48 hrs) to an infected tick must occur before the organisms can infect the human host. The principal reservoir for R. rickettsii is the ixodid (hard) tick in which transovarian passage occurs. Wild rodents can become infected and act as a reservoir for the bacteria but they are not considered to be the main reservoir.
 

 

rocky-bact.jpg (6187 bytes)  Figure 3
Gimenez stain of tick hemolymph cells infected with R. rickettsii  CDC
 

Figure 4

rocky-age.gif (4873 bytes)  Average annual incidence of Rocky Mountain spotted fever by age group, 1993-1996  CDC


rocky year.gif (8822 bytes)  Reported cases of Rocky Mountain spotted fever in the United States, 1942-1996   CDC

rocky-month.gif (7960 bytes)  Seasonal distribution of reported cases of Rocky Mountain spotted fever, 1993-1996 CDC

rocky-map3.gif (22329 bytes)  Number of reported cases of Rocky Mountain spotted fever by state and region, 1994-1998 CDC

rocky map.gif (5613 bytes)  Approximate distribution of the American dog tick CDC

rocky-tick2.jpg (5085 bytes)  
Rocky Mountain wood tick (Dermacentor andersoni) CDC

rocky-map2.gif (5683 bytes)  Approximate distribution of the Rocky Mountain wood tick CDC

rocky-tick.jpg (7244 bytes)    American dog tick (Dermacentor variabilis) CDC
rocky-tickcycle.gif (18545 bytes) Figure 5
Generalized Life Cycle of Dermacentor variabilis and Dermacentor andersoni Ticks (Family Ixodidae)  CDC


Clinical syndromes

Rocky Mountain spotted fever begins with the abrupt onset of fever, chills headache and myalgia usually 2 - 12 days after the tick bite. Patients may not recall being bitten by a tick. Rash usually (90% of cases) appears 2 - 3 days later. The rash begins on the hands and feet and spreads centripetally towards the trunk. Rash on the palms and soles is common. Initially, the rash is maculopapular but in the later stages may become petechial and hemorrhagic (figure 6).

Complications from widespread vasculitis can include gastrointestinal symptoms, respiratory failure, seizures, coma and acute renal failure. Complications occur most frequently in cases in which the rash does not develop, since treatment is usually delayed. Mortality rate in untreated patients is 20%.

Figure 6
rocky-feet.gif (38245 bytes)  Characteristic spotted rash of late-stage Rocky Mountain spotted fever on legs of a patient, ca. 1946  CDC

rocky-foot2.jpg (5493 bytes)  Early (macular) rash on sole of foot  CDC

rocky-arm.jpg (8438 bytes)  Late (petechial) rash on palm and forearm  CDC
 
 


Laboratory diagnosis

Initial diagnosis should be made on clinical grounds and treatment should not be delayed until laboratory confirmation is obtained. A fluorescent antibody test to detect antigen in skin punch biopsies is the fastest way to confirm a diagnosis. However, this test is available only in reference laboratories. PCR based methods are also available but limited to reference laboratories. The Weil-Felix test, which is an agglutination test to detect antibodies that cross react with Proteus vulgaris, is no longer recommended. The primary laboratory diagnostic tool is serology. Indirect fluorescent antibody tests (figure 7) and latex agglutination tests are available for serological diagnosis of Rocky Mountain spotted fever.

rocky-ifa.jpg (13644 bytes)  Figure 7
IFA reaction of a positive human serum on Rickettsia rickettsii grown in chicken yolk sacs, 400X  CDC

rocky-stain.jpg (21525 bytes)  Figure 8
Red structures indicate immunohistological staining of Rickettsia rickettsii in endothelial cells of a blood vessel from a patient with fatal RMSF CDC

Treatment, prevention and control

R. rickettsii is susceptible to tetracyclines and chloramphenicol. Prompt treatment is necessary since morbidity and mortality increases if treatment is delayed. No vaccine is available. Prevention of tick bites (protective clothing, insect repellents, etc.) and prompt removal of ticks are the best preventative measures. It is not feasible to attempt to control the tick reservoir.

See also Parasitology Chapter 7B:
Ticks

Rickettsia akari (rickettsialpox)

Epidemiology

R. akari is found in the United States and sporadic infections occur. The vector is a mouse mite and the reservoirs are mites and mice. In mites, the bacteria are maintained by transovarian transmission. Humans are accidentally infected.

Clinical syndromes

Rickettsialpox is typically a mild disease that has two phases. In the first phase a papule develops at the site of the mite bite and quickly ulcerates and forms an eschar. This initial phase occurs approximately 1 week after the bite. After an incubation time of 7 to 24 days, the second phase of the disease occurs. This phase is characterized by sudden onset of fever, chills headache and myalgia and is followed 2 to 3 days later with a generalized rash. The rash is papulovesicular and crusts over in the later stages. The pox heal within 2 to 3 weeks without scarring. Fatalities are rare.

Laboratory diagnosis

Not available except in certain reference laboratories

Treatment and prevention and control

Tetracycline and chloramphenicol can speed up recovery. Measures aimed at controlling mouse populations help to prevent the disease.

 

Rickettsia prowazekii (Epidemic typhus or louse-borne typhus)

Epidemiology

Epidemic typhus is a disease transmitted by the human body louse. When an infected louse bites a human, it defecates and the bacteria are found in the feces. Irritation caused by the bite causes the person to scratch the bite and thereby to inoculate the bacteria into abraded skin. Unlike the other rickettsial diseases, humans are the primary reservoir for R. prowazekii. Epidemic typhus occurs among people living in crowded, unsanitary conditions such as those found in wars, famine and natural disasters. Transovarian transmission in the louse does not occur since lice die several weeks after being infected. The disease occurs sporadically in the United States, primarily in the Eastern states where the reservoirs are flying squirrels and their fleas. The fleas are the vector that transmit the disease.

Clinical syndromes

a. Epidemic typhus is characterized by sudden onset of fever, chills, headache myalgia and arthralgia, after an average incubation period of 8 days. Approximately 7 days later, a rash develops in most patients. The rash is maculopapular but can be petechial or hemorrhagic. In contrast to the rash seen with Rocky Mountain Spotted Fever, the rash in epidemic typhus develops on the trunk first and spreads to the extremities (centrifugal spread). Complications include: myocarditis, stupor and delirium. The name typhus comes from the Greek for "smoke" underscoring the fact that stupor and delirium often complicate the disease. Recovery may take several months. The mortality rate varies but can be quite high (60 - 70%) in some epidemics.

b. Brill-Zinsser disease is recrudescent epidemic typhus. It occurs decades after the initial infection. In the United States it is most commonly seen in those who were exposed to epidemic typhus in World War II. The clinical course of the disease is similar to epidemic typhus but is milder and recovery is faster. The skin rash is rarely seen. Diagnosis is made on the basis of a fever with unknown origin and a history of previous exposure to epidemic typhus.

Laboratory diagnosis

Diagnosis should be made on clinical findings and treatment should begin before laboratory confirmation. Weil-Felix antibodies are produced but the test is not recommended. Serology is the primary laboratory test used for diagnosis of R. prowazekii. Indirect fluorescent antibody tests and latex agglutination tests are available. Patients with epidemic typhus initially have an IgM response followed by IgG antibodies whereas patients with Brill-Zinsser disease initially have an anamnestic IgG response. Isolation of the organism is possible but dangerous.

Treatment, prevention and control

Tetracyclines and chloramphenicol are highly effective. Louse control measures can prevent infection. A killed typhus vaccine is available and is recommended for use in high-risk populations.

See also Parasitology Chapter 7A:
Arthropods

 

 

Rickettsia typhi (Murine or endemic typhus)

Epidemiology

Murine typhus occurs worldwide with approximately 40 - 60 cases being reported in the United States annually. Rats are the primary reservoir for the disease which is transmitted by the rat flea vector. The normal cycle is rat to flea to rat and humans are accidentally infected. Since there is no transovarian transfer in the flea, the flea is not a reservoir for the disease. The cat flea can also be a vector for the disease in the United States. The bacteria are in the flea feces and are inoculated into abraded skin by scratching the area irritated by the bite.

Clinical syndromes

The symptoms of fever, chills headache and myalgia appear abruptly 1 - 2 weeks after infection. A rash develops in many but not all cases. The rash begins on the trunk and spreads to the extremities, unlike the rash seen in Rocky Mountain Spotted Fever. The disease is mild and resolves within 3 weeks even if untreated.

Laboratory diagnosis

A serological indirect fluorescent antibody test is used to detect antibodies to R. typhi.

Treatment, prevention and control

Tetracyclines and chloramphenicol are effective. Controlling the rodent reservoir is useful in preventing infection. A vaccine is not available.

 

ricket-em.jpg (96970 bytes) Figure 9
Phagocytosis of Rickettsia tsutsugamushi by mouse peritoneal mesothelial cell.  CDC/Dr. Edwin P. Ewing, Jr. epe1@cdc.gov

Orientia (Rickettsia)  tsutsugamushi (Scrub typhus)

Epidemiology

Scrub typhus occurs in Asia, Australia and the Pacific Islands. The disease is transmitted to humans by chiggers, the larval form of a mite. The mite is both the reservoir and the vector and passes the bacteria transovarially. Rodents can also act as a reservoir. The normal cycle is mite to rodent to mite; humans are accidentally infected.

Clinical syndromes

The disease is characterized by sudden onset of fever, chills headache and myalgia 1 - 3 weeks after contracting the bacteria. A maculopapular rash develops 2 - 3 days later. The rash appears first on the trunk and spreads to the extremities (centrifugal spread). Mortality rate in outbreaks are variable.

Laboratory diagnosis

Serological tests for antibody are available.

Treatment, prevention and control

Tetracyclines and chloramphenicol are effective. Avoiding exposure to chiggers will prevent the disease.

See also Parasitology Chapter 7A:
Arthropods

 

WEB RESOURCES
CDC Ehrlichia Site

 

 

Ehrlichia and Anaplasma

Replication

The Ehrlichia and Anaplasma preferentially infect leukocytes. They enter the cell by phagocytosis and once in the host cell they inhibit phagolysosome fusion. The organisms grow within the membrane-bound phagosome and are released by lysis of the cell (figure 10). The inclusion body containing the organisms is called a morula.

Epidemiology 

The Ehrlichia are divided into three groups based on genetic homology. Table 3 (Adapted from: Murray, et al., Medical Microbiology) summarizes the human diseases caused by the Ehrlichia and Analplasma, the vectors, reservoirs and the geographic distributions.

rick3.jpg (43974 bytes) Figure 10
Infection of leukocytes by Ehrlichia
Figure 11

ehrlich-us.gif (6426 bytes)  Reported Cases of Ehrlichiosis in the United States CDC

ehrlich-sewas.gif (5945 bytes)  Approximate seasonal distribution of HGE in the United States CDC

ehrlich-map3.gif (32970 bytes)  Areas where human ehrlichiosis may occur based on approximate distribution of  vector tick species  CDC

 
 

 

 

Table 3

Organism

Disease

Vector

Reservoir

Distribution

E chaffeensis

Human monocytic ehrlichiosis

Lone Star tick

White tailed deer

Southeastern, Mid-Atlantic and South Central United States

E. ewingii

Primarily a dog disease
Human granulocytic ehrlichiosis

Lone Star tick

White tailed deer

Southeastern, Mid-Atlantic and South Central United States

A. phagocytophilum Human granulocytic anaplasmosis (human anaplasmosis) Deer and dog ticks Small mammals Wisconsin, Minnesota, Connecticut

E. sennetsu

Sennetsu fever

Unknown

Unknown

Japan

 

 


Ehrlichia chaffeensis (human monocytic ehrlichiosis)

Clinical syndromes

The disease resembles Rocky Mountain Spotted Fever, except that the rash does not develop in most (80%) patients. In addition, leukopenia is observed due to destruction of the leukocytes. Mortality is low (5%).

Laboratory diagnosis

Microscopic observation of morula in blood smears is rare and ,although culture is possible, it is rarely attempted. Serological test are available and are the most commonly employed test. DNA probes are available and may replace serological tests.

Treatment, prevention and control

Patients should be treated with doxycycline. Avoidance of tick infected areas and protective measures (clothing and insect repellents) can prevent the disease.

See also Parasitology Chapter 7B:
Ticks

 

Figure 12

ehrlich-em.jpg (16055 bytes)  Electron-photomicrograph of morulae in a bone marrow leukocyte in a patient with ehrlichiosis. Arrows indicate individual ehrlichiae  CDC

ehrlich-chaff.jpg (5338 bytes)  Ehrlichia chaffeensis primarily infects mononuclear leukocytes (predominantly monocytes and macrophages), but may also be seen occasionally in the granulocytes of some patients with severe disease.  
(Morulae in cytoplasm of monocyte)  CDC

ehrlicj-tick.gif (16724 bytes)  Lone star tick (Amblyomma americanum) CDC

ehrlich-map1.gif (14691 bytes) Approximate distribution of the lone star tick  CDC

ehrlich-ifa.jpg (19841 bytes)  IFA of Ehrlichia chaffeensis in DH82 cells, 400X  CDC

ehrlich-stain.jpg (18019 bytes)  Diff-Quik Stain of Ehrlichia chaffeensis in DH82 cells, 1000X CDC

 

ehr2ml.jpg (95531 bytes)  Ehrlichia sp. develop within host cell vacuoles first as reticulate cells (RC) and then as dense-core cells (DC). A vacuole containing an ehrlichial microcolony is called a morula. Several morulae are seen in this host cell, including one filled with what appear to be dead ehrlichiae (shown at the arrow).

ehr3ml.jpg (96924 bytes)  A cultured cell, experimentally infected with E. chaffeensis (causative agent of HME), shows morulae of different sizes. Small morulae (shown at white arrows) contain few RC and are apparently in earlier stages of infection.

ehr4ml.jpg (65931 bytes)  Dense-core cells of E. chaffeensis are seen exiting the host cell following rupture of the morula and the host cell cytoplasmic membrane. These ehrlichiae will now go on to infect additional host cells or they may be ingested by a feeding tick, thus spreading the infection.
 
ehr1ml.jpg (106315 bytes)  A number of the bacteria are clustered in a vacuole in an infected host cell. The gram negative ehrlichiae have an inner and an outer membrane represented by the arrows. (All bars represent 0.5 mm.)
ehrlich-nh-hge.gif (35154 bytes)  Figure 13
Proposed life cycle for the agent of Human Granulocytic Ehrlichiosis
CDC



Ehrlichia ewingii and Anaplasma phagocytophilum (human granulocytic ehrlichiosis)

Clinical syndromes

The disease is similar to human monocytic ehrlichiosis except that mortality rates may be higher (10%)

Laboratory diagnosis

Same as E. chaffeensis

Treatment, prevention and control

Same as E. chaffeensis

Figure 14

ehrlich-equi.jpg (5311 bytes)   The pathogen that causes human granulocytic ehrlichiosis (HGE) primarily infects granulocytes (neutrophils and rarely eosinophils). The pathogen is often referred to as the agent of HGE or the HGE agent. This species is very similar, or likely identical, to E. phagocytophila and E. equi.  (Morulae in cytoplasm of neutrophil) CDC

ehrilich-bltick.gif (14979 bytes) Blacklegged tick (Ixodes scapularis)  CDC

ehrlick-bltickmap.gif (15402 bytes) Approximate distribution of the blacklegged tick CDC

ehrlich=bltick2.jpg (3326 bytes)  Western blacklegged tick (Ixodes pacificus) CDC
 
ehrlich-map2.gif (16811 bytes) Figure 15 Approximate distribution of the western blacklegged tick  CDC



Ehrlichia sennetsu (Sennetsu fever)

Clinical syndromes

The disease resembles infectious mononucleosis with fever, lethargy, cervical lymphadenopathy, increased number of peripheral blood mononuclear cells and atypical lymphocytes.

Laboratory diagnosis

Serological tests are available

Treatment

Tetracycline has been used but the disease is benign with no fatalities or serious complications.

 

WEB RESOURCES 
CDC Q fever site


COXIELLA

Coxiella burnetii (Q fever)  [Q for query]

Replication

C. burnetii  infects macrophages (figure 16) and survives in the phagolysosome where they multiply. The bacteria are released by lysis of the cells and phagolysosomes.

Pathogenesis and immunity 

Infection occurs by inhalation of airborne particles. The organism multiplies in the lungs and is disseminated to other organs. Pneumonia and granulomatous hepatitis are observed in patients with severe infections. In chronic disease, immune complexes may play a role in pathogenesis. Phase variation occurs in the LPS of C. burnetii. In acute disease, antibodies are produced against the phase II antigen. In chronically infected patients, antibodies to both phase I and phase II antigens are observed. Cellular immunity is important in recovery from the disease.

Epidemiology 

C. burnetii is extremely stable in the environment and has "spore-like" characteristics. C. burnetii infects a wide range of animals including goats sheep cattle and cats. The organism is found in the placenta and in the feces of infected livestock. The organisms persist in contaminated soil which is a focus for infection. C. burnetii is also passed in milk and people who consume non-pasteurized milk can become infected. Arthropods are not  common vectors for transmission of C. burnetii in humans but ticks are a primary vector for transmission among veterinary species.

C. burnetii is found worldwide and infection is common in ranchers, veterinarians, abattoir workers and others associated with cattle and livestock.

Clinical syndromes  

The disease can be mild and asymptomatic and is often undiagnosed. The disease can be acute or chronic. In acute Q fever, the patient presents with headache fever, chills and myalgia. Respiratory symptoms are usually mild ("atypical pneumonia"). Hepatomegaly and splenomegaly may be observed. Granulomas can be seen in histological sections of most patients with Q fever. Chronic Q fever typically presents as endocarditis generally on a damaged heart valve. Prognosis of chronic Q fever is not good.

Laboratory diagnosis  

Serology is most commonly used to diagnose Q fever. Antibodies to phase II antigen is used to diagnose acute disease and antibodies to both phase I and phase II antigens to diagnose chronic disease.

Treatment, prevention and control  

Tetracycline in used to treat acute Q fever. Chronic disease is treated by a combination of antibiotics. A vaccine is available in some countries, such as Australia, but it has not been approved for use in the United States.
 

rick2.jpg (42781 bytes)  Figure 16
Infection of Macrophages by Coxiella
Bartonellosis8.jpg (160749 bytes)  Figure 17
Bartonellosis- a bacterial onfection caused by Bartonella bacilliformis and found in South America. The infection can occur as either an acute febrile anemia (Oroya fever) or as a chronic cutaneous eruption (Verruga peruana). Dr V. Lloyd, Mount Allison University



Bartonella

Microbiology  

The Bartonella are small, Gram-negative aerobic bacilli that are difficult to grow in culture. They are found in many different animals but they cause no apparent disease in animals. Insects are thought to be vectors in human disease. Some species are able to infect erythrocytes while others simply attach to host cells. Table 4 (Adapted from: Murray, et al., Medical Microbiology) summarizes the organisms and the diseases they cause.

 

Table 4

Organism

Disease

B. quintana  (formerly Rochalimaea quintana)

Trench fever (shin-bone fever, 5 day fever), bacillary angiomatosis, bacillary peliosis endocarditis

B. henselae

Cat-scratch disease, bacillary angiomatosis, bacillary peliosis endocarditis

B. bacilliformis

Oroya fever (bartonellosis, Carrion's disease)

B. elizabethae

Endocarditis (rare)

 

Bartonella quintana (Trench fever)

Epidemiology

Trench fever is a disease associated with war. The vector is the human body louse and there is no known reservoir except man. Transovarian transmission in the louse does not occur. The organism is found in the feces of the louse and is inoculated into humans by scratching. The cycle is human to louse to human.

Clinical syndromes

Infection with B. quintana can result in asymptomatic to severe debilitating illness. Symptoms include fever, chills, headache and severe pain in the tibia. A maculopapular rash may or may not appear on the trunk. The symptoms may reappear at five day intervals and thus the disease is also called five day fever. Mortality rates are very low.

Laboratory diagnosis

Serological tests are available but only in reference laboratories. PCR based tests have been developed.

Treatment, prevention and control

Various antibiotics have been used to treat trench fever. Measures to control the body louse are the best form of prevention.
 

 

Bartonella henselae - (Cat-scratch disease)

Epidemiology

Cat-scratch disease is acquired after exposure to cats (scratches, bites, and possible cat fleas).

Clinical syndromes

The disease in usually benign, characterized by chronic regional lymphadenopathy.

Laboratory diagnosis

Serological tests are available

Treatment

Cat-scratch disease does not appear to respond to antimicrobial therapy.

 

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