|55 Kenosia Avenue
Danbury, CT 06810
Toll Free: 1.800.999.6673
The National Organization for Rare Disorders (NORD) web site, its databases, and the contents thereof are copyrighted by NORD. No part of the NORD web site, databases, or the contents may be copied in any way, including but not limited to the following: electronically downloading, storing in a retrieval system, or redistributing for any commercial purposes without the express written permission of NORD. Permission is hereby granted to print one hard copy of the information on an individual disease for your personal use, provided that such content is in no way modified, and the credit for the source (NORD) and NORD’s copyright notice are included on the printed copy. Any other electronic reproduction or other printed versions is strictly prohibited.
The information in NORD’s Rare Disease Database is for educational purposes only. It should never be used for diagnostic or treatment purposes. If you have questions regarding a medical condition, always seek the advice of your physician or other qualified health professional. NORD’s reports provide a brief overview of rare diseases. For more specific information, we encourage you to contact your personal physician or the agencies listed as “Resources” on this report.
Copyright 1986, 1994, 2001, 2009, 2012
NORD is very grateful to Edward B. Breitschwerdt, DVM, Professor of Medicine and Infectious Diseases, Center for Comparative Medicine and Translational Research, College of Veterinary Medicine, North Carolina State University, for assistance in the preparation of this report.
Bartonellosis is a group of emerging infectious diseases caused by bacteria belonging to the Bartonella genus. Bartonella includes at least 22 named species of bacteria that are mainly transmitted by carriers (vectors), including fleas, lice, or sandflies. Both domestic and wild animals can be infected with Bartonella species (Bartonella spp) by these vectors. Among the Bartonella spp, at least 14 have been implicated in diseases that can be transmitted from animals to people (zoonotic disease). Of these zoonotic species, several may be transmitted to humans by companion animals (dogs and cats), typically through a bite or scratch.
Human diseases that have been identified to be caused by one of the Bartonella spp bacteria include cat scratch fever (Bartonella henselae), Carrion’s disease (Bartonella bacilliformis), and trench fever (Bartonella quintana). Symptoms of a Bartonella infection include fever, fatigue, malaise, swollen lymph nodes, joint aches and swelling, neurological abnormalities, and skin rash or markings.
Bartonella spp have also been associated with diseases of the skin (bacillary angiomatosis), liver (peliosis hepatis), heart (endocarditis), eyes (neuroretinis), blood (bacteremia), and brain (encephalopathy). Emerging research suggests an association of Bartonella with chronic health conditons affecting the central nervous system, joints, and vascular system in patients with both healthy and compromised immune systems.
Bartonella infection does not always result in manifestation of illness. A number of studies have detected clinically healthy people that have tested positive (seropositive) for Bartonella and those who become ill usually develop mild disease that tends to end without treatment (self-limiting). Immunocompromised patients, such as those undergoing immunosuppressive treatments for cancer, organ transplant patients, and people with HIV/AIDS, are more likely to develop severe, life-threatening disease.
In 1909, Dr. Alberto Barton discovered the organism that became named Bartonell bacilliformis. Diseases caused by Bartonella spp occur all over the United States and in all major regions of the world, with higher prevalence occurring in areas that harbor insect carriers (arthropod vectors).
Diseases in humans that have been identified to be caused by one of the Bartonella spp include cat scratch disease, Carrion’s disease, trench fever.
Cat scratch disease (CSD)
CSD, caused by Bartonella henselae (B henselae), is a self-limiting infectious disease whose symptoms can vary from mild to severe. Symptoms may not appear for several days after exposure and may last for several weeks. Although in most patients the disease resolves spontaneously within 2-4 months without treatment, in people with severe cases and/or patients with a suppressed immune system, such as HIV/AIDS, antibiotic treatment is recommended.
The major symptoms of cat scratch disease may not appear for several days or weeks after exposure. A red spot (macule) may appear on the skin at the site of infection, and may become raised (papule) 3 to 10 days after exposure. The papule is painless and does not itch. It may become filled with fluid (vesicle), then crust over and heal with a scar similar to those left by chicken pox. The papule persists for 1 to 3 weeks, but may go unnoticed or be attributed to an injury.
Within 1-3 weeks, swelling of lymph nodes (lymphadenopathy) develops in a single node or group of regional nodes near the site of the bite or scratch. Swollen lymph nodes frequently occur under arms, on the neck, or in the groin regions. These nodes usually become very tender and the surface of the skin may appear red and feel hot to the touch. Pus may develop in the involved lymph nodes (suppuration) and become fluctuant. Lymphadenopathy remains regional and typically resolves within 2-4 months but may last up to 6-12 months. Rarely, it may persist for a year or more.
Other symptoms of cat-scratch disease may include achiness and overall discomfort (malaise), fatigue, headache, and in some patients, fever. Less common symptoms include loss of appetite, sore throat, and weight loss. In some cases chills, backache, abdominal pain, and/or convulsions have been reported. Other atypical manifestations of CSD include pericarditis (inflammation of the two layers of the thin, sac-like membrane that surrounds the heart) and pleural effusion (water on the lungs). Increasingly these atypical manifestations have been reported in patients without the typical symptoms of CSD. Children in particular appear to develop inflammation in the liver (granulomatous hepatitis) or spleen (splenitis) and bone (osteolytic) lesions. A more severe, systemic form of cat scratch disease has been reported. Major symptoms may include prolonged fever, joint pain (arthralgia), rash, weight loss, and/or enlargement of the spleen (splenomegaly).
Rare complications of Bartonella henselae infection more typically occur in people with immunocompromised conditions, such as those undergoing immunosuppressive treatments for cancer, organ transplant patients, and people with HIV/AIDS, although they are being increasingly reported in immunocompetent people, too. These include encephalopathy (inflammation of the brain), neuroretinitis (inflammation of the retina and optic nerve of the eye), osteomyelitis (acute or chronic bone infection), bacillary angiomatosis, and Parinaud's oculolandular syndrome.
Bacillary angiomatosis, caused by B quintana or B henselae, is a skin disorder that is characterized by reddish elevated lesions often surrounded by a scaly ring that may spread to produce a more widespread systemic disorder that can involve bone, liver, spleen, lymph nodes, the gastrointestinal and respiratory tracts, and bone marrow. Bacillary angiomatosis has occasionally been reported in immunocompetent patients.
Bacillary peliosis, a form of peliosis hepatis, is a vascular condition caused by B henselae. It is characterized by presence of blood-filled cavities in the liver.
Parinaud's oculoglandular syndrome, which affects the eye, presents in approximately 5% of patients with CSD. Symptoms include red, irritated, and painful eye (similar to conjunctivitis or "pink eye"), fever, general ill-feeling, and swelling of nearby lymph glands, often in front of the ear (preauricular lymphadenopathy).
Two thirds of patients with neuroretinitis have been found to present with serological evidence in blood work of previous B henselae infection. Some patients may persist in having the presence of bacteria (bacteremic) at a level that is below microbiological detection.
Neurologic complications occur in approximately 2% of infected patients, with
encephalopathy being the most common presentation. Symptoms generally occur 2 to 3
weeks after the onset of lymphadenopathy, although some patients have been known to
present with neurological symptoms without a CSD history. Greater than 90% of these
patients have complete, spontaneous recovery with no negative after effects.
Other rare symptoms of bartonellosis may include swelling of the largest salivary gland
(parotid gland), cardiac manifestation with inflammation of the lining of the heart and its
valves (endocarditis), renal inflammation (glomerulonephritis), granulomatous
inflammation of the liver (hepatitis), splenitis, and/or abscesses of the spleen. In very rare
cases, bartonellosis has been associated with atypical pneumonia, an inflammatory
reaction to infection characterized by bumps on the lower legs (erythema nodosum),
and/or a skin discoloration associated with a decreased blood platelet count
Carrion’s disease, caused by Bartonella bacilliformis (B bacilliformis), is a rare infectious disease that was originally thought to be localized to the Peruvian Andes. Other South American countries have more recently been included. New cases of the disease have been found in individuals who have traveled to other parts of the world.
In most affected individuals, Carrion’s disease is characterized by two well-defined stages: a sudden, acute phase known as Oroya fever and a chronic, benign skin (cutaneous) eruption consisting of raised, reddish-purple nodules known as verruga peruana (Peruvian wart). The first stage usually develops about three to 12 weeks following exposure to the B bacilliformis bacterium.
Oroya fever may be characterized by a sudden onset of high fever, profuse sweating, severe headache, chills, weakness, and paleness of the skin. In addition, in many cases, mental changes may develop, including confusion and disorientation or a coma. Such abnormalities occur in association with rapidly developing, severe hemolytic anemia or markedly reduced levels of red blood cells (erythrocytes) due to bacterial invasion and destruction of these cells. The first phase of the disease is very similar to malaria.
Additional associated findings may include abdominal pain, severe muscle aches (myalgia) and arthralgia, lymphadenopathy, inflammation of the brain and its protective membranes (meningoencephalitis), seizures, and/or other abnormalities. In addition, some affected individuals may develop chest pain due to insufficient oxygen supply to heart muscle (angina), thrombocytopenia, labored breathing (dyspnea), impaired digestive and liver function, and/or other abnormalities. Such findings are thought to result from severe hemolytic anemia and the abnormal formation of blood clots within small blood vessels (microvascular thrombosis), leading to an insufficient supply of oxygen to tissues (ischemia), impaired functioning of organs, and potentially life-threatening complications.
In addition, in some cases, the acute stage of Carrion’s disease may be complicated by and increased in severity due to the presence of other infections, such as salmonellosis or malaria (i.e., intercurrent infections). (For more on salmonellosis, see below. For further information on malaria, please choose "malaria" as your search term in the Rare Disease Database.)
In its mildest form, Carrion’s disease may not be noted until the development of characteristic skin lesions (verruga peruana). In such instances, it may have a gradual onset and initially be characterized by a fever that may be present for less than a week and be unrecognized as a manifestation of Carrion’s disease.
In those affected by Oroya fever, the period of recovery is typically associated with gradually reduced fever and disappearance of the bacterium as seen on microscopic examination of small blood specimens. However, some individuals remain persistently infected for years and blood smear examination, although the historical standard of care in Peru, is a very insensitive test. Furthermore, some affected individuals may temporarily have an increased susceptibility to certain, subsequent infections, such as with Salmonella bacteria (salmonellosis). Infection with certain strains of Salmonella bacteria may cause high fever, abdominal pain, bloody diarrhea, nausea, vomiting, rash, and/or other symptoms and findings. In addition, in some cases, without appropriate antibacterial therapy, B bacilliformis bacterium may remain present in the blood (bacteremia) for months to years without apparent symptoms (asymptomatic), potentially resulting in continued spread of the disease to others (i.e., as a "reservoir" or an ongoing source of infectious disease). Reports suggest that relapses or recurrences of Oroya fever are rare. According to experts, recurrence of fever after initial improvement of symptoms is considered suggestive of a secondary infection.
Following resolution of the acute stage of infection (Oroya fever), untreated individuals typically develop distinctive skin lesions within weeks or months. This second stage is known as verruga peruana. As noted above, verruga peruana may develop in individuals who have or have not had previous symptoms of Oroya fever.
Verruga peruana is typically characterized by reddish, purple skin lesions occurring in a series of outbreaks that may develop in one area as they heal in another and recur in certain sites. The lesions may initially be minute, eventually become nodular and range from about 0.2 to 4 centimeters in diameter, and potentially bleed, ulcerate, or become pus-containing blisters (pustules). Although they typically erupt on exposed skin, such as on the face, arms, and legs, they may also sometimes develop within mucous membranes and internal organs. In untreated individuals, verruga peruana may persist over a period of months to years.
Trench fever, caused by Bartonella quintana (B quintana), shows symptoms within a few days or up to five weeks following exposure to the bacterium. Affected individuals may develop sudden fever, chills, weakness, headache, dizziness, leg and back pain, and/or other abnormalities. Initial fever may last about four to five days and may recur one or several times, with each episode lasting about five days. Additional findings may include a temporary skin rash consisting of flat (macular) or raised (papular) lesions, splenomegaly, and/or enlargement of the liver (hepatomegaly). Trench fever is usually a self-limiting disease, although relapses and chronic bacteremic states are well known. A severe form of B quintana infection has also been reported in immunocompromised individuals, such as in association with AIDS.
Bartonella bacteria invade erythrocytes and the lining of the blood vessels (endothelial cells), where the organism proliferates. Inside the erythrocytes, it is protected from the host’s primary and secondary immune response, thus explaining bacterial persistence that can occur in some cases.
Cat scratch disease:
Cat scratch disease is caused by the B henselae bacterium. Most cases follow a lick, scratch, or bite from a cat or kitten when the bacterium is present on the cat’s claws or oral cavity. A feline infected with B henselae is a common occurrence. Up to half of domestic cats have antibodies to B henselae. Cats are infected with B henselae by fleas, therefore preventing flea exposure will prevent B henselae infection in cats and kittens and thereby prevent human infection. Kittens under 12 months of age are 15 times more likely to transmit the disease than adult cats. Outdoor cats and cats infested with fleas are also more likely to show antibodies (test seropositive) to B henselae. Fleas transmit the bacteria between cats. No evidence exists to suggest transmission from cat fleas to humans. Cat to cat and person-to-person transmission has not been documented. There is increasing evidence supporting vector transmission of B henselae by fleas, ticks and likely other arthropods. A deep puncture wound such as from a thorn or splinter may also introduce infection. There have also been cases reported of the disease following the scratch or bite of dogs in 5% of cases and occasional cases of infection have been associated with monkeys. Animals that are carrying the disease are not ill, and will not exhibit any symptoms. Not every person exposed to the carrier animal will develop cat scratch disease, and in most cases the symptoms are temporary (transient) and mild.
B bacilliformis is the etiologic agent of Carrion’s disease or Oroya fever (acute phase of infection) and Verruga peruana or Peruvian wart (chronic phase of infection). The bacterium is primarily carried and transmitted by the night-biting sand fly known as Lutzomyia (formerly Phlebotomus).
The B bacilliformis bacterium enters the bloodstream via the bite of the sand fly, enabling the bacterium to attach to the surface of erythrocytes. Bacterial invasion and reproduction leads to abnormal fragility and premature destruction of many erythrocytes in the bloodstream (hemolysis). This results in abnormally decreased red blood cell levels and reduced concentrations of hemoglobin, the oxygen-carrying component of the blood (hemolytic anemia). In addition, the bacterium may invade cells lining small blood vessels (capillary endothelial cells), potentially leading to blockage of normal blood flow (vascular occlusion). Severe hemolytic anemia and the abnormal formation of blood clots within small blood vessels may potentially lead to life-threatening complications without prompt appropriate treatment.
With developing immunity, levels of the bacterium markedly decrease in the blood. However, without appropriate antibiotic therapy, asymptomatic low-grade bacteremia may persist for months or years in some cases.
Following the symptom-free (latent) period, most untreated individuals develop the distinctive skin lesions characteristic of verruga peruana. The nodular lesions consist of newly formed blood vessels (neovascular proliferation) infiltrated by certain white blood cells that play an important role in fighting and destroying invading microorganisms (e.g., lymphocytes, macrophages).
Trench fever is caused by infection with B quintana most likely transmitted by the human body louse (Pediculus humanus) and is commonly found in homeless, alcoholic, and poverty-stricken populations where poor sanitation and poor hygiene often occurs. Other diseases that have been identified to be caused by B quintana include bacillary angiomatosis (angioproliferative lesions), chronic lymphadenopathy, bacteremia, and endocarditis. Human endocarditis has now been associated with at least nine different Bartonella spp.
Bartonella vinsonii subsp. berkhoffii has been isolated from immunocompetent patients with endocarditis, arthritis, neurological disease and vasoproliferative neoplasia. Dogs and wild canines (foxes, coyotes, wolves), who are the primary reservoir hosts, are the suspected reservoir hosts for this bacterium, and ticks are the suspected vectors, but this has not been scientifically proven.
Most infections in immunocompromised patients are caused by B henselae and B quintana. Unlike immunocompetent individuals who usually develop milder diseases such as cat scratch disease and trench fever, immunocompromised patients, including HIV/AIDS and posttransplant patients, are more likely to develop more severe, potentially life-threatening disease.
More studies are emerging that document the role that ticks may play in the transmission of Bartonella spp. These include studies that have documented Bartonella spp DNA in ticks (most often B henselae). A study in 2011 was the first to report the detection of B rochalimae, B quintana, and B elizabethae DNA in ticks from Peru. Vector competence for tick transmission of bartonellae was demonstrated in a study in 2011. Flea transmission to dogs in an experimental setting has been demonstrated. In addition, B henselae is the most frequent Bartonella spp to infect sick dogs. Several investigators have reported B quintana infection in research monkeys.
Cat scratch disease caused by B henselae infection occurs in approximately 1 per 10,000 persons. Cat-scratch disease has been shown in some studies to occur more frequently in males than females with a ratio of 3:2. However, other studies have shown equal rates between males and females. One hypothesis to explain a greater incidence among males than females is the tendency toward rougher play with cats and consequently an increased risk of bites and scratches. A database analysis in 1993 showed 55% of patients with CSD were 18 years of age or younger. Older literature suggests that more than 80% of cases of CSD occur in people under 21 years of age, and about 95% have a history of a scratch from a cat or exposure to cats.
Cases of CSD occur throughout the United States and worldwide, with the incidence greater in regions with higher temperatures and humidity, which supports heavy flea populations. In the United States, the majority of cases occur between the months of July and January. One study in 1993 concluded that incidence of CSD in the United States is higher in the south and lower in the west.
Carrion’s disease has, until recently, been restricted in its geographic distribution to the Andes Mountains regions of the South American countries of Columbia, Peru, and Ecuador at elevations of 1000-3000 meters because of the habitat of the sand fly Lutzomyia. Cases elsewhere in the world are found in travelers, who presumably acquired their infections while visiting one of these countries. Oroya fever was first recognized in the nineteenth century as the cause of acute fever and highly fatal, hemolytic anemia in railroad workers in Peru. Reports suggest that the chronic skin (cutaneous) stage was described earlier.
The common bacterial cause of Oroya fever and verruga peruana was confirmed by a Peruvian medical student, Daniel Carrion, in 1885, when he succumbed to acute hemolytic anemia after injecting himself with blood from a verruga peruana skin lesion. The spectrum of B. bacilliformis infection as manifested in Oroya fever and verruga peruana has since been named "Carrion's Disease."
Trench fever was first described during World War I when it affected nearly one million soldiers. B quintana has caused geographically widespread disease, although little data exists regarding incidence among specific populations. Though the true incidence of contemporary (urban) trench fever is unknown, one study of patients in a downtown poor Seattle clinic found 20% had antibodies to Bartonella spp, though most of these patients were asymptomatic.
Certain features of the following disorders may be similar to those of bartonellosis:
Adenitis (Bacterial, Fungal, Pyogenic, and Tuberculous) is an inflammatory disease characterized by lymphadenopathy. Differential diagnosis may be accomplished through skin testing and/or microscopic examination of the involved lymph nodes.
Atypical mycobacterial infections are caused by nontuberculous mycobacteria, but can be very difficult to distinguish from tuberculosis. Lymphadenopathy is caused by nontuberculous mycobacteria, surgical removal and examination (biopsy) of involved tissue may be necessary for diagnosis.
Brucellosis is an infection of livestock that can be transmitted to humans. It is caused by different species of the bacteria Brucella. Initial infection may result in an acute flu-like illness, or may evolve over months. Untreated cases may take months to resolve, and some cases become chronic. Symptoms may include a gradual onset of fever, weakness, headache, joint pain, and/or night sweats. Other symptoms may include lymphadenopathy, splenomegaly, and/or hepatomegaly. (For more information on this disorder, choose "Brucellosis" as your search term in the Rare Disease Database.)
Lymphogranuloma venereum is a sexually transmitted infection characterized by a primary skin lesion at the site of infection. This lesion may be a raised bump (papule) that heals spontaneously or may go unnoticed. This is followed by lymphadenopathy on one or both sides of the body. The site of the first infection or lesion will determine the region affected.
Lymphomas are growths (tumors) of the lymphoid tissue. These tumors are divided into two types, Hodgkin's and non-Hodgkin's lymphoma. Symptoms will depend upon the type and location of the tumor. Symptoms may include lymphadenopathy, hoarseness, a high- pitched respiratory sound when inhaling (stridor), and/or difficulty in swallowing (dysphagia).
Sarcoidosis is a rare disorder which affects many body systems. It is characterized by small round lesions (tubercles) of granulated tissue. Symptoms may vary depending on the severity of the disease and how much of the body is affected. Symptoms of sarcoidosis depend on the site of involvement and may be absent, slight, or severe. Lymphadenopathy is common. Both enlarged and normal-sized lymph nodes may contain the characteristic sarcoid tubercles. (For more information on this disorder, choose "Sarcoidosis" as your search term in the Rare Disease Database.)
Kaposi's sarcoma is a cancerous tumor that often appears as bluish-red or purple bump on the skin and is often associated with AIDS.
Pyogenic granulomas are small, reddish bumps on the skin whose exact cause is unknown but often appear on the hands, arms or face following injury.
Hemangioma is a benign tumor made up of blood vessels that typically occurs as a purplish or reddish slightly elevated area of skin.
Lyme disease is a tick-borne infection. The most common initial symptom is an expanding flat or slightly raised red spot skin lesion (bull's eye" rash known as erythema migrans) that develops at the site of the bite of a tick. Within days or weeks after infection, flu-like symptoms can develop. Later manifestations may include arthritis, the central nervous system, or cardiac involvement.
Most cases of CSD can be diagnosed by the individual's symptoms and history, such as the development of papules or pustules after vector exposure or a cat scratch or bite. Development of swollen lymph nodes and fever further reinforce a clinical diagnosis. Blood (serological) testing is available to confirm the diagnosis. However, serology is often negative in patients with chronic symptoms and repeatedly documented bacteremia. In these patients an enrichment blood culture using an insect cell culture based growth medium followed by PCR amplification of bacterial DNA (see Clinical Testing and Work-up below) provides a much greater test sensitivity and allows documentation of active infection.
Carrion's disease may be diagnosed based upon thorough clinical evaluation, detection of characteristic symptoms and physical findings, a complete patient history, including information concerning recent travel to regions where Carrion's disease is known to occur; and specialized laboratory tests. For example, during the acute stage, the bacterium may easily be seen within red blood cells on blood smears. With this diagnostic test, a drop of blood is smeared on a slide, stained with special dyes to make blood cells more visible, and examined under a microscope. During the chronic, cutaneous stage, the bacterium may be isolated from skin lesions. Blood smears are typically negative during this second stage. However, the bacterium may be cultured from the blood and grown under controlled conditions in the laboratory, enabling identification of the causative microorganism. In some cases, other laboratory studies may be used to help diagnose Carrion's disease.
Serological testing is used to diagnose Trench fever. However, it is difficult to diagnose in the laboratory, especially with blood cultures, since results are often negative even when infection is present and growth often takes 20-40 days.
Clinical Testing and Work-Up
Bartonella infection can be difficult to diagnosis. Serological testing is the most cost-effective diagnostic tool in laboratory detection of bartonellosis when positive results are found. However, as previously discussed, false negatives often occur, leading to undiagnosed, untreated patients when further testing is not performed. Detection of IgG and IgM antibodies in blood serum to Bartonella henselae by Indirect Immunofluorescence Assays (IFA) is an accurate way to identify CSD. Microscopic examination of Giemsa-stained blood smears (Giemsa-stained) is used to detect B bacilliformis in patients who may have Carrion’s disease. Other Bartonella species are visible only with silver stains (Warthin-Starry, Steiner, Dieterle), although they sometimes resist staining or are present in such low numbers as to not be detectable.
A polymerase chain reaction (PCR) test is a molecular technique used to detect specific genetic material in blood. Because of the serological cross-reactivity between Bartonella species and other bacteria, PCR analysis of tissue and body fluid is the most specific diagnostic test, especially in identifying distinct genotypes among Bartonella species.
A patented culturing process developed by the Intracellular Pathogens Research Laboratory at North Carolina State University, College of Veterinary Medicine and available through Galaxy Diagnostics Inc. (http://www.galaxydx.com) may increase the odds of detecting the presence of Bartonella spp bacteria if it is present in a patient sample.
Intradermal skin testing, using hypersensitivity reaction to B henselae antigen, is a test that is no longer used as more accurate testing is now available. Stains of biopsied tissue from lymph nodes examined microscopically may show small curved Gram-negative rods characteristic of B henselae, but this staining method is not a definitive diagnosis of CSD. PCR of lymph nodes and other tissues, when used in conjunction with DNA sequencing, allows for diagnostic confirmation of Bartonella spp and strains.
Complications involving the liver and/or spleen are now identified more frequently with the use of improved serologic, PCR and diagnostic imaging tests. Abdominal imaging is an important diagnostic tool for patients with suspected hepatosplenic disease and who present with prolonged fever.
Cat scratch disease typically subsides without any treatment, usually within 2 to 4 months. Therapy is symptomatic and supportive. Antipyretics (fever reducers) and analgesics may be administered as needed. Local heat may be applied to the involved lymph nodes.
Cat scratch disease usually has a very good prognosis, with no long-term health effects. When secondary disorders (i.e., encephalitis) develop, the secondary disorder is usually resolved when the lymphadenopathy and associated symptoms are resolved. Although rare, adults can have recurrent illnesses and elimination of bacteremia in some chronically infected patients is not easy to achieve.
If the affected lymph node produces pus (suppurates) and becomes large and/or painful, it may be necessary to drain the node. Draining the pus through a needle (aspiration) is preferred over making an incision. Usually one aspiration is sufficient to relieve discomfort.
Antibiotics may be considered for severe or systemic disease. Reduction of lymph node size has been demonstrated with a 5-day course of azithromycin. Other antibiotics that have been considered effective include rifampin, ciprofloxacin, intramuscular gentamicin, trimethoprim/sulfamethoxazole. Bartonella henselae is generally resistant to penicillin, amoxicillin, and nafcillin. Doxycycline is the preferred medication for treating neuroretinitis. Effective antibiotic therapy for the complication of endocarditis should include an aminoglycoside prescribed for a minimum of 2 weeks.
The treatment of choice for Carrion's disease is administration of the antibiotic chloramphenicol (due to frequent, intercurrent infection with Salmonella). In some cases, appropriate alternatives may include doxycycline, other tetracyclines, or ampicillin. Antibiotic therapy may rapidly treat acute febrile illness associated with Carrion's disease and speed healing of chronic skin lesions. Blood transfusions may be required to treat severe anemia. Other treatment for this disorder is symptomatic and supportive.
Carrion's disease may be prevented by avoiding the sandflies that transmit the bacterium to humans. Insect repellents, bed nets, and long-acting insecticides can help prevent exposure to these insects.
Tetracycline-group antibiotics (doxycycline, tetracycline) are commonly used to treat trench fever. Uncomplicated disease responds to doxycycline and gentamicin. Chloramphenicol is an alternative medication recommended when tetracycline usage is undesirable, such as in severe liver malfunction, kidney deficiency, in children under nine years and pregnant women. Macrolides and ceftriaxone have also been effective. It is important to treat with 2 antibiotics in severe, chronic, or complicated cases of bartonellosis.
A longer duration of treatment is recommended for immunocompromised patients and when the liver or other organs are involved. In patients with AIDS and bacillary angiomatosis, the primary choices of antibiotics include erythromycin, doxycycline, or more expensive drugs such as azithromycin, clarithromycin, or a fluoroquinolone. Doxycycline combined with rifampin is effective in patients with severe disease. An extended treatment if often required in these cases.
Though the course of the disease can be far more severe and potentially life-threatening for immunocompromised patients, these patients typically experience full resolution of disease with appropriate antibiotic use and management of complications. The response of immunocompromised patients to antibiotics is significantly more dramatic than immunocompetent patients. Some researchers believe that less virulent strains tend to infect immunocompromised patients and are perhaps more antibiotic responsive.
Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.
For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:
Toll free: (800) 411-1222
TTY: (866) 411-1010
For information about clinical trials sponsored by private sources contact:
Versalovic J, Carroll KC, Funke G, Jorgensen JH, Landry ML, Warnock DW, eds. Manual of Clinical Microbiology. 10th ed. Washington, DC: ASM Press; 2011.
Mandell GL, et al, eds. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 5th ed. Philadelphia, PA: Churchill Livingstone; 2000:2444-56.
Beers MH, et al, eds. The Merck Manual. 17th ed. Whitehouse Station, NJ: Merck Research Laboratories; 1999:1233-37.
Nelson Textbook of Pediatrics. 14th ed. Behrman RE, ed. Philadelphia, PA: W.B. Saunders Company: 1992:863-864.
Wyngaarden JB, et al, eds. Cecil Textbook of Medicine. 19th ed. Philadelphia, PA: W.B. Saunders Company; 1992:1729, 1732.
Ballenger JJ. Diseases of The Nose, Throat, Ear, Head & Neck. 14th ed. Philadelphia, PA: Lea & Febiger; 1991:302.
Newell FW. Ophthalmology: Principles And Concepts. 7th ed. St. Louis, MO: Mosby Year Book; 1991:230.
Clinical Dermatology. 2nd ed. Thomas P. Habif TP, ed. St. Louis, MO: The C.V. Mosby Company; 1990:396.
Dictionary of Medical Syndromes. 3rd ed. Magalini SI, Magalini SC, de Francisci S, eds. Philadelphia, PA: Lippincott Williams & Wilkins; 1990:684-685.
Maggi RG, Mozayeni BR, Pultorak EL, et al. Bartonella spp. bacteremia and rheumatic symptoms in patients from Lyme disease-endemic region. Emerg Infect Dis. 2012;18(5):783-91. http://www.ncbi.nlm.nih.gov/pubmed/22516098
Mosepele M, Mazo D, Cohn J. Bartonella infection in immunocompromised hosts: immunology of vascular infection and vasoproliferation. Clin Dev Immunol. 2012;2012:612809. http://www.ncbi.nlm.nih.gov/pubmed/22162717
Diaz MH, Bai Y, Malania L, Winchell JM, Kosoy MY. Development of a novel genus-specific real-time PCR assay for detection and differentiation of Bartonella species and genotypes. J Clin Microbiol. 2012;50(5):1645-9. http://www.ncbi.nlm.nih.gov/pubmed/22378904
VanderHeyden TR, Yong SL, Breitschwerdt EB, et al. Granulomatous hepatitis due to Bartonella henselae infection in an immunocompetent patient. BMC Infect Dis. 2012;12:17. http://www.ncbi.nlm.nih.gov/pubmed/22269175
Karris MY, Litwin CM, Dong HS, Vinetz J. Bartonella henselae infection of prosthetic aortic valve associated with colitis. Vector Borne Zoonotic Dis. 2011;11(11):1503-5. http://www.ncbi.nlm.nih.gov/pubmed/21702667
Graveleau J, Grossi O, Lefebvre M, et al.Vertebral osteomyelitis: an unusual presentation of Bartonella henselae infection. Semin Arthritis Rheum. 2011;41(3):511-6. http://www.ncbi.nlm.nih.gov/pubmed/21840042
Reis C, Cote M, Le Rhun D, et al. Vector competence of the tick Ixodes ricinus for transmission of Bartonella birtlesii. PLoS Negl Trop Dis. 2011;5(5):e1186. http://www.ncbi.nlm.nih.gov/pubmed/21655306
Mascarelli PE, Iredell JR, Maggi RG, Weinberg G, Breitschwerdt EB. Bartonella species bacteremia in two patients with epithelioid hemangioendothelioma. J Clin Microbiol. 2011;49(11):4006-12. http://www.ncbi.nlm.nih.gov/pubmed/21918021
Breitschwerdt EB, Mascarelli PE, Schweickert LA, et al. Hallucinations, sensory neuropathy, and peripheral visual deficits in a young woman infected with Bartonella koehlerae. J Clin Microbiol. 2011;49(9):3415-7. http://www.ncbi.nlm.nih.gov/pubmed/21734026
Billeter SA, Cáceres AG, Gonzales-Hidalgo J, Luna-Caypo D, Kosoy MY. Molecular detection of Bartonella species in ticks from Peru. J Med Entomol. 2011;48(6):1257-60. http://www.ncbi.nlm.nih.gov/pubmed/22238888
Breitschwerdt EB, Maggi RG, Chomel BB, Lappin MR. Bartonellosis: an emerging infectious disease of zoonotic importance to animals and human beings. J Vet Emerg Crit Care. 2010;20(1):8-30. http://www.ncbi.nlm.nih.gov/pubmed/20230432
Breitschwerdt EB, Maggi RG, Lantos PM, Woods CW, Hegarty BC, Bradley JM. Bartonella vinsonii subsp. berkhoffii and Bartonella henselae bacteremia in a father and daughter with neurological disease. Parasit Vectors. 2010;3(1):29. http://www.ncbi.nlm.nih.gov/pubmed/20377863
Sykes JE, Lindsay LL, Maggi RG, Breitschwerdt EB. Human coinfection with Bartonella henselae and two hemotropic mycoplasma variants resembling Mycoplasma ovis. J Clin Microbiol. 2010;48(10):3782-5. http://www.ncbi.nlm.nih.gov/pubmed/20702675
Maguiña C, Guerra H, Ventosilla P. Bartonellosis. Clin Dermatol. 2009;27(3):271-80. http://www.ncbi.nlm.nih.gov/pubmed/19362689
Florin TA, Zaoutis TE, Zaoutis LB. Beyond cat scratch disease: widening spectrum of Bartonella henselae infection. Pediatrics. 2008;121(5):e1413-25. http://pediatrics.aappublications.org/content/121/5/e1413.full.html
Vermeulen MJ, Herremans M, Verbakel H, Serological testing for Bartonella henselae infections in The Netherlands: clinical evaluation of immunofluorescence assay and ELISA. Clin Microbiol Infect. 2007;13(6):627-34. http://www.ncbi.nlm.nih.gov/pubmed/17378931
Vikram HR, Bacani AK, DeValeria PA, Cunningham SA, Cockerill FR 3rd. Bivalvular Bartonella henselae prosthetic valve endocarditis. Clin Microbiol. 2007;45(12):4081-4. http://www.ncbi.nlm.nih.gov/pubmed/17942646
Brunt J, Guptill L, Kordick DL, Kudrak S, Lappin MR. American Association of Feline Practitioners 2006 Panel report on diagnosis, treatment, and prevention of Bartonella spp. infections. Journal of Feline Medicine and Surgery. 2006;8(4):213-226. http://www.ncbi.nlm.nih.gov/pubmed/16846781
Maggi RG, Duncan AW, Breitschwerdt EB. Novel chemically modified liquid medium that will support the growth of seven bartonella species. J Clin Microbiol. 2005;43(6):2651-5. http://www.ncbi.nlm.nih.gov/pubmed/15956379
Tsujino K, Tsukahara M, Tsuneoka H, et al. Clinical implication of prolonged fever in children with cat scratch disease. J Infect Chemother. 2004;10:227-33. http://www.ncbi.nlm.nih.gov/pubmed/15365864
Lamps LW, Scott MA. Cat-scratch disease: historic, clinical and pathologic perspectives. Am J Clin Pathol. 2004;121:S71-80. http://www.ncbi.nlm.nih.gov/pubmed/15298152
Raoult D, Fournier PE, Vandenesch F, et al. Outcome and treatment of Bartonella endocarditis. Arch Intern Med. 2003;163(2):226-30. http://www.ncbi.nlm.nih.gov/pubmed/12546614
Wheeler SW, Wolf SM, Steinberg EA. Cat-scratch encephalopathy. Neurology. 1997;49(3):876-8. http://www.ncbi.nlm.nih.gov/pubmed/9305359
Amano Y, Rumbea J, Knobloch J, Olson J, Kron M. Bartonellosis in Ecuador: serosurvey and current status of cutaneous verrucuous disease. Am J Trop Med Hyg. 1997;57(2):174-79. http://www.ncbi.nlm.nih.gov/pubmed/9288812
Zangwill KM, Hamilton DH, Perkins BA, et al. Cat scratch disease in Connecticut. Epidemiology, risk factors, and evaluation of a new diagnostic test. N Eng J Med. 1993;329(1):8-13. http://www.ncbi.nlm.nih.gov/pubmed/8505963
Arrese Estrada J, Pié rard GE. Dendrocytes in verruga peruana and bacillary angiomatosis. Dermatology. 1992;184(1):22-25. http://www.ncbi.nlm.nih.gov/pubmed/1348435
Holley HP Jr. Successful treatment of cat-scratch disease with ciproflaxin. JAMA. 1991;265(12):1563-5. http://www.ncbi.nlm.nih.gov/pubmed/1999905
Garcia-Caceres U, Garcia FU. Bartonellosis. An immunodepressive disease and the life of Daniel Alcides Carrion. Am J Clin Pathol. 1991; 95(4 Suppl 1):S58-66. http://www.ncbi.nlm.nih.gov/pubmed/2008885
Gray GC, Johnson AA, Thornton SA, et al. An epidemic of Oroya fever in the Peruvian Andes. Am J Trop Med Hyg. 1990;42(3):215-21. http://www.ncbi.nlm.nih.gov/pubmed/2316791
Bogue CW, Wise JD, Gray GF, Edwards KM. Antibiotic therapy for cat-scratch disease? JAMA. 1989;262(6):813-6. http://www.ncbi.nlm.nih.gov/pubmed/2746837
Lea A., Trench Fever. Emedicine. http://emedicine.medscape.com/article/230294-overview. Updated January 12, 2012. Accessed August 13, 2012.
Nervi SJ, Ressner RA, Drayton JR, Kapila R. Catscratch Disease. Emedicine. http://emedicine.medscape.com/article/214100-overview. Updated November 21, 2011. Accessed June 11, 2012.
Davis CP. Cat Scratch Disease (CSD or Cat Scratch Fever). Emedicine. http://www.emedicinehealth.com/cat_scratch_disease/article_em.htm. Accessed June 11, 2012.
Cat scratch disease. MedlinePlus. http://www.nlm.nih.gov/medlineplus/ency/article/001614.htm. Last updated August 24, 2011. Accessed June 11, 2012.
Anderson A, McQuiston J. Bartonella-Associated Infections. Centers for Disease Control and Prevention. http://wwwnc.cdc.gov/travel/yellowbook/2012/chapter-3-infectious-diseases-related-to-travel/bartonella-associated-infections.htm. Updated July 1, 2011. Accessed August 13, 2012.
Cat Scratch Disease (Bartonella henselae Infection). Centers for Disease Control and Prevention. http://www.cdc.gov/healthypets/diseases/catscratch.htm. Last Updated June 23, 2011. Accessed June 11, 2012.
Hammoud KA, Hinthorn DR, Edwards B. Bartonellosis. Emedicine. http://emedicine.medscape.com/article/213169-overview. Updated December 23, 2010. Accessed August 13, 2012.
Report last updated: 2012/09/26 00:00:00 GMT+0