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originally printed in July 1997 issue
Cat Scratch Disease
Bartonella henselae (formerly Rochalimaea henselae) is a small gram-negative rod, that has recently been identified as the causative agent of Cat Scratch Disease in humans. The organism is zoonotic with the domestic cat as its reservoir. Other Bartonella spp. cause a number of disease in humans including Carrion’s disease (B. bacilliformis) occurring in South America, Trench fever (B. quintana) occurs worldwide, and endocarditis and bacteremia (B. elizabethae). Both B. bacilliformis and B. quintana are transmitted to humans via an arthropod vector.
Disease in Humans
Bacillary Angiomatosis (BA) is a potentially fatal proliferative vascular disease that occurs primarily in immunocompromised people. Proliferative vascular skin lesions are the most commonly reported sign; however, lesions can occur in the bones and bone marrow, gastrointestinal and respiratory tract, lymph nodes and CNS. Fever, weight loss and organomegaly are commonly seen. Cat scratches and bites are risk factors for the disease.
Bacillary Peliosis results from B. henselae infection of the vascular parenchyma occurring in immunocompromised people. Cystic, blood-filled spaces develop in the liver, spleen or lymph nodes. Fever, abdominal pain, GI signs, weight loss and cachexia are seen. Cat scratches or bites are risk factors for the disease.
A Febrile Bacteremia Syndrome occurs secondary to B. henselae bacteremia. Signs in immunocompromized patients, include malaise, fatigue, weight loss and recurring, increasing fevers. In immunocompetent patients signs include persistent or relapsing fevers with arthralgia, myalgia and headaches. Long term asymptomatic persistent bacteremia can develop. Exposure to cats does not appear to be a risk factor for the disease.
Cat Scratch Disease (CSD) is typically a benign, self-limiting disease occurring primarily in young people (less than 18 years old). The classic sign of CSD is regional lymphadenopathy with painful nodes, low grade fever and malaise. Signs typically last up to 2-4 months without antibiotic therapy. A primary cutaneous inoculation lesion at the site of a cat bite or scratch occurs in up to one-half of the cases. Atypical signs of the disease occur in approximately 15% of cases and include Perinauds oculoglandular syndrome, encephalopathy, hepatic granulomas, osteomyelitis, and pulmonary disease.
Epidemiologic studies have indicated that intimate contact with a domestic cat or their fleas is a major risk factor for developing B. henselae-associated diseases. Traumatic injury (bite or scratch) by a cat appears to be the primary route of infection for humans. Bacterial contamination of cat’s claws or saliva (probably obtained from scratching or chewing of flea bites and flea feces by the cat) is suspected to be the source of infection; however, B. henselae has been rarely isolated from cat saliva and claw scraping samples. The role of fleas in the direct transmission of B. henselae from cats to humans is unknown. Humans may inoculate themselves by scratching the flea bite and contaminating the flea bite wound with bacteria-laden flea feces. This mode of arthropod transmission is consistent with other Bartonella diseases.
Disease in cats
Cat fleas appear to be essential for the transmission of B. henselae between cats. Recent work has indicated that fleas are infected by ingesting blood from a positive cat. B. henselae replicates in the flea’s digestive tract and viable organisms are excreted in the flea’s feces. Experimental transmission of B. henselae from bacteremic cats to SPF cats using infected fleas has been demonstrated. Cats are probably infected by inoculating bacteria laden flea feces into a flea bite wound or directly into the skin. Direct cat-to-cat transmission of B. henselae between bacteremic cats and negative cats does not appear to occur without the presence of fleas. Direct cat-to-cat vertical transmission from bacteremic queen to kittens does also not appear to occur. However, kittens born from seropositive queens will be seropositive for B. henselae antibodies up to 40-60 days of age due to maternal derived antibodies.
Disease prevention in humans includes avoiding rough play with cats; handling cats gently to prevent scratches and bites; promptly washing bites or scratches once they occur; preventing cats from licking or coming into contact with open wounds; and washing hands and arms after contact with a cat. In households with children or immunocompromized people, the adoption of stray kittens or cats that are not used to human contact should be avoided. Epidemiologic studies suggest that onychetomy does not reduce the risk of B. henselae infection in humans.
B. henselae usually causes an asymptomatic infection in cats although cats become bacteremic following infection. Regional or generalized lymphadenopathy has been described in experimentally infected cats. Following both experimental and natural infections, cats can remain bacteremic for months to years. In general, high levels of B. henselae (greater than 10,000 CFU/mL blood) are found in the blood of cats during the first few months after infection. With time, the level of bacteremia gradually declines (10 - 1000 CFU/mL) and the cat enters a relapsing bacteremic stage. Experimental studies suggest that cats can mount an immune response and spontaneously clear the infection. At this time it is not know if this is a normal sequalae to infection in all cats. Cats that spontaneously clear the infection appear to be resistant to reinfection. The duration of the resistance is not known.
Epidemiology in cats
B. henselae infections are fairly common in cats. Positive cats have been reported worldwide (US, Canada, Austria, Netherlands, France, Israel, Australia, Japan, Zimbabwe and South Africa) A number of serologic surveys indicate that the prevalence of antibodies to B. henselae on average ranges between 20-30% of cats tested. Regional differences in seroprevalence have been described for the US. Seroprevalence was found the be highest (35-55% of cats tested) in warm or moist areas (southeast and southcentral US, Hawaii, Coastal California and Pacific Northwest). A lower seroprevalence (5-7% of cats tested) was found for colder and drier regions (Alaska, Rocky Mountains, Great Plains, and northern Midwest). Young cats (less than 1 year of age), impounded cats, former stray cats, and cats infested with fleas are more likely to be bacteremic. FIV infected cats do not have a higher prevalence of B. henselae bacteremia.
Identifying infected cats is not easy. The immunoflorescent antibody test indicates exposure to the organism, but is not predictive of bacteremia. Bacteremia has been demonstrated in seronegative cats. Culture of the organism from cat blood is difficult and requires using an enriched non-selective blood agar incubated over a prolonged period (up to 40 - 60 days) in a CO2 atmosphere. Negative cultures do occur due to fluctuations in the level of the organism in the cat’s blood. Four to six negative blood cultures over a 4-6 month period are needed before a cat is considered B. henselae negative.
Prevention and Control
Flea control is essential for prevention of infection in cats. The use of antibiotics to treat infected cats has been proposed, but experimental studies have produced conflicting results. In one study, treatment of experimentally infected cats with enrofloxacin (0.6mg/kg q12h) and amoxicillin (2.3-4.5mg/kg q8h) appear to have no effect on the level or duration of bacteremia; whereas erythromycin (2.3-4.5mg/kg q8h) and tetracycline (11.4mg/kg q4h) resulted in a decrease in the level and duration of bacteremia when compared to untreated controls. In an uncontrolled study, treatment with doxycycline (50mg/cat (7.3-21.7mg/kg ) q12h) cleared the organism in 4 of 8 experimentally infected cats. Subsequent treatment of the remaining 4 bacteremic cats with amoxicillin (18.5-43.5 mg/kg q12h) or amoxicillin-clavulanate (23.5mg/kg q8h) resulted in elimination of the bacteremia. It should also be noted that differences in the level of bacteremia in cats was also observed between the two studies, with cats in the first study having 10-100 fold higher levels of organism in their blood. To date, no antibiotic therapy has be found that uniformly clears B. henselae infection in cats.
-- by Michael Coyne VMD
References:
1. Abbot RC, Chomel BB, Kasten RW, et al. 1997. Experimental and natural infection with Bartonella henselae in domestic cats. Comp Immun Microbiol Infec Dis 20:41-51.
2. Chomel BB, Abbot RC, Kasten RW, et al. 1995. Bartonella henselae prevalence in domestic cats in California: Risk factors and association between bacteremia and antibody titers. J Clin Microbiol 33:2445-2450.
3. Chomel BB, Kasten RW, Floyd-Hawkins K, et al. 1996. Experimental transmission of Bartonella henselae by the cat flea. J Clin Microbiol 34:1952-1956.
4. Greene CE, McDermott M, Jameson PH, et al. 1996. Bartonella henselae infection in cats: Evaluation during primary infection, treatment, and rechallenge infection. J Clin Microbiol 34:1682-1685.
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9. Kordick DL, Wilson KH, Sexton DJ, et al. 1995. Prolonged Bartonella bacteremia in cats associated with Cat-Scratch Disease patients. J Clin Microbiol 33: 3245-3251.
10. Regnery R, Tappero J. 1995. Unraveling mysteries associated with Cat-Scratch Disease, Bacillary Angiomatosis, and related syndromes. Emerging Infectious Diseases 1:16-21.
11. Regnery RL, Rooney JA, Johnson AM, et al. 1996. Experimentally induced Bartonella henselae infections followed by challenge exposure and antimicrobial therapy in cats. AJVR 57:1714-1719.
12. Ueno H, Hohdatsu T, Yasukazu M, et al. 1996. Does coinfection of Bartonella henselae and FIV induce clinical disorders in cats? Microbiol Immunol 40:617-620.