| Cat scratch disease | |
|---|---|
| Other names | Cat-scratch fever, felinosis, Teeny's disease, inoculation lymphoreticulosis, subacute regional lymphadenitis[1] |
 | |
| An enlarged lymph node in the armpit region of a person with cat-scratch disease, and wounds from a cat scratch on the hand. | |
| Specialty | Infectious disease |
| Symptoms | Bump at the site of the bite or scratch, swollen and painful lymph nodes[2] |
| Complications | Encephalopathy,parotitis,endocarditis,hepatitis[3] |
| Usual onset | Within 14 days after infection[2] |
| Causes | Bartonella henselae from a cat bite or scratch[2] |
| Diagnostic method | Based on symptoms, blood tests[3] |
| Differential diagnosis | Adenitis,brucellosis,lymphogranuloma venereum,lymphoma,sarcoidosis[3] |
| Treatment | Supportive treatment,azithromycin[2][3] |
| Prognosis | Generally good, recovery within 4 months[3] |
| Frequency | 1 in 10,000 people[3] |
Cat-scratch disease (CSD) is aninfectious disease that most often results from a scratch or bite of acat.[4] Symptoms typically include a non-painful bump or blister at the site of injury and painful and swollenlymph nodes.[2] People may feel tired, have a headache, or afever.[2] Symptoms typically begin within 3–14 days following infection.[2]
Cat-scratch disease is caused by thebacteriumBartonella henselae which is believed to be spread by the cat's saliva.[2] Young cats pose a greater risk than older cats.[3] Occasionally dog scratches or bites may be involved.[3] Diagnosis is generally based on symptoms.[3] Confirmation is possible by blood tests.[3]
The primary treatment issupportive.[3]Antibiotics speed healing and are recommended in those with severe disease or immune problems.[2][3] Recovery typically occurs within 4 months but can require a year.[3] About 1 in 10,000 people are affected.[3] It is more common in children.[4]
Cat-scratch disease commonly presents as tender, swollen lymph nodes near the site of the inoculating bite or scratch or on the neck, and is usually limited to one side. This condition is referred to as regionallymphadenopathy and occurs 1–3 weeks after inoculation.[5] Lymphadenopathy most commonly occurs in theaxilla,[6] arms, neck, or jaw, but may also occur near the groin or around the ear.[4] Avesicle or anerythematouspapule may form at the site of initial infection.[4]
Most people also develop systemic symptoms such asmalaise,decreased appetite, and aches.[4] Other associated complaints includeheadache,chills,muscular pains,joint pains,arthritis,backache, and abdominal pain. It may take 7 to 14 days, or as long as two months, for symptoms to appear. Most cases arebenign and self-limiting, butlymphadenopathy may persist for several months after other symptoms disappear.[4] The disease usually resolves spontaneously, with or without treatment, in one month.
In rare situations, CSD can lead to the development of serious neurologic or cardiacsequelae such asmeningoencephalitis,encephalopathy,seizures, orendocarditis.[4] Endocarditis associated withBartonella infection has a particularly high mortality.[5]Parinaud's oculoglandular syndrome is the most common ocular manifestation of CSD,[4] and is a granulomatousconjunctivitis with concurrent swelling of the lymph node near the ear.[7]Optic neuritis or neuroretinitis is one of the atypical presentations.[8]
People who areimmunocompromised are susceptible to other conditions associated withB. henselae andB. quintana, such asbacillary angiomatosis orbacillary peliosis.[4] Bacillary angiomatosis is primarily a vascular skin lesion that may extend to bone or be present in other areas of the body. In the typical scenario, the patient hasHIV or another cause ofsevere immune dysfunction.Bacillary peliosis is caused byB. henselae that most often affects people with HIV and other conditions causing severe immune compromise. Theliver andspleen are primarily affected, with findings of blood-filled cystic spaces on pathology.[9]
Bartonella henselae is afastidious,[5] intracellular,Gram-negative bacterium.
The cat was recognized as thenatural reservoir of the disease in 1950 by Robert Debré.[5]Kittens are more likely to carry thebacteria in theirblood, so may be more likely to transmit the disease than adult cats.[10] However, fleas serve as avector for transmission ofB. henselae among cats,[5] and viableB. henselae are excreted in the feces ofCtenocephalides felis, the cat flea.[11] Cats could be infected withB. henselae through intradermal inoculation using flea feces containingB. henselae.[12]
As a consequence, a likely means of transmission ofB. henselae from cats to humans may be inoculation with flea feces containingB. henselae through a contaminated cat scratch wound or by cat saliva transmitted in a bite.[5]Ticks can also act as vectors and occasionally transmit the bacteria to humans.[4] Combined clinical and PCR-based research has shown that other organisms can transmit Bartonella, including spiders.[13][14] CrypticBartonella infection may be a much larger problem than previously thought, constituting an unrecognized occupational health hazard of veterinarians.[15]
The best diagnostic method available ispolymerase chain reaction, which has a sensitivity of 43-76% and a specificity (in one study) of 100%.[5] TheWarthin–Starry stain can be helpful to show the presence ofB. henselae, but is often difficult to interpret.B. henselae is difficult to culture and can take 2–6 weeks to incubate.[5]
Cat-scratch disease is characterized by granulomatous inflammation on histological examination of the lymph nodes. Under the microscope, the skin lesion demonstrates a circumscribed focus of necrosis, surrounded byhistiocytes, often accompanied by multinucleated giant cells,lymphocytes, andeosinophils. The regional lymph nodes demonstrate follicularhyperplasia with central stellate necrosis withneutrophils, surrounded by palisading histiocytes (suppurativegranulomas) and sinuses packed with monocytoidB cells, usually without perifollicular and intrafollicular epithelioid cells. This pattern, although typical, is only present in a minority of cases.[16]
Cat-scratch disease can be primarily prevented by taking effectiveflea control measures; since cats are mostly exposed to fleas when they are outside, keeping cats inside can help prevent infestation. Strictly-indoor cats without exposure to indoor-outdoor animals are generally at negligible risk of infestation.[17] Cats which are carrying the bacterium,B. henselae, are asymptomatic,[18] thus thoroughly washing hands after handling a cat or cat feces is an important factor in preventing potential cat-scratch disease transmission from possibly infected cats to humans.[17]
Most healthy people clear the infection without treatment, but in 5 to 14% of individuals, the organisms disseminate and infect the liver, spleen, eye, or central nervous system.[19] Although some experts recommend not treating typical CSD in immunocompetent people with mild to moderate illness, treatment of all people with antimicrobial agents (Grade 2B) is suggested due to the probability of disseminated disease. The preferred antibiotic for treatment isazithromycin, since this agent is the only one studied in a randomized controlled study.[20]
Azithromycin is preferentially used in pregnancy to avoid theteratogenic side effects ofdoxycycline.[21] However, doxycycline is preferred to treatB. henselae infections with optic neuritis due to its ability to adequately penetrate the tissues of the eye andcentral nervous system.[5]
Cat-scratch disease has a worldwide distribution, but it is a nonreportable disease in humans, so public health data on this disease are inadequate.[22] Geographical location, present season, and variables associated with cats (such as exposure and degree offlea infestation) all play a factor in the prevalence of CSD within a population.[23] In warmer climates, the CSD is more prevalent during the fall and winter,[23] which may be attributed to the breeding season for adult cats, which allows for the birth of kittens.[23] B henselae, the bacterium responsible for causing CSD, is more prevalent in younger cats (less than one year old) than it is in adult cats.[22]
To determine recent incidence of CSD in the United States, the Truven Health MarketScan Commercial Claims and Encounters database was analyzed in a case control study from 2005 to 2013.[24] The database consisted of healthcare insurance claims for employees, their spouses, and their dependents. All participants were under 65 years of age, from all 50 states. The length of the study period was 9 years and was based on 280,522,578 person-years; factors such as year, length of insurance coverage, region, age, and sex were used to calculate the person-years incidence rate to eliminateconfounding variables among the entire study population.[24]
A total of 13,273 subjects were diagnosed with CSD, and both in- and outpatient cases were analyzed. The study revealed an incidence rate of 4.5/100,000 outpatient cases of cat-scratch disease. For inpatient cases, the incidence rate was much lower at 0.19/100,000 population.[24] Incidence of CSD was highest in 2005 among outpatient cases and then slowly declined. The Southern states had the most significant decrease of incidence over time. Mountain regions have the lowest incidence of this disease because fleas are not commonly found in these areas.[24]
Distribution of CSD among children aged 5–9 was of the highest incidence in the analyzed database, followed by women aged 60–64. Incidence among females was higher than that among males in all age groups.[24] According to data on social trends, women are more likely to own a cat over men;[25] which supports higher incidence rates of this disease in women. Risk of contracting CSD increases as the number of cats residing in the home increases.[22] The number of pet cats in the United States is estimated to be 57 million.[23] Due to the large population of cats residing in the United States, the ability of this disease to continue to infect humans is vast. Laboratory diagnosis of CSD has improved in recent years, which may support an increase in incidence of the disease in future populations.[23]
Historically, the number of reported cases of CSD has been low, there has been a significant increase in reports in urban and suburban areas in the northeast region of United States. An example of the increased incidence can be found in Essex County, New Jersey. In 2016, there were 6 reported cases. In 2017, there were 51 reported cases. In 2018, there were 263 reported cases. Although usually treated with antibiotics and minimal long-term effects, there have been 3 reported case of tachycardia more than one year after exposure.[26]
Symptoms similar to CSD were first described byHenri Parinaud in 1889, and the clinical syndrome was first described in 1950 byRobert Debré.[27][5] In 1983, theWarthin-Starry silver stain was used to discover a Gram-negative bacillus which was namedAfipia felis in 1991 after it was successfully cultured and isolated. The causative organism of CSD was originally believed to beAfipia felis, but this was disproved by immunological studies in the 1990s demonstrating that people with cat-scratch fever developed antibodies to two other organisms,B. henselae (originally known asRochalimea henselae before the generaBartonella andRochalimea were combined) andB. clarridgeiae, which is arod-shapedGram-negative bacterium.[5]
