Cat scratch disease (CSD), also known as subacute regional lymphadenitis or cat scratch fever, is a common bacterial infection caused by Bartonellahenselae. As one may deduce, infected cats are disease vectors and transmit the bacteria, which is found in their saliva via bites or scratches. It is estimated that up to 50 percent of cats may be carriers of the microorganism responsible for CSD and these cats may show no signs of infection.
Occasionally, fleas which are responsible for spreading the infection from one cat to another may also transmit the disease to people. In addition to fleas, bites from infected ticks may also lead to disease transmission.
The first description of CSD may have been as early as 1889 by Henri Parinaud, who observed enlargement of the preauricular lymph nodes with conjunctivitis. However, he did not make any association of his findings with cats and the clinical oculoglandular syndrome was only seen to be present in a small number of patients with CSD.
In 1931, doctors Debre and Semelaigne observered a young boy with cat scratches and a suppurating adenitis who tested negative for tuberculosis. This finding led them to search for a possible link to a feline transmitted disease.
While they were unable to find a link bacteriologically, they observed several more similar cases within their pediatric population. They made notes accordingly while trying to rule out other differential diagnoses such as infectious mononucleosis.
In 1951, the first report of CSD was published in American literature by Greer and Keefer. In their report, they were able to describe a broad spectrum of the clinical manifestations of the disease, which led to further investigations into CSD. The microorganism implicated in CSD was first successfully isolated and cultured in 1988.
Ultimately, the discovery of the etiologic agent for CSD and its classification was considered a great success of contemporary microbiology. This allowed for understanding its pathogenesis and developing effective means to diagnose, manage, and prevent it.
The clinical hallmark of CSD is lymphadenopathy near the site of inoculation. The small gram-negative, fastidious, and pleomorphic intracellular bacilli that cause CSD may lead to a granulomatous or vasculoproliferative immunological response in immunocompetent or immunocompromised individuals, respectively. Infected lymph nodes typically become tender and enlarged within 1 – 2 weeks of inoculation.
CSD is a very common cause of chronic adenopathy in adolescents and children. In addition to the lymphatic system, CSD may also affect the central nervous system (CNS). Its most common neurological presentation is encephalopathy, seen most in adults as opposed to children.
While the incidences of CSD is unknown globally, it has been observed to have a higher prevalence in regions with humid and warm climates. Regions in temperate zones tend to see an increase in cases during the autumn and winter months, while those in tropical areas do not show such season variation in disease frequency.
The rates of infection between males to females may vary, but males may have a slightly greater incidence, possibly due to being more prone to injury from rough play with cats and increased risk of exposure. Moreover, the incidence is higher in children and adolescents as opposed to adults due to the greater likelihood of exposure.