Cat-Scratch Disease in Children
Introduction
Cat-scratch disease (CSD), also known as cat-scratch fever or benign inoculation lymphoreticulosis, is a bacterial infection caused by Bartonella henselae, a gram-negative bacillus. The disease predominantly affects children and adolescents, with a peak incidence between 5 and 9 years of age. CSD is typically transmitted through scratches, bites, or licks from infected cats, which are the primary reservoir for the causative agent.
Epidemiology
CSD is a relatively common disease, with an estimated annual incidence ranging from 3.7 to 12.9 cases per 100,000 population in the United States. The disease is more prevalent in regions with warmer climates, as fleas, which act as vectors for the transmission of B. henselae, thrive in these environments. Additionally, CSD is more common in households with cats, particularly those that are allowed to roam outdoors.
Pathogenesis
The pathogenesis of CSD involves the transmission of B. henselae from infected cats to humans through scratches, bites, or exposure to cat saliva. The bacteria are inoculated into the skin or mucous membranes, where they invade and replicate within endothelial cells and erythrocytes. The resulting inflammation and immune response lead to the formation of lymphadenopathy, the hallmark clinical manifestation of CSD.
Cats acquire B. henselae infection through exposure to infected fleas or flea feces. The bacteria can persist in the cat's bloodstream for prolonged periods, leading to a chronic carrier state. Kittens and immunocompromised cats are particularly susceptible to developing more severe manifestations of the disease, such as fever, lethargy, and anorexia.
Clinical Manifestations
CSD typically presents with a primary lesion at the site of inoculation, followed by regional lymphadenopathy several days to weeks later. The primary lesion may appear as a papule, pustule, or small crusted lesion, and is often overlooked or may have resolved by the time the patient seeks medical attention.
The lymphadenopathy is the most characteristic feature of CSD and is typically unilateral, affecting the lymph nodes draining the area of the primary lesion. The involved lymph nodes are usually tender, firm, and may become matted or suppurative. Systemic symptoms, such as fever, malaise, anorexia, and headache, may also occur.
In some cases, CSD can lead to more severe or atypical manifestations, including:
- Parinaud's oculoglandular syndrome: Conjunctivitis and preauricular lymphadenopathy, resulting from inoculation of the conjunctiva.
- Encephalopathy: Ranging from mild confusion to seizures and coma, affecting 1-7% of patients with CSD.
- Hepatosplenic involvement: Hepatomegaly, splenomegaly, and elevated liver enzymes, occurring in approximately 2% of cases.
- Neuroretinitis: Optic nerve inflammation and visual impairment, a rare complication.
- Osteolytic lesions: Lytic bone lesions, particularly in the skull and long bones, occurring in a small percentage of cases.
Diagnosis
The diagnosis of CSD is based on a combination of clinical presentation, epidemiological factors, and laboratory findings.
Clinical Evaluation
A thorough history, including exposure to cats (particularly kittens), scratches, or bites, should be obtained. Physical examination should focus on identifying the primary lesion, regional lymphadenopathy, and any systemic manifestations.
Laboratory Findings
Laboratory tests can aid in the diagnosis of CSD, but their utility is limited due to the lack of a single definitive test. The following tests may be helpful:
- Complete blood count (CBC): May reveal leukocytosis, predominantly lymphocytosis, and occasionally anemia or thrombocytopenia.
- Serology: Enzyme immunoassays (EIAs) or indirect fluorescent antibody (IFA) tests can detect antibodies against B. henselae. However, antibodies may not be detectable until several weeks after symptom onset, and serologic testing has limited sensitivity and specificity.
- Polymerase chain reaction (PCR): PCR testing for B. henselae DNA can be performed on lymph node aspirates or tissue biopsies, but it is not widely available and has variable sensitivity.
- Histopathology: Lymph node biopsy may show granulomatous inflammation and stellate necrosis, but these findings are not specific for CSD.
In many cases, a presumptive diagnosis is made based on the clinical presentation and exposure history, with laboratory testing playing a supportive role.
Treatment
Most cases of CSD are self-limiting and resolve spontaneously within 2-4 months without specific treatment. However, antibiotic therapy may be considered in certain situations:
- Severe or complicated cases: Antibiotic treatment is recommended for patients with severe lymphadenopathy, systemic symptoms, or atypical manifestations such as encephalopathy, neuroretinitis, or osteolytic lesions.
- Immunocompromised patients: Patients with underlying immunodeficiency or immunosuppression may benefit from antibiotic therapy to prevent disseminated infection.
- Persistent or worsening symptoms: If symptoms persist or worsen after several weeks, antibiotics may be prescribed to hasten recovery.
The recommended antibiotic regimen for CSD is azithromycin or trimethoprim-sulfamethoxazole for 5-10 days. Alternative options include doxycycline, gentamicin, or rifampin. In cases of severe or complicated disease, combination therapy or prolonged antibiotic courses may be required.
Symptomatic treatment, such as warm compresses or drainage of suppurative lymph nodes, may also be necessary in some cases.
Prevention
Preventive measures for CSD focus on reducing the risk of transmission from infected cats and controlling flea infestations. Recommendations include:
- Avoiding rough play with cats, particularly kittens, to minimize the risk of scratches or bites.
- Keeping cats indoors to reduce exposure to fleas and other potential sources of B. henselae.
- Using appropriate flea control measures, such as topical or oral flea prevention products, on household pets.
- Washing hands thoroughly after handling cats or their litter boxes.
- Avoiding contact with feral or stray cats, as they are more likely to harbor B. henselae and have a higher flea burden.
While CSD is generally a self-limiting disease in healthy individuals, prompt diagnosis and appropriate management are crucial, particularly in cases with severe or atypical manifestations.
Differential Diagnosis
The clinical presentation of CSD, particularly the presence of regional lymphadenopathy, can mimic several other infectious and non-infectious conditions. Differential diagnoses to consider include:
- Bacterial lymphadenitis: Caused by other bacterial pathogens, such as Staphylococcus aureus, Streptococcus pyogenes, or Mycobacterium species.
- Viral lymphadenitis: Infectious mononucleosis (caused by Epstein-Barr virus), cytomegalovirus, human immunodeficiency virus (HIV), and other viral infections can present with lymphadenopathy.
- Lymphoma: Lymphoproliferative disorders, such as Hodgkin's and non-Hodgkin's lymphoma, can manifest with lymphadenopathy and constitutional symptoms.
- Tularemia: A bacterial zoonosis caused by Francisella tularensis, which can result in lymphadenopathy and systemic illness.
- Tuberculosis: Both pulmonary and extrapulmonary tuberculosis can involve lymph node enlargement.
- Reactive lymphadenopathy: Non-specific lymph node enlargement due to various infections, autoimmune disorders, or malignancies.
- Sarcoidosis: A granulomatous disease that can present with hilar lymphadenopathy and systemic manifestations.
A thorough clinical evaluation, including exposure history, physical examination, and appropriate laboratory investigations, is essential to distinguish CSD from these differential diagnoses.
Complications
While most cases of CSD resolve without significant complications, some patients may experience more severe or persistent manifestations. Potential complications include:
- Suppurative lymphadenitis: Progression to suppurative or draining lymph nodes, which may require drainage or surgical excision.
- Neurological complications: Encephalopathy, seizures, neuroretinitis, and other neurological manifestations can occur in a small percentage of cases, potentially leading to long-term neurological sequelae.
- Hepatosplenic involvement: Severe hepatic or splenic involvement, although uncommon, can lead to organ dysfunction or failure.
- Osteolytic lesions: Bone lesions, particularly in the skull or long bones, can result in pain, deformity, or pathologic fractures.
- Prolonged illness: In some cases, CSD can persist for several months or even years, leading to chronic fatigue, malaise, and impaired quality of life.
Early recognition and appropriate management of severe or complicated cases are crucial to minimize the risk of long-term complications.
Special Considerations
Immunocompromised Patients
Patients with underlying immunodeficiency or immunosuppression, such as those with HIV/AIDS, organ transplant recipients, or those receiving immunosuppressive therapy, are at increased risk for severe or disseminated CSD. In these individuals, prompt recognition and aggressive antibiotic treatment are recommended to prevent potentially life-threatening complications.
Pregnancy
CSD is generally considered a low-risk infection during pregnancy. However, some studies have suggested an increased risk of adverse pregnancy outcomes, such as preterm delivery and low birth weight, in cases of CSD during gestation. Close monitoring and appropriate management are recommended for pregnant women with CSD.
Epidemiological Considerations
CSD is more prevalent in certain geographical regions, particularly areas with warmer climates that favor flea infestations. Healthcare professionals should maintain a high index of suspicion for CSD in patients presenting with compatible symptoms and epidemiological risk factors, such as residing in or traveling to endemic areas, owning cats, or having occupational exposure to cats (e.g., veterinary workers).
Additionally, understanding the local epidemiology of CSD can aid in tailoring preventive measures and public health strategies to reduce the burden of the disease in the community.
Further Reading
Objective QnA: Cat-Scratch Disease in Children
- What is the causative agent of cat-scratch disease (CSD)?
Bartonella henselae - What is the primary vector for transmitting B. henselae to cats?
Cat fleas (Ctenocephalides felis) - How is cat-scratch disease typically transmitted to humans?
Through scratches, bites, or licks from infected cats - What age group is most commonly affected by cat-scratch disease?
Children and adolescents under 18 years old - What is the typical incubation period for cat-scratch disease?
3-14 days - What is the most common clinical presentation of cat-scratch disease in children?
Regional lymphadenopathy near the site of inoculation - Can cat-scratch disease cause systemic symptoms in children?
Yes, including fever, fatigue, and headache - What percentage of cats carry B. henselae?
Approximately 40% of cats carry the bacteria at some point - Which diagnostic test is considered most reliable for detecting B. henselae?
Polymerase Chain Reaction (PCR) on lymph node tissue or aspirate - Are serological tests useful for diagnosing cat-scratch disease in children?
Yes, but they may have limited sensitivity in early infection - What is the recommended first-line antibiotic treatment for uncomplicated cat-scratch disease in children?
Azithromycin - Is antibiotic treatment always necessary for cat-scratch disease?
No, mild cases may resolve without antibiotic treatment - What is the most common ocular manifestation of cat-scratch disease?
Parinaud oculoglandular syndrome - Can cat-scratch disease cause neurological complications in children?
Yes, including encephalitis, meningitis, and transverse myelitis - What is the typical duration of lymphadenopathy in cat-scratch disease?
2-4 months, but can persist for up to 6-12 months - Can cat-scratch disease cause hepatosplenic involvement in children?
Yes, hepatosplenic abscesses can occur in some cases - What is the role of imaging studies in diagnosing cat-scratch disease?
Ultrasound or CT can help characterize lymph node involvement and detect complications - Can cat-scratch disease be transmitted from person to person?
No, human-to-human transmission has not been documented - What is the significance of immunocompromised status in cat-scratch disease?
Immunocompromised individuals are at risk for more severe and disseminated disease - Can cat-scratch disease cause endocarditis in children?
Rarely, B. henselae can cause culture-negative endocarditis - What is the role of lymph node aspiration in managing cat-scratch disease?
It can be both diagnostic and therapeutic, relieving pain in suppurative nodes - Can cats show symptoms of B. henselae infection?
Most cats are asymptomatic carriers - What is the significance of bacillary angiomatosis in relation to B. henselae?
It's a severe vascular proliferative form of the disease, primarily affecting immunocompromised individuals - How does B. henselae evade the host immune response?
By invading endothelial cells and triggering angiogenesis - What is the impact of cat-scratch disease on school attendance in children?
It can lead to prolonged absences due to persistent lymphadenopathy and fatigue - Can cat-scratch disease cause erythema nodosum in children?
Yes, erythema nodosum is a rare manifestation of cat-scratch disease - What is the role of cat age in the transmission of B. henselae?
Kittens under one year old are more likely to transmit the bacteria - Can cat-scratch disease cause osteomyelitis in children?
Rarely, B. henselae can cause osteomyelitis, typically in the vertebrae or pelvis - What is the significance of granulomatous hepatitis in cat-scratch disease?
It's a rare complication that can occur in systemic infections - How does climate affect the prevalence of cat-scratch disease?
Cases tend to increase in fall and winter, correlating with flea activity and cat breeding seasons
