7. About Disease
Cat scratch disease
is a disease caused
by bartonella
bacteria. It is
believed to be
transmitted by cat
scratches and bites,
or exposure to cat
saliva.
9. MORPHOLOGY
B. henselae is a small Gram negative bacillus measuring
2.0-2.5 X 0.5-0.6µ.
Like other Bartonella species, it can grow on chocolate
agar or Columbia agar supplemented with 5% sheep or
rabbit blood.
B. henselae produces 2 morphological types of
colonies:
1. Irregular, raised,rough, dry white cauliflower-like
colonies.
2. Small, circular, tan & moist, tending to pit the agar
and adhere to the agar after 5-15 days of incubation at
35-37°C in the presence of 5% CO 2 .
10. Presence of B. henselae )
arrow) within naturally
infected cat erythrocytes,
as seen by confocal
microscopy.
Natural History of
Bartonella Infections (an
Exception to Koch’s
Postulate) CVI, 2002
12. History
1950: Clinical syndrome described
1889: Similar disease reported
1983: Bacterial cause described
Gram negative bacillus
Found in lymph nodes of patients
1988: Organism successfully
isolated and cultured
13. History
1991: CSD bacillus named Afipia felis
1992: Rochalimaea henselae isolated
Patients with bacillary angiomatosis
Refuted role of A. felis in CSD
1993: Genera Rochalimaea
and Bartonella united
B. henselae currently recognized
as causative agent of CSD
16. Geographic Distribution
Worldwide
B. henselae type I
Eastern U.S.
Asia
B. henselae type II
Europe
Temperate climates
Seasonal variation
Peak August to October (North)
22. Symptoms
Bump (papule) or blister (pustule) at
site of injury (usually the first sign
occurs 3-10 days after infected)
Fatigue
Fever (in some patients)
Headache
Lymph node swelling near the scratch
or bite (occurs 1 to 4 weeks after
infected)
Overall discomfort (malaise)
Less common symptoms:
Draining lymph nodes'
Enlarged spleen
Loss of appetite
Sore throat
Weight loss
24. Worst Case Scenario
It is usually worse with
those who have weaker
immune systems and those
with AIDS. Also with
younger children symptoms
can be worse. Causing
bigger bumps, lymph nodes
to swell bigger, wider
spread of lesions, and
sometimes bumps can
appear on eyes (Parinaud
oculoglandular syndrome).
Plus an inflammation of the
brain can occur causing
seizures. In any of these
cases it is recommended to
take antibiotics.
25.
26. PATHOGENESIS
Endothelial Cell Invasion and
Colonization:
Human umbilical endothelial cells (HUVECs)
Bacterial adhesion and invasion
Actin-dependant mechanisms
Intracellular membrane-bound compartments
B. henselaeinfection leads to:
Secretion of vascularproliferative compounds
Inhibition of host cell apoptosis
Host cell proliferation
27. Morbidity and Mortality
Humans
22,000 to 24,000 annual cases in U.S.
3 to 6% of general
population seropositive
Higher in veterinarians
Most cases in children
Most infections self-limiting
Death is rare
28. Morbidity and Mortality
Seroprevalence in cats
14 to 55% in U.S.
40 to 70% in warm, humid climates
30% of captive wild felids
Higher in feral cats vs. pets
No reported morbidity or mortality
31. Species Affected
Cats, felids are
reservoir hosts
Experimental infection
Dog
Armadillo
Mice
32. Feline Infections
Erythrocytes
Firm bacterial adhesion
Internalization
Membrane-bound compartments
Bacteria replicate within erythrocytes
Circulate in the bloodstream (weeks to months)
Long-lasting intraerythrocytic infection
Specific adaption to the mode of
transmission
33. Disease in Other Animals
Experimental infections
Dogs
No bacteremia
Rodents
Asymptomatic
Granulomatous hepatitis
Non-human primates
Asymptomatic
Fever
Subcutaneous skin lesions at inoculation site
34. Post Mortem Lesions
Lymphadenomegaly
Multiple histopathologic lesions
Blood-filled cysts and cavities
in the liver Peliosis hepatitis
Granulomatous hepatitis
38. Disinfection
Susceptibility of B. henselae not
specifically known
Closely related organism B. bacilliformis
Susceptible to:
70% ethanol
1% sodium hypochlorite
2% formaldehyde
