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SADAT CITY UNIVERSITY
FACULTY OF VETRINARY MEDICINE
ZOONOSES DEPT
CAT SCRATCH DISEASE
“ C S D ”
CAT SCRATCH DISEASE
“ C S D ”
PREPARED BY :-
Dr / AHMED ABDEL_RAHMAN
MOHAMED ESMAIL
Well you might just want to take a step back……
Cat Scratch Fever/Disease
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.
The Organism
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 .
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
History
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
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
Epidemiology
EPIDEMIOLOGY
 Worldwide distribution
Prevalence in warm/humid climates
 ~ 20,000 cases annually in US
80% under the age of 20yrs
 30% of domestic cats are infected
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)
Transmission
Cat contact
(scratch, bite,
? cat flea bite)
1 - 3 weeks
Resolution
in weeks to
months
Dissemination
in immuno-
compromised
hosts
Human Infections
 Vascular endothelial cells
Monocytes/macrophages
 Immunocompenent host
Self-limiting CSD
Swollen lymph nodes and fever
 Immunocompromised host
Bacilliaryangiomatosis-peliosis (BAP)
Tumour-like vasoproliferative lesions
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
Cat-scratch disease
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.
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
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
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
Cat Scratch Disease:
Complications
 Parinaud’s oculoglandular
syndrome
 Encephalitis
 Endocarditis
 Disseminated disease
 AIDS patients
 Rashes
 Bone/joint lesions
 Pneumonia
Disease in Animals
Species Affected
 Cats, felids are
reservoir hosts
 Experimental infection
 Dog
 Armadillo
 Mice
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
Disease in Other Animals
 Experimental infections
 Dogs
 No bacteremia
 Rodents
 Asymptomatic
 Granulomatous hepatitis
 Non-human primates
 Asymptomatic
 Fever
 Subcutaneous skin lesions at inoculation site
Post Mortem Lesions
 Lymphadenomegaly
 Multiple histopathologic lesions
 Blood-filled cysts and cavities
in the liver Peliosis hepatitis
 Granulomatous hepatitis
Diagnosis
 Diagnosis
Culture
Time consuming, used mainly in
research
Serology
Cross reactions possible
PCR
Cure
Usually the
disease does not
need medical
treatment, but in
severe cases
treatment with
antibiotics such
as azithromycin
can be helpful.
Prevention
 Avoid bites and scratches
 Kittens
 Wash wounds
immediately
 Flea control?
 Clip nails
 Keep cats indoors
 Antimicrobials?
Disinfection
 Susceptibility of B. henselae not
specifically known
 Closely related organism B. bacilliformis
 Susceptible to:
 70% ethanol
 1% sodium hypochlorite
 2% formaldehyde
Cat scratch disease

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Cat scratch disease

  • 1. SADAT CITY UNIVERSITY FACULTY OF VETRINARY MEDICINE ZOONOSES DEPT CAT SCRATCH DISEASE “ C S D ”
  • 3. PREPARED BY :- Dr / AHMED ABDEL_RAHMAN MOHAMED ESMAIL
  • 4.
  • 5. Well you might just want to take a step back……
  • 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
  • 15. EPIDEMIOLOGY  Worldwide distribution Prevalence in warm/humid climates  ~ 20,000 cases annually in US 80% under the age of 20yrs  30% of domestic cats are infected
  • 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)
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  • 19. Cat contact (scratch, bite, ? cat flea bite) 1 - 3 weeks Resolution in weeks to months Dissemination in immuno- compromised hosts
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  • 21. Human Infections  Vascular endothelial cells Monocytes/macrophages  Immunocompenent host Self-limiting CSD Swollen lymph nodes and fever  Immunocompromised host Bacilliaryangiomatosis-peliosis (BAP) Tumour-like vasoproliferative lesions
  • 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.
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  • 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
  • 29. Cat Scratch Disease: Complications  Parinaud’s oculoglandular syndrome  Encephalitis  Endocarditis  Disseminated disease  AIDS patients  Rashes  Bone/joint lesions  Pneumonia
  • 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
  • 35. Diagnosis  Diagnosis Culture Time consuming, used mainly in research Serology Cross reactions possible PCR
  • 36. Cure Usually the disease does not need medical treatment, but in severe cases treatment with antibiotics such as azithromycin can be helpful.
  • 37. Prevention  Avoid bites and scratches  Kittens  Wash wounds immediately  Flea control?  Clip nails  Keep cats indoors  Antimicrobials?
  • 38. Disinfection  Susceptibility of B. henselae not specifically known  Closely related organism B. bacilliformis  Susceptible to:  70% ethanol  1% sodium hypochlorite  2% formaldehyde