Catscratch Disease Medication
- Author: Stephen J Nervi, MD; Chief Editor: Michael Stuart Bronze, MD more...
In general, treatment beyond analgesia and recommendation for warm compresses is unnecessary for patients with catscratch disease (CSD) because the condition spontaneously resolves without sequelae in most cases.
Currently, only limited and/or anecdotal evidence supports the use of antibiotics in the treatment of typical CSD in immunocompetent hosts. Bartonella henselae is susceptible to many antibiotics in vitro. However, the susceptibility patterns do not predict efficacy in vivo. Bartonella is an intracellular bacterium and responds poorly to penicillin derivatives in vivo despite susceptibility in vitro.
A single treatment for all Bartonella -related diseases has not been identified, so treatment must be tailored to specific situations. Immunocompromised patients tend to develop more-severe Bartonella infections and may require prolonged antibiotic treatment.
Some patients, usually ones who are immunocompromised, develop a Jarisch-Herxheimer–like reaction shortly after receiving antibiotic therapy.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. These agents reduce the duration of lymphadenopathy and decrease constitutional symptoms. B henselae, a gram-negative bacillus, is sensitive to various antibiotics in vitro. Few clinical studies are available, but not all of the antibiotics to which the organism is sensitive in vitro are effective in vivo.
This agent inhibits RNA-dependent protein synthesis at the chain elongation step. It Acts by binding to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected.
Azithromycin concentrates in phagocytes and fibroblasts, as demonstrated by in vitro incubation techniques. In vivo studies suggest that concentration in phagocytes may contribute to drug distribution to inflamed tissues.
This agent treats mild-to-moderate microbial infections. Plasma concentrations are very low but tissue concentrations are much higher, giving it value in treating intracellular organisms. It has a long tissue half-life.
Doxycycline inhibits protein synthesis by binding with the 30S and possibly the 50S ribosomal subunit(s) of susceptible bacteria; may also cause alterations in the cytoplasmic membrane.
Ciprofloxacin is a fluoroquinolone with activity against pseudomonads, streptococci, methicillin-sensitive Staphylococcus aureus (MSSA), S epidermidis, and most gram-negative organisms. It has no activity against anaerobes. This agent inhibits bacterial DNA gyrase and consequently growth; it inhibits relaxation of supercoiled DNA and promotes breakage of double-stranded DNA. Continue treatment for at least 2 d after signs and symptoms have disappeared (7-14 d typically).
Rifampin inhibits bacterial RNA synthesis by binding to the beta subunit of DNA-dependent RNA polymerase, blocking RNA transcription.
Erythromycin inhibits RNA-dependent protein synthesis at the chain elongation step; it binds to the 50S ribosomal subunit, resulting in blockage of transpeptidation.
Gentamicin is an aminoglycoside antibiotic for gram-negative coverage. This agent binds bacterial 30S and 50S ribosomal subunits. It is used in combination with both an agent against gram-positive organisms and an agent that covers anaerobes.
Gentamicin is not the drug of choice for CSD. Consider using it if penicillins or other less toxic drugs are contraindicated, when clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms.
Dosing regimens are numerous; adjust dose based on creatinine clearance (CrCl) and changes in volume of distribution. Gentamicin may be given IV or IM. Follow each regimen by at least a trough level drawn on the third or fourth dose (0.5 h before dosing); a peak level may be drawn 0.5 h after 30-min infusion.
This combination agent inhibits bacterial growth by inhibiting dihydrofolate reductase, depleting folic acid. Its antibacterial activity includes common urinary tract pathogens, except Pseudomonas aeruginosa.
Clarithromycin is a semisynthetic macrolide antibiotic that reversibly binds to P site of 50S ribosomal subunit of susceptible organisms. It may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl t-RNA from ribosomes, causing bacterial growth inhibition.
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|Sign or Symptom||Percentage, %||Average Duration, d|
|Fever >101°F (38.3°C)||32-60||6|
|Anorexia, weight loss, emesis||14||5|
n = 1174, %
n = 1200, %
|Inoculation lesion (skin, eye, mucous membrane)||58.6|
|Parinaud oculoglandular syndrome||6.3||4|
|Systemic disease, severe, chronic||2|
500 PO bid
|"Dramatic improvement" in a few days; defined as resolution of symptoms (ie, malaise and pain)||Holley|
5 mg/kg/d IV/IM
3 febrile children; 2 with hepatitis, 1 with painful regional lymphadenopathy
|Resolution of fever and systemic symptoms in 1-2 days||Bogue et al|
6-8 mg TMP/kg/d PO
|Uncontrolled retrospective study
60 patients with prolonged fever and systemic symptoms
|58% effective, 7-day course (see above)||Margileth|
|Rifampin 10-20 mg/kg/d PO/IV||Uncontrolled retrospective study
60 patients with prolonged fever and systemic symptoms
|87% effective, 7- to 14-day course (see above)||Margileth|
500 mg PO qd for 1 day, then 250 mg PO qd for 4 days
|Prospective placebo-controlled, double-blind study
|80% of lymph node volume (as measured by ultrasonography) resolved in 30 days in 7 of 15 patients on azithromycin vs 1 of 15 control patients||Bass et al|