Thanks for the updates. Your posts could very well help other folks in a similar situation now or in the future. It's reassuring to know you have access to doctors who are doing their best to figure things out.
It sounds like the immunologist you saw is erring on the side of caution by recommending you discontinue the Keflex instead of further challenging your body (which is already dealing with more than enough).
As you mentioned previously, there are times when it is virtually impossible for patients and their doctor(s) to tell the difference between a temporary reaction to a medication (which may signal it is working) or an adverse reaction that could potentially get worse with continued use. A true allergic reaction isn't always that easy to spot either because the spectrum includes everything from a slightly annoying rash to life-threatening anaphylactic shock.
Cephalexin (Keflex) is a first generation cephalosporin, whereas Ceftriaxone (Rocephin) is a third generation cephalosporin, and this apparently makes a difference.
http://www.uic.edu/pharmacy/courses/pmp ... orins.html
VI. FIRST GENERATION CEPHALOSPORINS
SPECTRUM OF ACTIVITY. Gram-positive aerobic cocci: Very active against Streptococci pyogenes (Group A strep), Streptococcus agalactiae (Group B strep), viridans streptococci. Methicillin-resistant Staphylococci, Enterococci, penicillin-resistant Streptococcus pneumoniae are resistant.
Gram-negative aerobes: Commonly active against Escherichia coli, Proteus mirabilis, and Klebsiella pneumoniae, though susceptibilities may vary. Inadequate activity against Moraxella catarrhalis and Hemophilus influenzae.
Anaerobes: Active against most penicillin-susceptible anaerobes found in the oral cavity, except those belonging to the Bacteroides fragilis group.
GENERAL CLINICAL USES. Uncomplicated, community-acquired infections of the skin and soft tissue and urinary tract. Useful for respiratory tract infections caused by pencillin-sensitive Streptococcus pneumoniae but not for Hemophilus influenzae and Moraxella catarrhalis. While effective for these infections, other less expensive alternatives should be used when appropriate because of their efficacy and narrower spectrum of activity (eg: penicillins, trimethoprim/sulfamethoxazole). Parenteral 1st generation agents are used for surgical wound prophylaxis.
VI. THIRD GENERATION CEPHALOSPORINS
Improved activity against Enterobacteriaceae associated with hospital-acquired infections; some agents are also active against Pseudomonas aeruginosa which is a frequent cause of hospital-acquired pneumonia.
SPECTRUM OF ACTIVITY. Gram-positive aerobic cocci: Cefotaxime, ceftriaxone, and ceftizoxime are active against methicillin-susceptible Staphylococcus aureus (though less than 1st and some 2nd generation agents), very active against Groups A and B streptococci, and viridans streptococci. Cefotaxime and ceftriaxone are more active than ceftizoxime against Streptococcus pneumoniae, particularly intermediately-penicillin resistant Streptococcus pneumoniae. None are active against methicillin-resistant Staphylococci, Enterococci, and Listeria monocytogenes.
Gram-negative aerobes: Very active against Hemophilus influenzae, Moraxella catarrhalis, Neisseria meningitidis, and Enterobacteriaceae (eg: Escherichia coli, Klebsiella species, Proteus mirabilis, Providencia)found in hospital and community-acquired infections. Some Enterobacter species have a tendency to become resistant during cephalosporin therapy, and thus cephalosporins are not the drugs of choice for Enterobacter infections.
Only and ceftazidime and cefoperazone are active against Pseudomonas aeruginosa, and ceftazidime is preferred because it is more potent than cefoperazone against gram-negative bacteria.
Anaerobes: Cefotaxime, ceftriaxone, and ceftizoxime are adequate for oral anaerobes.
GENERAL CLINICAL USES. For infections involving gram-negative bacteria, particularly hospital-acquired infections or complicated community-acquired infections of the respiratory tract, blood, intra-abdominal, skin and soft tissue, and urinary tract. Because of their activity includes the aerobic gram negative bacteria covered by aminoglycosides, they may be an alternative to aminoglycosides in some patients with renal dysfunction.
The clinical situations requiring use of 3rd generation cephalosporins are likely to be encountered in patients who are hospitalized, have recently received antibiotics, or are immunocompromised.
A. Cefotaxime (Claforan), Ceftriaxone (Rocephin), Ceftizoxime (cefizox) . IV/IM formulations. Activity against Enterobacteriaceae (eg: Escherchia coli, Klebsiella pneumoniae) are similar. None are active against Pseudomonas aeruginosa. Only cefotaxime and ceftriaxone achieve adequate drug levels in the cerebral spinal fluid to constitute reliable empiric therapy for bacterial meningitis. Ceftriaxone is eliminated to a significant degree by the biliary system, and as a result, biliary pseudo-lithiasis has been reported as a side effect of this agent.
The following article abstract explains why cephalexin (Keflex) is not recommended for the treatment for Lyme disease:
Arch Fam Med. 2000 Jun;9(6):563-7.
Failure of treatment with cephalexin for Lyme disease.
Nowakowski J1, McKenna D, Nadelman RB, Cooper D, Bittker S, Holmgren D, Pavia C, Johnson RC, Wormser GP.
1Division of Infectious Diseases, Westchester Medical Center, New York Medical College, Valhalla, USA.
Lyme disease typically presents with a skin lesion called erythema migrans (EM), which though often distinctive in appearance may be confused with cellulitis. The first-generation cephalosporin, cephalexin monohydrate, is effective for treating bacterial cellulitis but has not been recommended or studied for treating Lyme disease because of poor in vitro activity.
To describe the outcome of patients with EM who were treated with cephalexin.
PATIENTS AND METHODS:
Patients presenting with EM to the Lyme Disease Diagnostic Center in Westchester, NY (May 1992-September 1997). A 2-mm punch biopsy specimen of the leading edge of the EM lesion and/or blood was cultured for Borrelia burgdorferi.
Eleven (2.8%) of 393 study patients had been initially treated with cephalexin prior to our evaluation; 9 (82%) were originally diagnosed with cellulitis. Cephalexin was administered for 8.6 days (range, 2-21 days) prior to presentation. All 11 patients had clinical evidence of disease progression, including 8 whose rash enlarged, 2 who developed seventh-nerve palsy (1 with new EM lesions), and 1 who developed new EM lesions. Borrelia burgdorferi grew in cultures from 5 patients despite a mean of 9.8 days of treatment with cephalexin (range, 5-21 days).
Cephalexin should not be used to treat early Lyme disease and should be prescribed with caution during the summer months for patients believed to have cellulitis in locations where Lyme disease is endemic.
[PubMed - indexed for MEDLINE]
My guess is that the precise reason(s) for the flare in symptoms experienced by Lyme disease patients prescribed Keflex (yourself included) may never be known with any certainty -- and especially since the reason(s) could well vary from person to person.
I think it's worth noting that people react differently to medications for a variety of reasons, further complicating matters:
Definition : "Study of hereditary sources of variation in drug response, their prevalence and mechanism."
Patients vary widely in their responses to drugs. Important factors in variability are drug metabolism and drug transport. Interindividual variation of drug metabolism is due to several factors. Genetic polymorphism is one of them and is defined by the presence, in a normal population, of monogenic traits that exist in at least two phenotypes, neither of which is rare (less than 1%).
Genetic polymorphism of metabolic enzymes may be due to:
- Allelic variants that lead to enzymes with different catalytic activities from that of the wild type form.
- Gene suppression.
- Gene duplication.
- Modification in gene inducibility.
Genetic variability has been historically illustrated by the metabolism of isoniazid. Isoniazid is primarily acetylated in the liver to N-acetylisoniazid, a precursor of a hepatotoxic compound. Large genetically controlled ethnic differences exist in the distribution of acetylator status (slow and rapid acetylators). Adverse effects may occur prevalently in slow acetylators. On the other hand, rapid acetylators may be more susceptible to adverse reactions such as isoniazid-induced hepatic damage. Later on, it has been found that the majority of metabolic polymorphisms involve the isoenzymes of the cytochrome P450 system.
The clinical implications of genetic polymorphism in drug metabolism depend on whether activity or toxicity lies with the affected substrate or the metabolite, as well as the importance of the pathway to overall elimination. If the parent drug is active, there is a greater likelihood of adverse reactions in poor metabolizers and ineffective therapy in extensive metabolizer. Likewise, if the metabolite is active or toxic, there is a greater likelihood of adverse reactions in the extensive metabolizers and ineffective therapy in the poor metabolizers.
Genetic variability may effect drug clearance but also drug bioavailability ...
I wish you the best of luck in figuring this out with the help of your medical team. Most of all, I hope you are feeling better soon.