Buried in a contaminated Petri dish in 1928, Penicillin gave Alexander Fleming a bacterial killer that later spared thousands of soldiers – yet trained medicine to expect rescue from a single chemical class.
Penicillin changed fatal infection from routine terminal event to treatable episode. Modern broad-spectrum antibiotics inherited that victory while widening antibacterial reach far beyond streptococci and pneumococci.
The same lineage produced the field’s fixed contradiction: narrow agents such as penicillin preserve microbial ecology but miss many pathogens, whereas broad-spectrum drugs strike empirically and immediately but exact collateral damage through resistance selection, microbiome disruption, and diagnostic laziness.
Shared origin, split liability.
During World War II, industrial fermentation amplified penicillin into an entrenched protocol – something that worked when you couldn’t wait for lab results – and that very success steered later drug development toward wider coverage whenever uncertainty threatened delay.
Effectiveness and spectrum of activity compared
Clutched by empiric prescribing, modern broad-spectrum antibiotics hit more bacterial targets than penicillin because medicinal chemists widened activity beyond many gram-positive organisms and into numerous gram-negative pathogens.
Penicillin still kills exquisitely susceptible bacteria with a precision broad agents rarely match, since classic beta-lactams can eradicate streptococci and Treponema pallidum without the expansive collateral pressure that later compounds impose on bystander flora.
Breadth changed the wager.
Aminopenicillins and later broad-spectrum classes gained clinical reach by chemical modification that improved acid stability, tissue penetration, and pathogen coverage in patients whose infection source remained uncertain at first contact.
In bloodstream sepsis, lobar pneumonia with unclear source, complicated urinary infection, and mixed intra-abdominal infection, broad-spectrum drugs often secure earlier appropriate coverage because the first dose can intercept organisms that plain penicillin would’ve left untouched.
Penicillin G retains greater intrinsic potency against selected susceptible organisms than many broader descendants, and that narrower force remains clinically valuable when cultures identify a target and resistance patterns permit de-escalation.
Methicillin-resistant Staphylococcus aureus resists most broad-spectrum beta-lactams.
Broader spectrum doesn’t mean stronger: MRSA resists most broad-spectrum beta-lactams but not narrow drugs.
That fact punctures the lazy equation that wider spectrum guarantees stronger action against bacteria, because spectrum measures range, not superiority against every organism.
Across wards and emergency departments, physicians trade ecological restraint for initial certainty whenever they choose broad coverage before culture data return. The same pharmacologic expansion that rescues undifferentiated patients also nourishes the resistance problem that penicillin first exposed in miniature.
Unsurprising, then, that the most effective agent is often the one with the smallest target list after the laboratory names the bacterium.
Penicillin G remains the treatment of choice for syphilis and many streptococcal infections where susceptibility is confirmed.
What is better, antibiotics or penicillin?
Penicillin is an antibiotic class, not a rival category.
Phenoxymethylpenicillin, or Penicillin V, sits inside the antibiotic family, and any comparison that treats “antibiotics” and “penicillin” as opposite options starts from a category error.
Doctors choose between penicillins and other antibiotics based on the organism, infection site, prior exposure, allergy history, renal function, and data on local resistance.
No universal winner exists. The microbe decides.
By NHS naming, phenoxymethylpenicillin remains “a type of antibiotic” used for defined bacterial infections rather than a stand-alone therapeutic universe with its own rules.
That wording matters because many patients ask for “antibiotics” after penicillin failure, as though one substance has been replaced by another species of treatment, when the real switch is from one antibiotic subclass to another with altered spectrum, pharmacokinetics, and burden of toxicity.
Mayo Clinic material dated July 19, 2024, kept the safety issue in plain view: penicillin allergy, whether proven or mislabeled, can steer clinicians toward non-penicillin drugs even when antimicrobial fit would otherwise favor a penicillin derivative.
Inside that choice sits the same old contradiction: the narrower drug protects more normal flora when it fits, but diagnostic uncertainty and allergy labels push physicians toward agents that cover more organisms and disturb more biology.
Penicillin remains better for infections caused by penicillin-susceptible bacteria, including many streptococcal syndromes and syphilis, whereas non-penicillin antibiotics become better when resistance, polymicrobial burden, gram-negative risk, atypical pathogens, or patient-specific hazards block the narrower route.
Precision wins late. Breadth wins early.
Side effects and safety profiles
Spilled into modern drug development, antibiotic safety moved from bedside anecdote toward randomized controlled trials, postmarketing surveillance, and label revisions that quantify harms with a rigor Fleming never possessed. (Source: FDA.gov, 2026 – fda.gov/drugs/surveillance/postmarketing-surveillance-programs)
Penicillin remains one of the cleaner agents when a susceptible organism and a nonallergic patient align. But penicillin also carries the archetypal fear in antimicrobial practice because immediate anaphylaxis can strike about 0.02% to 0.04% of exposed patients.
Small number. Hard stop.
Modern broad-spectrum agents widened microbiologic reach, they also widened toxicity portfolios through Clostridioides difficile risk, nephrotoxicity, QT prolongation, tendinopathy, marrow suppression, drug-drug interactions, and collateral microbiome injury.
It was old dogma that inflated cephalosporin fear in penicillin-labeled patients, not current evidence. (Source: JAMA / PubMed, 2019 – pubmed.ncbi.nlm.nih.gov/30644987)
A 2019 JAMA review placed penicillin-cephalosporin cross-reactivity at about 2% – far below the inherited teaching that kept many clinicians away from useful beta-lactams.
Penicillin-cephalosporin cross-reactivity is just 2%, debunking decades of exaggerated allergy fears.
That correction matters. False allergy labels drive substitution toward broader, more toxic alternatives.
In August 2024, FDA labeling for amoxicillin/clavulanate still listed hypersensitivity, gastrointestinal injury, hepatic effects, and severe cutaneous reactions – a reminder that even a familiar penicillin-class product keeps a substantial adverse-event ledger under contemporary scrutiny.
Across stewardship programs and emergency departments, the safety paradox shadows the spectrum paradox: the drug that spares flora and toxic burden in the right patient becomes unusable once an allergy label appears. And the substitute that covers uncertainty often imports a longer list of injuries than the discarded narrow agent ever posed.
A 2024 JAMA Internal Medicine meta-analysis found that reactions during direct penicillin challenge remained uncommon, which leaves institutions facing an old embarrassment. Many patients still carry labels that punish them more than penicillin would.
In most modern studies, penicillin allergy labels are incorrect in over 90% of patients who carry them.
Antibiotic resistance rates: penicillin vs modern drugs
Entangled with every gain in antibacterial reach, resistance has eroded penicillin more visibly than many later agents because decades of bacterial exposure selected enzymes and altered targets that nullify classic beta-lactams.
In 1940, Ernst Chain and Edward Abraham reported an Escherichia coli strain that produced penicillin resistance before mass civilian antibiotic use had even matured – a warning that arrived near the drug’s birth rather than after its overuse. (Source: CDC MMWR, 1989 – cdc.gov/mmwr/preview/mmwrhtml/00001575.htm)
The problem started early.
Penicillin resistance now limits first-line use for many common infections, especially where Staphylococcus aureus, respiratory pathogens, enteric gram-negatives, or mixed flora dominate the likely differential.
- Beta-lactamase production – many bacteria produce enzymes that destroy penicillin and related drugs, rendering them ineffective
- Altered penicillin-binding proteins – resistance mechanisms such as PBP2a in MRSA block penicillin action at the target site
- Efflux pumps and porin loss – gram-negative bacteria evolve ways to expel or exclude antibiotics, limiting their reach
- Plasmid-mediated resistance – genetic elements allow rapid spread of resistance traits through bacterial populations
Modern drugs did not escape the same evolutionary pressure, they merely redistributed it across newer molecular scaffolds, reserve classes, and combination products.
MRSA resists methicillin and most beta-lactams chiefly through altered penicillin-binding proteins such as PBP2a, not through beta-lactamase alone. That mechanism defeats an old reflex that was used in clinics that blamed enzyme destruction for nearly every penicillin failure.
Penicillin resistance emerged before widespread use; bacteria anticipated the drug’s attack from the very start.
Clavulanic acid, sulbactam, and tazobactam inhibit many beta-lactamases and restore activity for selected combinations. Yet those pairings still fail against organisms with carbapenemases, porin loss, efflux systems, inducible AmpC enzymes, or remodeled binding proteins.
Across hospitals, agriculture, and community prescribing, each broadened antimicrobial answer has fed the next resistance workaround – the field keeps making wider chemical umbrellas under a sky already altered by earlier rain.
Modern broad-spectrum antibiotics often resist obsolescence longer than penicillin did against many pathogens. But none retain innocence once selective pressure accumulates.
Why isn’t penicillin no longer effective?
Penicillin often fails because many bacteria now destroy the drug with beta-lactamase or evade it by altering penicillin-binding proteins.
Bacteria didn’t need to invent a single escape route – different species built different defenses, and clinicians paid for that plural ingenuity with collapsing susceptibility.
Penicillin once treated gonorrhea and many invasive coccal infections with high reliability. Present-day practice can’t assume that historical success predicts current activity.
Old charts mislead. Microbes changed first.
In Neisseria gonorrhoeae, penicillin effectiveness fell across decades as chromosomal mutations and plasmid-mediated beta-lactamase spread through sexual networks, travel corridors, and repeated treatment campaigns; CDC-reviewed surveillance converted that collapse from anecdote into policy. (Source: CDC MMWR, 1989 – cdc.gov/mmwr/preview/mmwrhtml/00001575.htm)
Neisseria meningitidis – once managed with penicillin in many settings – also acquired reduced susceptibility in some strains through altered penicillin-binding proteins, which narrowed the margin for empiric confidence in meningococcal disease.
Staphylococcus aureus took a harsher route. MRSA replaced the target itself with PBP2a, and that altered protein leaves penicillins functionally sidelined even when laboratory language tempts clinicians to think in older beta-lactam categories.
Inside that retreat lies the same inheritance that shaped modern antibiotic practice: the first narrow miracle trained clinicians to depend on precise killing, then bacterial populations converted that precision into a vulnerability by learning the exact structure they needed to block.
Broad-spectrum successors emerged partly to outrun the failures of penicillin. Yet every wider substitute repeats the same bargain under a different label.
Selection never sleeps. That’s why penicillin remains brilliant for a shrinking set of susceptible targets and unreliable for many pathogens that medicine once believed it’t already subdued.
Cost and accessibility comparison
Forced by wartime demand, penicillin became cheaper and more reachable at industrial speed once U.S. production infrastructure stopped treating the drug as a laboratory curiosity and started treating it as military necessity.
Penicillin now sits among the least expensive antibiotic options in many health systems when manufacturers supply generic oral or injectable forms. Newer broad-spectrum agents often carry higher prices for acquisition, tighter formulary controls, infusion-center dependence, or patent-era premiums that shrink access outside hospitals.
Price changed with scale. Access changed with chemistry.
World War II production drove that turn with brutal arithmetic: one U.S. scale-up reported output rising from 21 billion units in 1943 to 1,663 billion units in 1945.
- Generic penicillin – typically low cost and widely available in both oral and injectable forms
- Broad-spectrum antibiotics – often higher cost due to patent protection, complex synthesis, or limited manufacturers
- Supply chain vulnerability – shortages of old sterile injectables like benzathine penicillin can disrupt care despite low production cost
- Formulary restrictions – newer agents may be reserved for hospital use or specific indications due to expense
By the end of World War II, monthly penicillin production rose from 400 million units in early 1943 to 650 billion units, and mass fermentation crushed unit cost far faster than bedside demand alone could have managed. (Source: NBER Working Paper, 2024 – nber.org/system/files/working_papers/w27909/w27909.pdf)
Cheap penicillin does not always mean easier treatment, though.
Even cheap penicillin can be inaccessible – neglect of the supply chain turns abundance into shortage for key infections.
Benzathine penicillin shortages have periodically disrupted syphilis care despite the drug’s age and modest manufacturing cost, because old sterile injectables earn thin margins and attract fewer committed producers than premium broad-spectrum products.
Institutions neglected the cheap winner, supply chains didn’t forgive them.
Across public clinics and hospital formularies, every push toward broader agents has traded convenience in prescribing for greater financial strain. The narrow drug that costs little often requires a confirmed diagnosis, steady supply, and a clinician willing to resist empiric excess.
Penicillin owes its accessibility to abundance on an industrial scale more than molecular simplicity. Modern broad-spectrum antibiotics remain easier to start than to afford at scale.
Treatment duration and dosing differences
Carved out by pharmacokinetics, antibiotic dosing schedules depend less on drug age than on absorption, half-life, protein binding, tissue penetration, and the bacterial kill pattern each compound produces.
Beta-lactam antibiotics – including penicillins and many later broad-spectrum descendants – usually exert time-dependent killing, so clinicians aim to keep serum and tissue concentrations above the minimum inhibitory concentration for enough of the dosing that was standardized rather than chasing towering peak levels.
Timing rules efficacy. Miss the window, lose the edge.
Penicillin G illustrates the old constraint in raw form because stomach acid destroys it, forcing intravenous or intramuscular administration and tying effective treatment to supervised delivery, admission status, or injection access.
- Penicillin G – requires parenteral dosing due to acid lability, limiting outpatient use
- Penicillin V – orally bioavailable but less potent for severe infections
- Broad-spectrum agents – often available in oral, intravenous, and extended-release forms, improving adherence and outpatient feasibility
- Modern regimens – shorter courses possible for many indications due to better pharmacodynamic modeling
Penicillin V solved part of that problem by tolerating gastric acid and allowing oral administration, yet Penicillin V trades some potency for convenience and cannot simply replace Penicillin G in every severe infection.
Modern broad-spectrum agents often compress treatment through longer half-lives, better oral bioavailability, extended-release formulations, and pharmacodynamic modeling that permits dosing that was standardized to once-daily or twice-daily in many settings.
Shorter modern antibiotic regimens often cure as well as older, longer penicillin courses – less can be enough.
Longer treatment isn’t always stronger treatment.
But shorter modern regimens often work as well as older extended courses when source control, exposure to drugs, and organism susceptibility align.
Across wards and outpatient clinics, the old narrow drugs frequently demand more disciplined timing and route control, whereas newer agents purchase adherence with easier schedules at the price of broader ecological exposure, therefore convenience itself becomes another mechanism by which expanded coverage displaces restraint.
Dosing that was standardized decides more failures than brand age does.
What is the 60 90 rule for antibiotics?
The 60/90 rule states that susceptible isolates yield clinical success in about 90% of cases, while resistant isolates still yield success in roughly 60%. (Source: PubMed / Infectious Diseases in Clinical Practice, 2002 – pubmed.ncbi.nlm.nih.gov/12355386)
Rex and Pfaller coined the formulation to summarize a stubborn clinical reality: laboratory resistance does not guarantee bedside failure, and laboratory susceptibility does not deliver certainty.
Host immunity alters outcomes. Source control alters them too.
Susceptibility reports guide treatment, but they don’t function as prophecy because pneumonia, abscesses, urinary infections, endocarditis, catheter biofilms, and bacterial burden distort what the dish predicts.
A 2018 review in the American Society for Clinical Laboratory Science repeated the rule and stressed its origin in clinical microbiology interpretation rather than in a single universal trial dataset.
That same review placed a hard limit on its use: the rule generally doesn’t apply to immunocompromised patients, whose impaired host defenses compress the margin between microbiologic resistance and clinical collapse.
A veterinary internal medicine study using clinical samples collected from January 2014 through December 2016 examined the same discordance from another angle, reinforcing that organism-level test results and patient-level outcomes diverge under the pressure of dose, tissue penetration, inoculum size, drainage quality, and host factors.
Inside antibiotic choice, the 60/90 rule exposes the same contradiction that shaped penicillin’s descendants: clinicians want a narrow, exact answer from the laboratory, yet living infections answer to exposure to drugs, anatomy, immunity, and delay, which pushes many prescribers toward broader empiric coverage before cultures mature.
The rule doesn’t excuse sloppy prescribing. It indicts overconfidence in single numbers.
A susceptibility label remains useful, but the patient at the bedside still determines whether the old narrow drug suffices or whether the broader substitute enters because uncertainty keeps winning the first twenty-four hours.
When penicillin is still the right choice and when to switch
Microbiology keeps penicillin alive, not nostalgia. The drug still works against organisms that stay predictably susceptible – and for patients who can’t take a narrow beta-lactam without trouble.
Penicillin remains the right choice for syphilis, many infections caused by streptococci, selected mouth infections, and other syndromes where culture points to a specific target. Narrow killing protects normal flora. It avoids the ecological blast radius that comes with use for therapy that’s broad-spectrum.
Use it when you know the target. Drop it when the target widens.
But empiric uncertainty changes the math, polymicrobial burden shifts the odds, risk from gram-negative bacteria enters the picture. Prior resistance history matters. So does treatment failure. A severe beta-lactam allergy can all push treatment away from classic penicillin toward broader agents or molecules that are structurally different.
- Syphilis – penicillin remains the only recommended agent for all stages when susceptibility is confirmed
- Streptococcal pharyngitis – narrow-spectrum penicillin is preferred due to high target specificity and low collateral impact
- Severe allergy or resistance – switch to broader or structurally different antibiotics if penicillin is unsafe or ineffective
- Polymicrobial or gram-negative infections – broad-spectrum therapy is indicated when likely pathogens exceed penicillin’s reach
Cloxacillin and oxacillin show how the switch happened inside the penicillin family itself. These semi-synthetic antistaphylococcal antibiotics resist breakdown by staphylococcal penicillinase – they beat plain penicillin against penicillinase-producing methicillin-susceptible Staphylococcus aureus.
Penicillin’s own family had to evolve: new penicillins beat old ones for staphylococci that produced penicillinase.
That fact cuts against a common assumption that “penicillin” means one fixed molecule with one fixed role. In hospitals, the class already split into targeted descendants built for specific failures of the parent compound.
Antipseudomonal penicillins pushed this logic toward Pseudomonas aeruginosa – an organism that classic penicillin cannot cover in serious disease (not reliably, anyway).
At the bedside, the narrow drug stays the better tool when culture data lines up with syndrome recognition and local resistance patterns. The same clinician must switch the moment those anchors loosen. Precision without fit just delays the right answer.
Penicillin works when evidence narrows the field. Broader use for therapy enters when uncertainty tears the field open – or when resistance makes penicillin irrelevant.
Treatment failures, adverse reactions, and why penicillin use declined
At the bedside, penicillin lost ground less because physicians stopped trusting antibiotics than because repeated treatment failures and persistent allergy labels made the old narrow drug look unreliable under modern clinical pressure.
Use of penicillin declined when staphylococcal penicillinase, altered targets, polymicrobial infections, gram-negative pathogens, and empiric hospital practice kept pushing clinicians away from a molecule that worked magnificently only when the bacterium still fit its original design.
Failure drove substitution. Fear made it faster.
Methicillin entered UK clinical practice in 1959 as an alternative to penicillin for rising penicillin-resistant staphylococcal disease – just twelve years after penicillin reached widespread use – and that date marks how rapidly one corrective drug had to replace another within the same family.
- Staphylococcal penicillinase – enzyme-mediated resistance forced clinicians to abandon plain penicillin for staphylococcal infections
- Allergy labeling – widespread, often inaccurate penicillin allergy labels shifted use toward broader or unrelated antibiotics
- Adverse-event history – fear of anaphylaxis and severe rash attached to the entire class, even when risk was low
- Methicillin nephritis – the substitute for penicillin developed its own toxicity, leading to further drug turnover
Adverse reactions added a second blow.
Immediate hypersensitivity remained rare in absolute numbers, yet the cultural memory of anaphylaxis and rash attached itself to the entire penicillin class with unusual force, leaving many patients permanently labeled despite uncertain histories and later tolerance.
Methicillin, designed to rescue penicillin failures, was itself abandoned due to toxicity in the kidney.
Methicillin itself later vanished from routine use because interstitial nephritis and other liabilities undercut its value in medicine, which means the very substitute created to rescue penicillin’s failure became its own casualty.
Drug succession solved nothing cleanly.
Across hospitals and clinics, the same event kept repeating in new forms: a narrow agent cured elegantly when conditions aligned, then resistance, fear of an adverse-event, and diagnostic haste made broader successors appear safer than they often were. Those successors expanded collateral damage and pressure on future resistance, the cycle continued.
Penicillin declined because medicine rewarded immediate coverage more consistently than restraint over the long term.
How doctors choose the right antibiotic for each infection
Under diagnostic pressure, doctors choose antibiotics by matching the likely organism, infection site, patient risk, local susceptibility data, prior cultures, allergy history, renal and hepatic function, pregnancy status, drug interactions, and illness severity to the narrowest agent that can still credibly succeed.
Penicillin enters that calculation when the syndrome points toward highly susceptible organisms such as streptococci or Treponema pallidum. But modern broad-spectrum antibiotics dominate the first move when sepsis, hospital exposure, neutropenia, mixed infection, or gram-negative danger makes delay intolerable.
First doses are wagers. Laboratories settle them later.
Escherichia coli often defeats natural penicillin, and Pseudomonas aeruginosa defeats many ordinary options from the outset – neither organism permits sentimental prescribing.
- Organism and syndrome – match the likely pathogen to the narrowest effective agent
- Allergy and safety history – avoid agents with known hypersensitivity or contraindications for the patient
- Local resistance data – use antibiograms and recent culture results to guide empiric choices
- Severity and urgency – initiate broad-spectrum therapy for severe, undifferentiated, or life-threatening infections, then de-escalate as data allow
For uncomplicated streptococcal pharyngitis, physicians can often prescribe a narrow penicillin with confidence because syndrome, epidemiology, and expected susceptibility converge tightly enough to support restraint.
For pyelonephritis, ventilator-associated pneumonia, abdominal sepsis, or bacteremia of unclear source, clinicians usually start broader because early undercoverage kills faster than later de-escalation injures.
Doctors prescribe broad antibiotics first, not for strength, but to outrun fatal delays before cultures return.
Aminopenicillins can treat some Escherichia coli infections when susceptibility holds. Plain penicillin doesn’t cover that organism reliably.
Site can outweigh spectrum.
Vancomycin, linezolid, or cefazolin may outrank a broader gram-negative agent if the patient most likely carries methicillin-resistant or methicillin-susceptible staphylococcal disease.
Across stewardship rounds (where infectious disease teams review every case), every antibiotic choice reenacts the old bind between immediate certainty and ecological restraint: physicians begin broad when uncertainty threatens the patient in front of them. They then try to narrow once cultures, imaging, and clinical response strip away the guesswork that broad drugs invited in the first place.
Good prescribing doesn’t eliminate the contradiction; it manages its timing.
From Fleming’s discovery to today’s antibiotic arsenal
By 12 February 1941, Albert Alexander received injected penicillin at the Radcliffe Infirmary. That single patient encounter converted a contaminated culture’s promise into a clinical fact with mortal stakes. (Source: University of Oxford, 2018 – phc.ox.ac.uk/news/blog/on-this-site-penicillin-a-historic-first)
Fleming identified the mold effect, but Howard Florey, Ernst Boris Chain, and Norman Heatley transformed that observation into purification, animal proof, human dosing, and industrial momentum – then carried the project to the United States in June 1941 to accelerate mass production.
The molecule hit bacterial cell walls with exquisite specificity.
The mechanism was plain: penicillins and other beta-lactams bind penicillin-binding proteins, inhibit final peptidoglycan transpeptidation, weaken the wall, and kill growing bacteria.
A laboratory accident didn’t build the arsenal. Teams did.
- Fleming’s initial discovery (1928) – identified the antibacterial effect of mold, launching the antibiotic era
- Florey, Chain, Heatley’s development – enabled purification, clinical testing, and mass production of penicillin
- Industrial scale-up (1941 – 1945) – transformed penicillin from laboratory rarity to global medicine
- Semi-synthetic derivatives – expanded the penicillin family to cover resistant organisms and new clinical indications
The 1945 Nobel Prize in Physiology or Medicine fixed the discovery narrative in public memory by honoring Fleming, Chain, and Florey, yet Norman Heatley – who designed the extraction vessels and scaled production from lab bench to factory floor – received no Nobel share despite his central role in extraction, assay, vessel design, and practical scale-up.
Norman Heatley enabled the mass production of penicillin but was excluded from the Nobel Prize story.
That omission exposes the forensic truth of antibiotic history: famous discoveries often depend on technical labor that prestige systems undercount.
Semi-synthetic penicillins later extended the parent scaffold into aminopenicillins, agents for use against staphylococci, and drugs for use against pseudomonas. Cephalosporins and further beta-lactam classes inherited the same wall-targeting logic and diversified it into a larger pharmacologic armory.
Across that entire lineage, the founding contradiction remains untouched: the mold-derived narrow weapon taught medicine the power of selective killing, and every expansion of that weapon into broader coverage increased the field’s ability to rescue uncertain infections while multiplying the ecological and evolutionary debts attached to rescue itself.
Fleming’s dish started the cure, and the cure still makes the problem it was built to outrun.