While typical drug side effects reactions are mild to moderate; sometimes serious adverse effects occur.

As of 2016, the U.S. FDA recommended that "serious side effects associated with fluoroquinolone antibacterial drugs generally outweigh the benefits for patients with acute sinusitis, acute bronchitis, and uncomplicated urinary tract infections who have other treatment options. For patients with these conditions, fluoroquinolones should be reserved for those who do not have alternative treatment options."

Partly as a result of the efforts of Public Citizen, in 2008 the U.S. FDA ordered boxed warnings on all fluoroquinolones, advising consumers of an enhanced risk of tendon damage.

Prominent among these are side effects that became the subject of a black box warning by the U.S. FDA in 2016. The FDA wrote: "An FDA safety review has shown that fluoroquinolones when used systemically (i.e. tablets, capsules, and injectable) are associated with disabling and potentially permanent serious side effects that can occur together. These side effects can involve the tendons, muscles, joints, nerves, and central nervous system."

Quinolones are associated with a small risk of tendonitis and tendon rupture; a 2013 review found the incidence of tendon injury among those taking fluoroquinolones to be between 0.08 and 0.2%. The risk appears to be higher among people older than 60 and those also taking corticosteroids; there may also be higher risk among people who are male, have a pre-existing joint or tendon issue, have kidney disease, and are highly active. Some experts have advised avoidance of fluoroquinolones in athletes. If tendonitis occurs, it generally appears within one month, and the most common tendon that is injured appears to be the Achilles tendon. The cause is not well understood.

Nervous system effects include insomnia, restlessness, and rarely, seizure, convulsions, and psychosis. Other rare and serious adverse events have been observed with varying degrees of evidence for causation.

More generally, fluoroquinolones are tolerated, with typical drug side effects being mild to moderate. Common side effects include gastrointestinal effects such as nausea, vomiting, and diarrhea, as well as headache and insomnia. Postmarketing surveillance has revealed a variety of relatively rare but serious adverse effects that are associated with all members of the fluoroquinolone antibacterial class. Among these, tendon problems and exacerbation of the symptoms of the neurological disorder myasthenia gravis are the subject of "black box" warnings in the United States.

The overall rate of adverse events in patients treated with fluoroquinolones is roughly similar to that seen in patients treated with other antibiotic classes. A U.S. Centers for Disease Control and Prevention study found patients treated with fluoroquinolones experienced adverse events severe enough to lead to an emergency department visit more frequently than those treated with cephalosporins or macrolides, but less frequently than those treated with penicillins, clindamycin, sulfonamides, or vancomycin.

Fluoroquinolones prolong the heart's QT interval by blocking voltage-gated potassium channels. Prolongation of the QT interval can lead to torsades de pointes, a life-threatening arrhythmia, but in practice this appears relatively uncommon in part because the most widely prescribed fluoroquinolones (ciprofloxacin and levofloxacin) only minimally prolong the QT interval.

"Clostridium difficile" colitis may occur in connection with the use of any antibacterial drug, especially those with a broad spectrum of activity such as clindamycin, cephalosporins, and fluoroquinolones. Fluoroquinoline treatment is associated with risk that is similar to or less than that associated with broad spectrum cephalosporins. Fluoroquinoline administration may be associated with the acquisition and outgrowth of a particularly virulent "Clostridium" strain.

Events that may occur in acute overdose are rare, and include renal failure and seizure. Susceptible groups of patients, such as children and the elderly, are at greater risk of adverse reactions during therapeutic use.

In 2017 the FDA included the following important warning:

"The U.S. Food and Drug Administration (FDA) has required the drug labels and Medication Guides for all fluoroquinolone antibacterial drugs be updated to better describe the serious side effect of peripheral neuropathy. This serious nerve damage potentially caused by fluoroquinolones (see Table for a list) may occur soon after these drugs are taken and may be permanent.

The risk of peripheral neuropathy occurs only with fluoroquinolones that are taken by mouth or by injection. Approved fluoroquinolone drugs include levofloxacin (Levaquin), ciprofloxacin (Cipro), moxifloxacin (Avelox), norfloxacin (Noroxin), ofloxacin (Floxin), and gemifloxacin (Factive). The topical formulations of fluoroquinolones, applied to the ears or eyes, are not known to be associated with this risk.

If a patient develops symptoms of peripheral neuropathy, the fluoroquinolone should be stopped, and the patient should be switched to another, non-fluoroquinolone antibacterial drug, unless the benefit of continued treatment with a fluoroquinolone outweighs the risk. Peripheral neuropathy is a nerve disorder occurring in the arms or legs. Symptoms include pain, burning, tingling, numbness, weakness, or a change in sensation to light touch, pain or temperature, or the sense of body position. It can occur at any time during treatment with fluoroquinolones and can last for months to years after the drug is stopped or be permanent. Patients using fluoroquinolones who develop any symptoms of peripheral neuropathy should tell their health care professionals right away.

FDA will continue to evaluate the safety of drugs in the fluoroquinolone class and will communicate with the public again if additional information becomes available. "

In most countries, fluoroquinolones are approved for use in children only under narrowly-defined circumstances, owing in part to the observation of high rates of musculoskeletal adverse events in fluoroquinolone treated juvenile animals. In the UK, the prescribing indications for fluoroquinolones for children are severely restricted. Only inhalant anthrax and pseudomonal infections in cystic fibrosis infections are licensed indications in the UK due to ongoing safety concerns. In a study comparing the safety and efficacy of levofloxacin to that of azithromycin or ceftriaxone in 712 children with community-acquired pneumonia, serious adverse events were experienced by 6% of those treated with levofloxacin and 4% of those treated with comparator antibiotics. Most of these were considered by the treating physician to be unrelated or doubtfully related to the study drug. Two deaths were observed in the levofloxacin group, neither of which was thought to be treatment-related. Spontaneous reports to the U.S. FDA Adverse Effects Reporting System at the time of the 20 September 2011 U.S. FDA Pediatric Drugs Advisory Committee included musculoskeletal events (39, including 5 cases of tendon rupture) and central nervous system events (19, including 5 cases of seizures) as the most common spontaneous reports between April 2005 and March 2008. An estimated 130,000 pediatric prescriptions for levofloxacin were filled on behalf of 112,000 pediatric patients during that period.

Meta-analyses conclude that fluoroquinolones pose little or no additional risk to children compared to other antibiotic classes.

Fluoroquinolines use in children may be appropriate when the infection is caused by multidrug-resistant bacteria, or when alternative treatment options require parenteral administration and oral therapy is preferred.

Antibiotics can cause severe reactions and add significantly to the cost of care. In the United States, antibiotics and anti-infectives are the leading cause of adverse effect from drugs. In a study of 32 States in 2011, antibiotics and anti-infectives accounted for nearly 24 percent of ADEs that were present on admission, and 28 percent of those that occurred during a hospital stay.

Prescribing by an infectious disease specialist compared with prescribing by a non-infectious disease specialist decreases antibiotic consumption and reduces costs.

Though antibiotics are required to treat severe bacterial infections, misuse has contributed to a rise in bacterial resistance. The overuse of fluoroquinolone and other antibiotics fuels antibiotic resistance in bacteria, which can inhibit the treatment of antibiotic-resistant infections. Their excessive use in children with otitis media has given rise to a breed of bacteria resistant to antibiotics entirely.

Widespread use of fluoroquinolones as a first-line antibiotic has led to decreased antibiotic sensitivity, with negative implications for serious bacterial infections such as those associated with cystic fibrosis, where quinolones are among the few viable antibiotics.

The Gonorrhea bacterium Neisseria gonorrhoeae has developed antibiotic resistance to many antibiotics.

The bacteria was first identified in 1879, although some Biblical scholars believe that references to the disease can be found as early as Parshat Metzora of the Old Testament.

In the 1940s effective treatment with penicillin became available, but by the 1970s resistant strains predominated. Resistance to penicillin has developed through two mechanisms: chromasomally mediated resistance (CMRNG) and penicillinase-mediated resistance (PPNG). CMRNG involves step wise mutation of penA, which codes for the penicillin-binding protein (PBP-2); mtr, which encodes an efflux pump that removes penicillin from the cell; and penB, which encodes the bacterial cell wall porins. PPNG involves the acquisition of a plasmid-borne beta-lactamase. "N. gonorrheoea" has a high affinity for horizontal gene transfer, and as a result, the existence of any strain resistant to a given drug could spread easily across strains.

Fluoroquinolones were a useful next-line treatment until resistance was achieved through efflux pumps and mutations to the gyrA gene, which encodes DNA gyrase. Third-generation cephalosporins have been used to treat gonorrhoea since 2007, but resistant strains have emerged. As of 2010, the recommended treatment is a single 250 mg intramuscular injection of ceftriaxone, sometimes in combination with azithromycin or doxycycline. However, certain strains of "N. gonorrhoeae" can be resistant to antibiotics usually that are normally used to treat it. These include: cefixime (an oral cephalosporin), ceftriaxone (an injectable cephalosporin), azithromycin, aminoglycosides, and tetracycline.

"N. gonorrhoeae" has also shown resistance to the aminoglycoside class of antibiotics. These antibiotics bind to the 16s rRNA of the 30S subunit of the bacterial ribosome, thereby stopping transcription of the bacterial genome. Resistance appears to be acquired through porin-related mechanisms, much like the cephalosporin resistance mechanism. This mechanism would result in the access of the antibiotic to the bacterial cell being inhibited. There is a possibility of future enzymes (made by the bacterium) that will be able to denature and inactivate the aminoglycosides.

Cases of MDR tuberculosis have been reported in every country surveyed. MDR-TB most commonly develops in the course of TB treatment, and is most commonly due to doctors giving inappropriate treatment, or patients missing doses or failing to complete their treatment. Because MDR tuberculosis is an airborne pathogen, persons with active, pulmonary tuberculosis caused by a multidrug-resistant strain can transmit the disease if they are alive and coughing. TB strains are often less fit and less transmissible, and outbreaks occur more readily in people with weakened immune systems (e.g., patients with HIV). Outbreaks among non immunocompromised healthy people do occur, but are less common.

As of 2013, 3.7% of new tuberculosis cases have MDR-TB. Levels are much higher in those previously treated for tuberculosis - about 20%. WHO estimates that there were about 0.5 million new MDR-TB cases in the world in 2011. About 60% of these cases occurred in Brazil, China, India, the Russian Federation and South Africa alone. In Moldova, the crumbling health system has led to the rise of MDR-TB. In 2013, the Mexico–United States border was noted to be "a very hot region for drug resistant TB", though the number of cases remained small.

It has been known for many years that INH-resistant TB is less virulent in guinea pigs, and the epidemiological evidence is that MDR strains of TB do not dominate naturally. A study in Los Angeles, California found that only 6% of cases of MDR-TB were clustered. Likewise, the appearance of high rates of MDR-TB in New York City in the early 1990s was associated with the explosion of AIDS in that area. In New York City, a report issued by city health authorities states that fully 80 percent of all MDR-TB cases could be traced back to prisons and homeless shelters. When patients have MDR-TB, they require longer periods of treatment—about two years of multidrug regimen. Several of the less powerful second-line drugs, which are required to treat MDR-TB, are also more toxic, with side effects such as nausea, abdominal pain, and even psychosis. The Partners in Health team had treated patients in Peru who were sick with strains that were resistant to ten and even twelve drugs. Most such patients require adjuvant surgery for any hope of a cure.

There are several ways that drug resistance to TB, and drug resistance in general, can be prevented:

1. Rapid diagnosis & treatment of TB: One of the greatest risk factors for drug resistant TB is problems in treatment and diagnosis, especially in developing countries. If TB is identified and treated soon, drug resistance can be avoided.

2. Completion of treatment: Previous treatment of TB is an indicator of MDR TB. If the patient does not complete his/her antibiotic treatment, or if the physician does not prescribe the proper antibiotic regimen, resistance can develop. Also, drugs that are of poor quality or less in quantity, especially in developing countries, contribute to MDR TB.

3. Patients with HIV/AIDS should be identified and diagnosed as soon as possible. They lack the immunity to fight the TB infection and are at great risk of developing drug resistance.

4. Identify contacts who could have contracted TB: i.e. family members, people in close contact, etc.

5. Research: Much research and funding is needed in the diagnosis, prevention and treatment of TB and MDR TB.

"Opponents of a universal tuberculosis treatment, reasoning from misguided notions of cost-effectiveness, fail to acknowledge that MDRTB is not a disease of poor people in distant places. The disease is infectious and airborne. Treating only one group of patients looks inexpensive in the short run, but will prove disastrous for all in the long run."- Paul Farmer

HCAP is a condition in patients who can come from the community, but have frequent contact with the healthcare environment. Historically, the etiology and prognosis of nursing home pneumonia appeared to differ from other types of community acquired pneumonia, with studies reporting a worse prognosis and higher incidence of multi drug resistant organisms as etiology agents. The definition criteria which has been used is the same as the one which has been previously used to identify bloodstream healthcare associated infections.

HCAP is no longer recognized as a clinically independent entity. This is due to increasing evidence from a growing number of studies that many patients defined as having HCAP are not at high risk for MDR pathogens. As a result, 2016 IDSA guidelines removed consideration of HCAP as a separate clinical entity.

Healthcare-associated pneumonia can be defined as pneumonia in a patient with at least one of the following risk factors:

- hospitalization in an acute care hospital for two or more days in the last 90 days;

- residence in a nursing home or long-term care facility in the last 30 days

- receiving outpatient intravenous therapy (like antibiotics or chemotherapy) within the past 30 days

- receiving home wound care within the past 30 days

- attending a hospital clinic or dialysis center in the last 30 days

- having a family member with known multi-drug resistant pathogens

Treatment for gastroenteritis due to "Y. enterocolitica" is not needed in the majority of cases. Severe infections with systemic involvement (sepsis or bacteremia) often requires aggressive antibiotic therapy; the drugs of choice are doxycycline and an aminoglycoside. Alternatives include cefotaxime, fluoroquinolones, and co-trimoxazole.

Penicillin is known to become less effective as strains of bacteria become resistant.

Many people have indicated that they have a side effect related to an allergic reaction to penicillin. It has been proposed that as many as 90% of those claiming to have an allergy to penicillin are able to take it. Identifying an allergy to penicillin requires a hypersensitivity skin test which diagnoses IgE-mediated immune responses caused by penicillin. This test is typically performed by an allergist who uses a skin-prick and intradermal injection of penicilloyl-polylysine, a negative control (normal saline), and a positive control (histamine).

There is a common side effect that can develop when other medications are used. This is the development of cross sensitivities to other antibiotics. If someone has developed side effects when taking penicillin, these side effects may develop with a new medication even though the person has not taken the new medication before. Those medications that may cause a cross sensitivity reaction are: carbapenems, ampicillin, cefazolin, cephalosporins and cloxacillin.

Yersiniosis is an infectious disease caused by a bacterium of the genus "Yersinia". In the United States, most yersiniosis infections among humans are caused by "Yersinia enterocolitica". The infection by "Y. enterocolitica" is also known as pseudotuberculosis. Yersiniosis is mentioned as a specific zoonotic disease to prevent outbreaks in European Council Directive 92/117/EEC.

Infection with " Y . enterocolitica" occurs most often in young children. The infection is thought to be contracted through the consumption of undercooked meat products, unpasteurized milk, or water contaminated by the bacteria. It has been also sometimes associated with handling raw chitterlings.

Another bacterium of the same genus, "Yersinia pestis", is the cause of Plague.

Prevention of bacterial pneumonia is by vaccination against "Streptococcus pneumoniae" (pneumococcal polysaccharide vaccine for adults and pneumococcal conjugate vaccine for children), "Haemophilus influenzae" type B, meningococcus, "Bordetella pertussis", "Bacillus anthracis", and "Yersinia pestis".

"Streptococcus pneumoniae" — amoxicillin (or erythromycin in patients allergic to penicillin); cefuroxime and erythromycin in severe cases.

"Staphylococcus aureus" — flucloxacillin (to counteract the organism's β-lactamase).

In addition to vaccine-specific factors, vets and owners should also consider pet-specific factors that have been shown to increase the risk of adverse reactions in both dogs and cats. Examples of such factors include:

- age,

- number of vaccinations per office visit,

- size,

- general health of the animal,

- breed,

- neutered status, and

- past vaccination history.

Fortunately, severe systemic reaction to vaccine allergy is very rare in dogs. When it does occur, however, anaphylaxis is a life-threatening emergency. More often, dogs will develop urticaria, or hives within minutes of receiving a vaccine. When this occurs, a veterinarian will treat the reaction with antihistamines and corticosteroid drugs and this is usually effective. Future vaccine protocols must be modified according to the vaccine component suspected to have triggered the reaction.

Infants may develop respiratory symptoms as a result of exposure to a specific type of fungal mold, called Penicillium. Signs that an infant may have mold-related respiratory problems include (but are not limited to) a persistent cough and/or wheeze. Increased exposure increases the probability of developing respiratory symptoms during their first year of life. Studies have shown that a correlation exists between the probability of developing asthma and increased exposure to "Penicillium". The levels are deemed ‘no mold’ to ‘low level’ , from ‘low’ to ‘intermediate’ , and from ‘intermediate’ to ‘high’.

Mold exposures have a variety of health effects depending on the person. Some people are more sensitive to mold than others. Exposure to mold can cause a number of health issues such as; throat irritation, nasal stuffiness, eye irritation, cough and wheezing, as well as skin irritation in some cases. Exposure to mold may also cause heightened sensitivity depending on the time and nature of exposure. People at higher risk for mold allergies are people with chronic lung illnesses, which will result in more severe reactions when exposed to mold.

There has been sufficient evidence that damp indoor environments are correlated with upper respiratory tract symptoms such as coughing, and wheezing in people with asthma.

It has been hypothesized that biofilm bacterial infections may account for many cases of antibiotic-refractory chronic sinusitis. Biofilms are complex aggregates of extracellular matrix and inter-dependent microorganisms from multiple species, many of which may be difficult or impossible to isolate using standard clinical laboratory techniques. Bacteria found in biofilms have their antibiotic resistance increased up to 1000 times when compared to free-living bacteria of the same species. A recent study found that biofilms were present on the mucosa of 75% of people undergoing surgery for chronic sinusitis.

Acute sinusitis is usually precipitated by an earlier upper respiratory tract infection, generally of viral origin, mostly caused by rhinoviruses, coronaviruses, and influenza viruses, others caused by adenoviruses, human parainfluenza viruses, human respiratory syncytial virus, enteroviruses other than rhinoviruses, and metapneumovirus. If the infection is of bacterial origin, the most common three causative agents are "Streptococcus pneumoniae", "Haemophilus influenzae", and "Moraxella catarrhalis". Until recently, "Haemophilus influenzae" was the most common bacterial agent to cause sinus infections. However, introduction of the "H. influenza" type B (Hib) vaccine has dramatically decreased "H. influenza" type B infections and now non-typable "H. influenza" (NTHI) are predominantly seen in clinics. Other sinusitis-causing bacterial pathogens include "Staphylococcus aureus" and other streptococci species, anaerobic bacteria and, less commonly, gram negative bacteria. Viral sinusitis typically lasts for 7 to 10 days, whereas bacterial sinusitis is more persistent. Approximately 0.5% to 2% of viral sinusitis results in subsequent bacterial sinusitis. It is thought that nasal irritation from nose blowing leads to the secondary bacterial infection.

Acute episodes of sinusitis can also result from fungal invasion. These infections are typically seen in patients with diabetes or other immune deficiencies (such as AIDS or transplant patients on immunosuppressive anti-rejection medications) and can be life-threatening. In type I diabetics, ketoacidosis can be associated with sinusitis due to mucormycosis.

Chemical irritation can also trigger sinusitis, commonly from cigarette smoke and chlorine fumes. Rarely, it may be caused by a tooth infection.

Symptoms of mold exposure can include:

- Nasal and sinus congestion, runny nose

- Respiratory problems, such as wheezing and difficulty breathing, chest tightness

- Cough

- Throat irritation

- Sneezing / Sneezing fits

Among US adults older than 55, 4% are taking medication and or supplements that put them at risk of a major drug interaction. Potential drug-drug interactions have increased over time and are more common in the low educated elderly even after controlling for age, sex, place of residence, and comorbidity.

A recent retrospective study of all cases of Ecthyma gangrenosum from 2004-2010 in a university hospital in Mexico shows that neutropenia in immunocompromised patients is the most common risk factor for ecthyma gangrenosum.

Carrion's disease is caused by "Bartonella bacilliformis".

Recent investigations show that "Candidatus Bartonella ancashi" may cause verruga peruana, although it may not meet all of Koch's postulates. There has been no experimental reproduction of the Peruvian wart in animals and there is little research on the disease's natural spread or impact in native animals.