What antibiotics are used for c diff. Comprehensive Guide to C. Difficile Infection: Antibiotics, Treatment, and Prevention

22.10.202108.06.2023 by alexxlab

What are the most effective antibiotics for treating C. difficile infection. How is CDI diagnosed and what are the recommended treatment options. What preventive measures can reduce the risk of developing or spreading C. difficile.

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Understanding C. Difficile Infection (CDI)

Clostridioides difficile, formerly known as Clostridium difficile, is a bacterium that can cause a serious infection of the large intestine. C. difficile infection (CDI) occurs when the normal balance of bacteria in the gut is disrupted, often following antibiotic use, allowing C. difficile to proliferate and produce toxins that damage the intestinal lining.

CDI affects approximately 500,000 people in the United States annually, with severity ranging from mild to life-threatening. The most common symptoms include:

Watery diarrhea (3+ times daily for 2+ days)
Abdominal cramping and pain
Fever
Loss of appetite
Nausea

In severe cases, CDI can lead to complications such as dehydration, electrolyte imbalances, toxic megacolon, and bowel perforation.

Antibiotics Used to Treat C. Difficile Infection

The primary treatment for CDI involves targeted antibiotic therapy. The choice of antibiotic depends on the severity of the infection and whether it’s an initial or recurrent case. The most commonly used antibiotics for CDI include:

Vancomycin

Vancomycin is a glycopeptide antibiotic that is highly effective against C. difficile. It is typically administered orally for CDI treatment. Vancomycin is often the first-line treatment for severe or recurrent cases of CDI.

Metronidazole

Metronidazole is a nitroimidazole antibiotic that has been historically used for mild to moderate CDI. However, its use has declined in recent years due to concerns about efficacy and potential side effects. Metronidazole is not FDA-approved for CDI treatment but may still be used in certain situations.

Fidaxomicin

Fidaxomicin is a newer, narrow-spectrum antibiotic specifically designed to target C. difficile while preserving the normal gut microbiota. It has shown efficacy in reducing CDI recurrence rates compared to vancomycin.

When treating CDI, it’s crucial to discontinue any other antibiotics that may have triggered the infection, if possible. Treatment duration is typically 10-14 days, depending on the severity of the infection and the chosen antibiotic.

Diagnosing C. Difficile Infection

Accurate diagnosis of CDI is essential for appropriate treatment. Diagnostic methods include:

Stool toxin tests: These detect the presence of C. difficile toxins in a stool sample.
PCR tests: These identify the genes responsible for toxin production in C. difficile.
Stool culture: This can isolate and grow C. difficile bacteria from a stool sample.
Endoscopy: In severe cases, a colonoscopy or sigmoidoscopy may be performed to visualize the colon and assess the extent of inflammation.

Healthcare providers should consider CDI in patients with recent antibiotic exposure who develop diarrhea, especially in healthcare settings where C. difficile is prevalent.

Managing Recurrent C. Difficile Infections

Recurrent CDI is a significant challenge, affecting approximately 20% of patients after initial treatment. Management strategies for recurrent CDI include:

Extended or pulsed vancomycin regimens
Fidaxomicin treatment
Bezlotoxumab, a monoclonal antibody that binds to C. difficile toxin B
Fecal microbiota transplantation (FMT)

Fecal microbiota transplantation has shown remarkable success in treating recurrent CDI. This procedure involves transferring stool from a healthy donor to the colon of a patient with CDI, effectively restoring a healthy gut microbiome. While FMT has demonstrated high efficacy, its long-term safety profile is still being studied, and availability may be limited in some areas.

Preventing C. Difficile Infection

Prevention is crucial in reducing the incidence of CDI, particularly in healthcare settings. Key preventive measures include:

Judicious use of antibiotics (antibiotic stewardship)
Proper hand hygiene with soap and water
Environmental cleaning and disinfection
Isolation precautions for infected patients
Personal protective equipment for healthcare workers

Can probiotics help prevent CDI? While some studies suggest that certain probiotic strains may reduce the risk of CDI, current guidelines do not recommend their routine use for CDI prevention due to limited data and potential risks. However, patients with recurrent CDI may benefit from specific probiotic strains, such as Saccharomyces boulardii, under medical supervision.

Emerging Therapies for C. Difficile Infection

Research into new treatments for CDI is ongoing. Some promising approaches include:

Novel antibiotics with enhanced selectivity for C. difficile
Microbiome-based therapies, including defined bacterial consortia
Immunotherapies targeting C. difficile toxins
Vaccines to prevent primary and recurrent CDI

These emerging therapies aim to improve treatment outcomes, reduce recurrence rates, and minimize disruption to the gut microbiome.

Special Considerations for Long-Term Care Facilities

Long-term care facilities (LTCFs) face unique challenges in managing CDI due to their vulnerable patient populations and the potential for rapid spread within the facility. Key considerations for LTCFs include:

Implementing robust infection control protocols
Educating staff, residents, and visitors about CDI prevention
Developing antibiotic stewardship programs
Ensuring prompt diagnosis and treatment of suspected cases
Coordinating with acute care facilities for seamless patient transitions

LTCFs should have clear policies and procedures in place for managing CDI outbreaks and preventing transmission within the facility.

The Impact of C. Difficile Infection on Public Health

CDI poses a significant burden on healthcare systems and society as a whole. The impact of CDI extends beyond individual patient outcomes and includes:

Increased healthcare costs
Prolonged hospital stays
Strain on healthcare resources
Potential for community spread
Contribution to antimicrobial resistance

Addressing CDI requires a coordinated effort from healthcare providers, public health officials, and researchers to improve prevention, diagnosis, and treatment strategies.

How does CDI contribute to antimicrobial resistance? While C. difficile itself is not typically resistant to antibiotics used for its treatment, the overuse of broad-spectrum antibiotics that can trigger CDI contributes to the larger problem of antimicrobial resistance. Additionally, the need for repeated antibiotic treatments in recurrent CDI cases can further exacerbate this issue.

The Role of Antimicrobial Stewardship

Antimicrobial stewardship programs play a crucial role in combating CDI and antimicrobial resistance. These programs aim to optimize antibiotic use through:

Evidence-based prescribing guidelines
Regular review of antibiotic prescriptions
Education for healthcare providers and patients
Monitoring and reporting of antibiotic use and resistance patterns

Effective antimicrobial stewardship can reduce the incidence of CDI, improve patient outcomes, and help preserve the efficacy of antibiotics for future use.

Patient Education and Empowerment

Educating patients about CDI is essential for prevention and early detection. Key points to communicate include:

The importance of proper hand hygiene
Understanding the risks associated with antibiotic use
Recognizing the symptoms of CDI
The significance of completing prescribed antibiotic courses as directed
When to seek medical attention for persistent or severe diarrhea

Empowering patients with this knowledge can lead to better health outcomes and reduce the spread of C. difficile in both healthcare and community settings.

The Future of C. Difficile Management

As our understanding of C. difficile and the gut microbiome evolves, so too will our approaches to managing CDI. Future directions in CDI management may include:

Personalized treatment strategies based on individual microbiome profiles
Advanced diagnostic tools for rapid and accurate CDI detection
Novel non-antibiotic therapies that target C. difficile without disrupting the gut microbiota
Improved infection control technologies for healthcare environments

Continued research and innovation in these areas hold promise for reducing the burden of CDI and improving patient outcomes.

In conclusion, C. difficile infection remains a significant challenge in healthcare, requiring a multifaceted approach to prevention, diagnosis, and treatment. By staying informed about the latest developments in CDI management and implementing evidence-based practices, healthcare providers and facilities can work towards reducing the impact of this potentially severe infection. Patients and caregivers also play a crucial role in CDI prevention and early detection, highlighting the importance of education and awareness in combating this healthcare-associated infection.

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Guidance for Long-term Care Facilities

Whenever possible, other antibiotics should be discontinued. In a small number of patients, diarrhea may go away when other antibiotics are stopped. Proton pump inhibitors (PPI) and antiperistaltic agents should also be avoided for all residents suspected of having or diagnosed with CDI.
Treatment of primary infection caused by C. difficile is an antibiotic such as metronidazole, vancomycin, or fidaxomicin. While metronidazole is not approved for treating C. difficile infections by the FDA, it has been commonly recommended and used for mild C. difficile infections; however, it should not be used for severe C. difficile infections. Whenever possible, treatment should be given by mouth and continued for a minimum of 10 days.
One problem with antibiotics used to treat primary C. difficile infection is that the infection returns in about 20 percent of patients. In a small number of these patients, the infection returns over and over and can be quite debilitating. While a first return of a C. difficile infection is usually treated with the same antibiotic used for primary infection, all future infections should be managed with oral vancomycin or fidaxomicin.
Transplanting stool from a healthy person to the colon of a patient with repeat C. difficile infections has been shown to successfully treat C. difficile. These “fecal transplants” appear to be the most effective method for helping patients with repeat C. difficile infections. This procedure may not be widely available and its long-term safety has not been established.
Probiotics are not recommended to prevent primary CDI due to limited data and risk of bloodstream infection. Patients with recurrent CDI may benefit from 500 mg of Saccharomyces boulardii twice a day.

How is CDI treated?
What have researchers found about treatments for CDI?
What are possible side effects of treatments for CDI?

If C. difficile bacteria in your intestines grow out of control, they can cause an infection. This can happen after a person takes antibiotics. Antibiotics are a type of medicine that fight infections caused by bacteria. When you take antibiotics, the normal bacteria in your intestines that help keep you healthy can also be killed. When this happens, bacteria such as C. difficile can grow out of control. When a person has CDI, chemicals called toxins produced by the C. difficile bacteria make him or her sick.

Fidaxomicin (Dificid®)
Fidaxomicin is much more expensive than both metronidazole and vancomycin. The cost to you depends on your health insurance plan.
Most health insurance plans will only cover fidaxomicin after you have tried metronidazole and vancomycin and neither one worked.

Findings about antibiotics for CDI
Antibiotic	What did researchers find?
Metronidazole (Flagyl®)	Works to treat CDI for most people. CDI is just as likely to come back with metronidazole (Flagyl®) as it is with taking vancomycin (Vancocin®).
Vancomycin (Vancocin®)	Works to treat CDI for most people. Works slightly better than metronidazole (Flagyl®). CDI is just as likely to come back with vancomycin (Vancocin®) as it is with taking metronidazole (Flagyl®).
Fidaxomicin (Dificid®)	Works as well as vancomycin (Vancocin®) does. CDI is less likely to come back with fidaxomicin (Dificid®) than after taking vancomycin (Vancocin®).

Possible side effects of antibiotics to treat CDI
Antibiotic	Possible Side Effects
Metronidazole (Flagyl®)	Nausea Vomiting Headache Loss of appetite Diarrhea Pain in the belly Constipation Metallic taste in the mouth Warning: Metronidazole (Flagyl®) may cause nerve damage and seizures, although these are rare.
Vancomycin (Vancocin^®)	Nausea Pain in the belly Low potassium in the blood
Fidaxomicin (Dificid^®)	Nausea Vomiting Pain in the belly Low red blood cell count (anemia) Low white blood cell count (neutropenia) Bleeding in the stomach

To help keep your CDI from coming back, your health care professional may suggest that you take probiotics along with the antibiotic to treat your CDI. Probiotics are healthy bacteria and other microscopic organisms that are normally found in your body. Probiotics are taken as dietary supplements. They come in some foods, such as yogurt, kefir (a drink made from fermented milk), soy drinks, buttermilk, some soft cheeses, and enriched milk. Probiotics also come as a pill you can take by mouth.

Findings About Probiotics
Types of Probiotics	What did researchers find?
Saccharomyces boulardii (also called S. boulardii)	Does not appear to help keep CDI from coming back when added to treatment with an antibiotic, but more research is needed to know this for sure.
Lactobacillus	Appears to help keep CDI from coming back when added to treatment with an antibiotic, but more research is needed to know this for sure.
A combination of two or more types of probiotics	Appears to help keep CDI from coming back when added to treatment with an antibiotic, but more research is needed to know this for sure.

Fecal microbiota transplantation (FMT) is a newer type of treatment for CDI. Your health care professional may suggest FMT if antibiotics do not help your CDI or if your CDI keeps coming back. FMT is meant to help put some of the “good” bacteria back into your intestines. To do this, your health care professional takes a small amount of stool containing healthy bacteria from a person who does not have CDI and places it into your intestine. The stool may come from a close family member or from a healthy donor from a stool bank.

When caring for someone with CDI:
Wash your hands often. To help prevent CDI, it is best to use soap and water instead of hand sanitizer.
Clean often-touched surfaces such as door knobs, sinks, and countertops with a disinfectant, such as bleach.

The information in this summary comes from Butler M, Olson A, Drekonja D, Shaukat A, Schwehr N, Shippee N, Wilt TJ. Early Diagnosis, Prevention, and Treatment of Clostridium difficile: Update. Comparative Effectiveness Review No. 172. (Prepared by the Minnesota Evidence-based Practice Center under Contract No. 290-2012-00016-I.) AHRQ Publication No. 16-EHC012-EF. Rockville, MD: Agency for Healthcare Research and Quality; March 2016.

Yersinia are psychrophiles. At a refrigerator temperature (4-8 °C), they are able to persist for a long time and multiply on vegetables, root crops and other food products. At the same time, some of the bacterial strains have increased heat resistance to high temperatures and are able to withstand the pasteurization regime. When boiled (100°C), all strains of Yersinia die within a few seconds. Sensitive to common disinfectants.

Yersinia (Y. enterocolitica and Y. pseudotuberculosis) are widely distributed in nature. They were found in soil, water, isolated from the body of many animal species. However, the main reservoir of the pathogen in nature, obviously, are small rodents, which, by seeding various environmental objects, food products, water, contribute to the spread of infection among other animals. Another reservoir of Yersinia is the soil. The frequent detection of pathogens in it is associated not only with contamination with animal feces, but also with the presence of saprophytic properties in Yersinia. Based on this, the disease can be classified as a saprozoonosis.

The main way of spread of both infections is food. Transmission factors for Y. enterocolitica are most often infected meat products, milk, vegetables, root crops, and water. Y. pseudotuberculosis transmission factors include vegetable dishes (cabbage salads, carrots, etc.) and dairy products that are eaten without prior heat treatment. The water route of transmission is incomparably less important for both infections. It is usually realized by drinking water from open reservoirs. Other routes of transmission are not significant in the epidemiology of yersiniosis.

The disease occurs in all age groups, but more often in children of the first years of life. The seasonal rise in the incidence of yersiniosis is observed in the cold season with a peak in November. In some regions, there are two seasonal rises – in autumn and spring. The peak incidence of pseudotuberculosis occurs in the spring months (March-May). Yersiniosis and pseudotuberculosis occur as sporadic and group diseases.

The entrance gate for causative agents of yersiniosis and pseudotuberculosis is the gastrointestinal tract. The most pronounced local reaction in response to Yersinia invasion is recorded from the mucous membrane of the ileum and its lymphoid formations. In the ileum, an inflammatory process of various severity develops – terminal ileitis. Through the lymphatic vessels, Yersinia penetrate into the mesenteric lymph nodes and cause mesadenitis. The appendix and the cecum may be involved in the pathological process.

Against the background of infectious and inflammatory changes, toxic and toxic-vasar (paresis of vasomotors) processes associated with toxinemia develop. At this stage, the infectious process, acquiring the features of a localized form, can be completed.
In the event of a breakthrough of the intestinal lymphatic barrier, bacteremia occurs, causing the development of generalized forms of the disease. There is a bacterial-toxic damage to many organs and systems, primarily the liver and spleen, it is possible to develop polylymphadenitis, polyarthritis, myositis, nephritis, urethritis, meningitis, etc.

Localized (gastrointestinomesenteric) form of manifest flow includes the following options: gastroentero-colitis , gastroenteritis , enterocolitis , enteritis , acute terminal ileitis , mesadenitis , an pendicitis . The asymptomatic course of the localized (gastrointestinomesenteric) form includes subclinical and convalescent variants. The latter is not characteristic of pseudotuberculosis.

The generalized form of the manifest course can have two varieties: toxicobacteremia and septic. Depending on the predominance of one symptom or another, the toxicobacteremic variety of the generalized form can occur in the following variants: exanthematous, arthritic, icteric (yersinia hepatitis), meningeal, catarrhal, mixed, and in the form of yersiniosis (pseudotuberculosis) of rare localizations. In rare cases (for example, in immunocompromised individuals with chronic liver pathology and signs of iron thesaurismosis), yersinia sepsis develops. An asymptomatic course with a generalized form can be represented by a convalescent variant. The latter is usually not characteristic of pseudotuberculosis.

The clinical picture of these variants is characterized by the presence of an intoxication syndrome and symptoms of damage to the gastrointestinal tract at one or another of its levels. The disease begins acutely: chills occur, body temperature rises to 38-38.5 ° C. Patients are concerned about headache, weakness, myalgia and arthralgia. Simultaneously with the intoxication syndrome, nausea occurs, in some patients – vomiting, abdominal pain, which are cramping or permanent. Localization of pain – in the epigastrium, around the navel, in the right iliac region, sometimes in the right hypochondrium. The chair is liquid, viscous, with a pungent odor. In some patients, when the colon is involved in the pathological process, an admixture of mucus, less often blood, is found in the stool. The frequency of stools is from 2-3 to 15 times a day. The duration of the disease is from 2 to 15 days. Along with a benign course, there are severe forms of the disease with pronounced intoxication, dehydration of the body.

Acute terminal ileitis is accompanied by an increase in body temperature up to 38-39°C, intense pain in the ileocecal region and diarrhea. Patients, as a rule, describe two types of pain: constant and against their background – cramping types. On x-ray examination, the affected part of the ileum is sharply narrowed and has a smooth relief of the mucous membrane (“cord symptom”). Terminal ileitis has a long and often complicated course. Among the possible complications: infarction and necrosis of the mucous membrane, followed by limited or (rarely) diffuse peritonitis, adhesive process, the development of intestinal obstruction, etc. It is possible to develop a clinic of consequences in the form of a chronic granulomatous-ulcerative lesion of the ileum, morphologically indistinguishable from Crohn’s disease.

Acute mesadenitis is characterized by moderately severe intoxication, subfebrile temperature, less than with terminal ileitis, the strength of cramping and constant type of pain. At the onset of the disease, nausea, vomiting, loose stools up to 3-5 times per day may occur. In the future, a significant part of the patients develop (for 4-6 days) “infiltrate” in the ileocecal region, which is a group of enlarged mesenteric nodes, and peritoneal symptoms. Positive symptoms of McFadden, Klein, Padalka, Sternberg’s “cross” symptom are revealed. The course of acute mesadenitis is often accompanied by exacerbations and relapses. The transition of the disease to a protracted and chronic course is possible. Some patients undergo surgery.

Acute yersinia (pseudotuberculous) appendicitis , unlike vulgar, has a slower rate of development from catarrhal to destructive forms. As a consequence of this – a higher frequency of detection of a catarrhal appendix during surgery than with vulgar appendicitis. However, this option does not differ in a smooth flow. Often, after surgery, signs of generalization develop: high fever, polylymphadenitis, hepatosplenomegaly, exanthema.

The toxicobacteremia course of the generalized form is best studied in the exanthematous variant of pseudotuberculosis, previously described as Far Eastern scarlet fever. The disease is characterized by an acute onset. Patients complain of chills, headache, myalgia and arthralgia. Body temperature rises to 38-40°C and stays at this level for 5-7 days, and in severe form even longer. In the first days of the disease, nausea, sometimes vomiting, loose stools, and abdominal pain are noted. Often there are catarrhal symptoms from the upper respiratory tract: perspiration and moderate pain when swallowing, coughing, runny nose.

During an objective examination in the 1st week of the disease, the skin of patients is dry, hot, the face is puffy. There is hyperemia of the conjunctiva, injection of the vessels of the sclera. Often, especially in children, a pale nasolabial triangle is determined. The mucous membrane of the oropharynx is diffusely hyperemic. In some patients, a dotted enanthema is found on the soft palate. Among the cardinal signs of this disease are punctate scarlatiniform exanthema in combination with symptoms of the “hood” (hyperemia of the face and neck), “gloves” and “socks” (limited hyperemia of the hands and feet). These cardinal symptoms appear most often on the 2-4th day of illness. The duration of the rash is 1-7 days. After its disappearance, from the 2nd week of the disease, most patients develop pityriasis peeling of the skin of the trunk, face and neck and lamellar (leaf-like) – the skin of the palms and feet.

Organs of the digestive system are naturally involved in the pathological process. The tongue, coated in the first days of the disease with a white coating, often clears up by the 5-7th day and becomes “raspberry”. On palpation of the abdomen, pain and rumbling are noted in the ileocecal region, with less persistence in the epi- and mesogastric region. Positive symptoms of Padalka, Sternberg’s “cross” are revealed. In malnourished patients, enlarged and tender mesenteric lymph nodes can be felt. Usually the liver is involved in the pathological process. It increases, becomes available for palpation by the end of the 1st week of the disease. In some patients, damage to the liver parenchyma leads to the appearance of icterus of the sclera and skin, hyperbilirubinemia, urobilin- and bilirubinuria, and moderate hypertransaminasemia. 9l, stab shift, sometimes eosinophilia, an increase in ESR up to 25-50 mm / h.

In some patients, the 2nd and 3rd weeks of illness are characterized by the appearance of symptoms indicating immunopathological restructuring. During this period, urticarial, macular and maculopapular rashes often appear with localization on the trunk and extremities, more often in the area of large joints. Erythema nodosum occurs. Some patients develop reactive polyarthritis, Reiter’s disease.

The septic course of the generalized form of yersiniosis and pseudotuberculosis is very rare. It usually develops with severe immunodeficiency, in individuals with chronic liver pathology and signs of iron thesaurismosis. The course of the disease is characterized by severe intoxication, microabscess formation of internal organs, hepatosplenomegaly, often diarrhea, a long relapsing course and, despite treatment, high mortality.

In all forms of the manifest course of yersinia infection, the duration of the disease usually does not exceed 1.5 months. However, sometimes there is a protracted course of the disease (from 1.5 to 3 months) and in rare cases chronic (more than 3 months). The presence of a disease etiologically associated with the transferred yersiniosis, but with a bacteriologically and serologically proven absence of the pathogen in the patient’s body, should be regarded as a clinic of the consequences of yersiniosis (residual phase).

Asymptomatic course can be acute (up to 3 months) and chronic (more than 3 months). The latter is not typical for pseudotuberculosis. In addition, with yersiniosis, in contrast to pseudotuberculosis, not only subclinical, but also convalescent bacterial excretion of pathogens is observed. Persons with an asymptomatic course of the disease are actively detected during the examination of workers in food enterprises and contact workers in the outbreaks.

Of the clinical signs, the combination of gastrointestinal tract injury syndrome and “extra-intestinal” toxic-vasar symptoms has the greatest diagnostic value. Epidemiological history data, especially in case of a group nature of morbidity, are also of great importance in recognizing yersiniosis and pseudotuberculosis. However, decisive in establishing the final diagnosis are specific diagnostic methods – bacteriological and serological.

Serological diagnosis is of great importance for confirming not only the clinical diagnosis, but also the etiological role of isolated Yersinia. It is carried out with the help of RA and RNGA by the method of paired sera. Blood sera taken at the beginning and at the 3rd week of illness are examined. An antibody titer of 1:80 and above is considered diagnostic for RA, and 1:160 and above for RNGA.

Antibiotics, sulfonamides and chemotherapy drugs are used as causal agents. Fluoroquinolones are the drugs of choice in the generalized form of the disease. Reserve drugs include 3rd generation cephalosporins, tetracyclines and chloramphenicol. Aminoglycosides are usually used in the treatment of patients with yersinia (pseudotuberculous) hepatitis. For the treatment of patients with gastrointestinal-mesenteric form (options: gastroenterocolitis, gastroenteritis, enterocolitis, enteritis), drugs from the group of cotrimoxazole and nitrofuran can be used. The duration of etiotropic therapy depends on the form of the disease. With a localized form, it is 7-10 days, with a generalized form – at least 12-14 days.

Asymptomatic patients receive therapy depending on the type (subclinical or convalescent) and duration of bacterial excretion. Treatment of an acute subclinical variant corresponds to the treatment of a mild course of a localized form. In the treatment of chronic subclinical and convalescent variants, fluoroquinolones, aminoglycosides, rifampicin are used in combination with immuno-oriented agents.

The vast majority of cases of ARS of viral origin are more often rhinovirus, influenza virus and parainfluenza. Acute bacterial infection occurs only in 0.5-2.0% of cases. ABRS usually occurs as a complication of a viral infection, but may also result from persistent obstruction of nasal breathing, decreased local or systemic immune function (allergic, non-allergic rhinitis, dental infection, cystic fibrosis, immunodeficiency). The most common bacteria associated with ABRS are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis, with the former two accounting for approximately 75% of sinusitis cases.

The main symptoms of OVRS resolve within 7-10 days. In most cases, the peak of the severity of the disease occurs on the 3-6th day, after which the state of health improves. Fever may be present in the early stages of the disease and disappear within the first 24 to 48 hours, with respiratory symptoms becoming more pronounced thereafter. Patients with ABRS have the same symptoms, but their duration is more than 10 days. The disease proceeds according to the scenario of “double deterioration” – an increase in symptoms occurs after an initial period of improvement.

Intranasal glucocorticoids (inGCS) – studies have shown little symptomatic benefit and minimal side effects with short-term use of inGCS in patients with both viral and bacterial ARS. InGCS are more effective in patients with concomitant allergic rhinitis. A meta-analysis of three studies in patients with ARS showed that the use of intranasal steroids increased the rate of symptom resolution compared with placebo. However, there is also evidence that only 1 out of 15 patients treated with inGCS will have a significant reduction in clinical symptoms.

The drugs of choice for ABRS are amoxicillin or amoxicillin-clavulanate. The use of an antibiotic with clavulanic acid in the composition expands the spectrum of action of the drug, including on ampicillin-resistant bacteria Haemophilus influenzae or Moraxella catarrhalis. This is not necessary in every case. There is evidence that the use of amoxicillin-clavulanate is more preferable in children than in adults. It should also be understood that resistance rates vary by region, which should also be taken into account when selecting therapy.

What antibiotics are used for c diff. Comprehensive Guide to C. Difficile Infection: Antibiotics, Treatment, and Prevention

Understanding C. Difficile Infection (CDI)