CDI Treatment Clostridioides (Clostridium) difficile Toolkit for Long-term Care Facilities

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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.

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Last Updated: 10/05/2022

Treating and Preventing C. difficile Infections

This information is right for you if:

What will this summary tell me?

This summary will answer these questions:

• What is a C. difficile infection?
• How is CDI treated?
  • What have researchers found about treatments for CDI?
  • What are possible side effects of treatments for CDI?
• What can I do to help prevent CDI?
• What should I think about when deciding on treatment for my CDI?

What is the source of this information?

This information comes from a research report that was funded by the Agency for Healthcare Research and Quality, a Federal Government agency.

To write the report, researchers looked at 56 scientific research articles reporting on studies to prevent and treat CDI. The studies were published through April 2015.

Health care professionals, researchers, experts, and the public gave feedback on the report before it was published.

Understanding Your Condition

What is a C. difficile infection?

A C. difficile infection (CDI) results from a type of bacteria (or germ) called Clostridium difficile infecting your large intestine. C. difficile bacteria are common and can be found everywhere. These bacteria can be found in the air, in water, or on items such as door knobs, sinks, and countertops. Small amounts of C. difficile bacteria are even found in many people’s intestines.

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.

CDI affects about 500,000 people in the United States each year. CDI can be mild to severe. The most common symptoms of CDI include watery diarrhea (three or more times a day for 2 or more days) and cramping in your belly. Some people with CDI can become very sick. In rare cases, severe CDI can be life threatening.

Symptoms of severe CDI may include:

• Having watery diarrhea often (as many as 15 times) throughout the day and night
• Cramping and pain in your belly that may be severe
• Blood or pus (a thick, yellowish substance) in your bowel movements
• Tenderness in your belly
• A swollen belly
• A fever
• Nausea
• Vomiting
• Not enough water in your body (called “dehydration”)
• Loss of appetite
• Weight loss

What increases the risk of CDI?

Anyone can get CDI, but some people have a higher risk. You may be at a higher risk for getting CDI if you:

Can CDI come back after treatment?

For some people, CDI may return after treatment ends. Out of every 10 people who have had CDI in the past, as many as 3 to 6 people will have CDI again.

Understanding Your Options

How is CDI treated?

There are several treatments for CDI, including:

• Antibiotics to treat your CDI.
• Probiotics to take with an antibiotic to help keep your CDI from coming back.
• Fecal microbiota transplantation if antibiotics do not help your CDI or if your CDI keeps coming back.

What about antidiarrhea medicines?
Talk with your health care professional before taking any over-the-counter antidiarrhea medicines (such as Pepto-Bismol®, Kaopectate®, or Imodium®) for your CDI. These medicines may make CDI worse.

Antibiotics

If your CDI happened after you took an antibiotic, your health care professional may have you stop taking the antibiotic. Your health care professional will likely give you a different antibiotic to help treat your CDI. The antibiotic your doctor recommends may depend on the availability and cost of the antibiotic, what is covered by your health insurance plan, and how severe your CDI is.

Note: You should never stop taking any medicine without first talking with your health care professional.

Your health care professional will likely first recommend one of these antibiotics:

• Metronidazole (Flagyl®)
• Vancomycin (Vancocin®)

If metronidazole (Flagyl®) and vancomycin (Vancocin®) do not work to treat your CDI, your health care professional may recommend a newer kind of antibiotic:

• 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.

What did researchers find about antibiotics for CDI?

What are possible side effects of antibiotics to treat CDI?

The U.S. Food and Drug Administration (FDA) lists the following possible side effects of antibiotics to treat CDI. Just because a side effect is possible does not mean you will have it.

Probiotics

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.

Note: The FDA approves the quality and safety of all prescription and over-the-counter medicines. But dietary supplements such as probiotics do not need FDA approval. When considering a dietary supplement, always check the label to see if the supplement has been tested for quality.

What did researchers find about probiotics?

The chart below lists some different types of probiotics and what researchers found about each.

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.

What are possible side effects of probiotics?

Probiotics are usually safe for people who are generally healthy. Possible side effects of probiotics may include gas and bloating.

For people with a weak immune system, S. boulardii may cause severe side effects, such as a life-threatening fungal infection. It is important to always talk with your health care professional before taking probiotics.

Fecal Microbiota Transplantation

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.

What did researchers find about FMT?

Researchers found that FMT appears to help stop diarrhea and to help keep CDI from coming back, but more research is needed to know this for sure.

What are possible side effects of FMT?

There is not much research on the short-term and long-term side effects of FMT. There is a chance of bleeding or infection, but the risk is low.

Other possible side effects of FMT may include:

• Diarrhea
• Stomach cramps
• Nausea
• Belching
• Constipation

What can I do to help prevent CDI?

• Only take antibiotics when your health care professional prescribes them. Take all antibiotics exactly as instructed. Never stop taking an antibiotic without first talking with your health care professional (even if you start to feel better).
• 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.

Making a Decision

What should I think about when deciding on treatment for my CDI?

You and your health care professional can decide what might be best to treat CDI and help keep it from coming back. Talk with your health care professional about whether this is your first time to have CDI or whether you have had CDI in the past and it has come back.

Ask your health care professional

• If my CDI happened after taking an antibiotic, should I stop taking the antibiotic? Is there a different antibiotic I can take with less risk of causing CDI?
• Which other antibiotic might be best to help treat my CDI?
• What possible side effects of the antibiotic for CDI should I watch for?
• Might probiotics help keep my CDI from coming back?
• If antibiotics do not work or if my CDI keeps coming back, might FMT help?
• What possible side effects from FMT would I need to watch for?

Source

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.

Additional information came from the MedlinePlus website, a service of the National Library of Medicine and the National Institutes of Health.

This summary was prepared by the John M. Eisenberg Center for Clinical Decisions and Communications Science at Baylor College of Medicine, Houston, TX. It was written by Amelia Williamson Smith, M.S., Daniel Musher, M.D., Frank Domino, M.D., and Michael Fordis, M.D. People who have had CDI gave feedback on this summary.

Yersiniosis and Pseudotuberculosis – Department of Infectious Diseases – Departments

Yersiniosis and Pseudotuberculosis are intestinal saprozoonoses caused by Yersinia, characterized by lesions of the gastrointestinal tract, severe toxic-vasar symptoms and inclination (most pronounced in pseudotuberculosis) to a generalized course . Both diseases have a distinct tendency to induce the development of immunopathology.

Etiology

The causative agents of yersiniosis (Y. enterocolitica) and pseudotuberculosis (Y. pseudotuberculosis) belong to the family of intestinal bacteria. Yersinia are gram-negative rods that grow on both normal and nutrient-poor media. The latter are used in bacteriological examination according to the method of Peterson and Cook (1963).

Yersinia contains O- and H-antigens. Differences in the structure of 0-antigens made it possible to isolate more than 50 Y. enterocolitica serovars. Serovars 03 are of the greatest importance in human pathology; 05.27; 07.8 and 09. The causative agent of pseudotuberculosis has 8 serovars. The most common disease in humans is caused by serovar 1.

Many strains of Yersinia produce exotoxin (a thermostable enterotoxin). When bacteria are destroyed, endotoxin is released. Yersinia also have the ability of adhesion, invasion and intracellular reproduction. Invasive properties in Y. pseudotuberculosis are more pronounced than in Y. entero-colitica.

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.

Epidemiology

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 source of infection for humans with yersiniosis are farm animals, less often synanthropic rodents. A sick person as a source of infection is incomparably less important. With pseudotuberculosis, the main sources of infection are synanthropic and wild rodents. A person, as a rule, is not a source of pseudotuberculosis.

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.

Pathogenesis

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.

When Yersinia and its toxins are kept in the blood and organs for a long time, the organism becomes sensitized. In some patients, usually with the HLA-B27 phenotype, yersiniosis and pseudotuberculosis can trigger the emergence of immunopathological reactions and conditions.

The final link in pathogenesis is the release of the body from the pathogen, leading to recovery.

The development of specific immunity in yersiniosis and pseudotuberculosis is slow and it is not strong enough, which is the reason for the frequent development of exacerbations and relapses of the disease.

Clinic

The duration of the incubation period for yersiniosis ranges from 1 to 7 days, and for pseudotuberculosis – from 3 to 21 days.

Based on the general pathogenetic patterns of intestinal zoonoses and clinical and pathogenetic features of yersiniosis and pseudotuberculosis, localized (gastro-intestinomesenteric) and general and yawning forms can be distinguished. They may be symptomatic or (rarely) asymptomatic.

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.

According to the severity of the manifest course of the disease, mild, moderate and severe are distinguished. By the nature of the course – smooth and complicated, including with exacerbations and relapses. According to the duration of the disease and its outcomes – acute (up to 3 months), chronic (more than 3 months) and clinical consequences (residual phase).

Localized (developing-intestinomesenteric) form occurs in 70% of cases of yersiniosis and almost 30% of pseudotuberculosis. The most common manifestations of this form are gastroenterocolitic , gastroenteric , enterocolitic and enteric disease course. They are registered in all age groups, but mostly in children under the age of 10 years.

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.

All variants of the localized form are characterized not only by abdominal (gastrointestinal), but also extra-abdominal symptoms due to the action of the toxin and excessive production of prostaglandins on vasomotors and vascular endothelium: injection of scleral vessels and conjunctival hyperemia, “crimson” tongue, soft palate hyperemia, arthralgia, myalgia, etc.

Leukocytosis, neutrophilia, stab shift, increased ESR, sometimes eosinophilia are observed in the peripheral blood.

The generalized form occurs in approximately 30% of cases of the manifest course of yersiniosis and 70% of cases of pseudotuberculosis. It has two types of flow: toxicobacteremia and septic. As with yersiniosis, and with pseudotuberculosis, a toxicobacteremic course of a generalized form is usually observed. A septic course in both diseases is extremely rare.

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.

It should be noted that this type of exanthema practically does not occur in yersiniosis. It is more characteristic of a small-spotted rash on symmetrical areas of the skin of the trunk and / or extremities, which disappears in a period of several hours to 3-4 days.

Palpation reveals moderately enlarged and painful peripheral lymph nodes. Determined lability and increased heart rate, corresponding to body temperature. Arterial pressure is somewhat reduced.

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.

The disease is often accompanied by the development of signs of infectious-toxic interstitial nephritis. In some cases of severe disease, signs of serous meningitis are observed.

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.

Sometimes during this period of the disease, myocarditis, nephritis, urethritis, cystitis, conjunctivitis, iridocyclitis and other lesions of internal organs are detected.

According to the predominance of one or another symptomatology within the toxic-bacteremic course of the generalized form of the disease, the following variants are distinguished: exanthematous, arthritic, icteric (yersinia / pseudotuberculosis hepatitis), meningeal, catarrhal and yersiniosis (pseudotuberculosis) of rare localizations.

Exacerbations and relapses often complicate the course of yersiniosis and pseudotuberculosis. They occur in 1/3 patients and are characterized by a repeated wave of fever and symptoms of local lesions.

During the period of convalescence, the body temperature drops to normal, the symptoms of intoxication disappear, and the functions of internal organs normalize.

The severity of the course of yersiniosis and pseudotuberculosis is determined by the severity of the intoxication syndrome and the degree of involvement of internal organs in the pathological process. More often the disease occurs in mild and moderate forms.

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.

The prognosis in most cases, with the exception of the septic course of the disease, is favorable.

Diagnosis

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.

The main materials for bacteriological examination are feces, blood, cerebrospinal fluid, resected lymph nodes and appendix. Enzyme-linked immunosorbent assay (ELISA) is used to determine the presence of pseudotuberculous antigens in faeces and other material.

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.

In the express diagnosis of yersiniosis, RNHA with immunoglobulin diagnosticums and MFA is used.

Histological examination of biopsies of lymph nodes and other organs is also of particular importance in diagnosis.

Differential diagnosis of yersiniosis and pseudotuberculosis depends on the clinical variant of the disease. Most often there is a need to differentiate these diseases from acute intestinal infections, appendicitis, various diseases of the joints, viral hepatitis, sepsis of a different etiology, etc.

Treatment

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.

Pathogenetic therapy involves the appointment of detoxification, general strengthening and stimulating, as well as desensitizing agents. In some cases, glucose electrolyte and polyionic rehydration solutions are used.

Patients with a septic course of the disease are treated in accordance with the principles of the treatment of sepsis, using 2-3 antibiotics (fluoroquinolones, aminoglycosides, cephalosporins) intravenously in combination with intensive pathogenetic therapy.

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.

Surgical treatment is carried out according to indications.

Prevention

Monitoring the condition of vegetable stores, rodent control.

Acute rhinosinusitis (sinusitis): symptoms and treatment

Acute rhinosinusitis (ORS, or sinusitis) is one of the most common inflammatory diseases of the nasal cavity and paranasal sinuses in adults and children.

It is preferable to use the term “rhinosinusitis” rather than “sinusitis”, since inflammation isolated in the sinuses is extremely rare.

Depending on the duration, rhinosinusitis is divided into types:

• acute – symptoms last less than 4 weeks;
• subacute – 4 to 12 weeks;
• chronic – symptoms persist for more than 12 weeks.

Recurrent ARS is four or more recurring episodes of the inflammatory process within a year, with complete recovery in between.

According to the etiology, acute viral rhinosinusitis (AVRS) is the most common form of the disease, uncomplicated acute bacterial rhinosinusitis (ABRS) and complicated ABRS (the inflammatory process spreads to the surrounding structures).

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.

Diagnosis of acute rhinosinusitis

Symptoms of ARS include difficulty breathing through the nose, nasal congestion, purulent discharge from the nose, discomfort or pain in the maxillary sinuses (cheeks) and teeth, which in some cases are aggravated by bending forward. General symptoms: fever, fatigue, cough, hyposmia or anosmia (impaired sense of smell), stuffy ears, headache.

The symptoms of OVRS and ABRS are very similar, which sometimes makes it difficult to diagnose and leads to inappropriate treatment.

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.

When viewed (anterior rhinoscopy) in the nasal cavity, diffuse swelling of the mucous membrane, narrowing of the middle nasal passages, hypertrophy and swelling of the inferior nasal concha, mucous or mucopurulent discharge in the nasal cavity are visualized.

Complications of ABRS, when infection spreads beyond the paranasal sinuses and nasal cavity into the central nervous system, orbit, or surrounding tissues, are extremely rare.

X-rays or computed tomography of the nose and paranasal sinuses may show changes such as fluid levels, swelling of the mucous membrane, air bubbles in the sinuses. All these signs are nonspecific and are often observed in banal ARVI. That is why, in uncomplicated ARS, X-ray examination is not indicated.

Microbiological studies (smears from the nasal cavity) are also not indicated in the standard situation. The need for them arises either in cases of ineffectiveness of empirical therapy, or in patients with suspected complicated course of the disease.

Differential diagnosis

OCR should be differentiated from the following processes:

• Fungal rhinosinusitis (acute invasive form) – symptoms are similar to ARS, but the disease progresses more rapidly, in many cases the infection spreads beyond the sinuses.
• Acute respiratory viral infection – symptoms of the common cold and ARS are often similar. However, patients with a cold usually do not have facial pain, and symptoms often include sneezing fits, nasal discharge, coughing due to mucus dripping from the nasopharynx.
• Allergic and vasomotor rhinitis. In contrast to ARS, symptoms of sneezing, rhinorrhea (copious mucous, watery discharge), nasal congestion, and nasal itching predominate. Facial pain is not noted.
• Facial pain. May be a manifestation of neuralgia, pathology of the temporomandibular joint. There are no nasal symptoms.
• Headache. Frontal sinus pain can be caused by a variety of causes, including migraines, tension headaches, and cluster headaches.

Treatment of acute rhinosinusitis

Symptomatic therapy is indicated for patients with OVRS.

• Analgesics and antipyretics – ibuprofen or paracetamol can be used to relieve pain and reduce fever as needed.
• Irrigation Saline Therapy – Nasal rinsing with saline or hypertonic saline may reduce the need for pain medication and improve general well-being. It is important that nasal irrigation solutions are sterile, as amoebic encephalitis has been reported from the use of tap water for nasal irrigation.
• 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.
• Ipratropium bromide is an anticholinergic spray that may help relieve rhinorrhea in patients with concomitant cold symptoms.
• Oral decongestants may be useful for Eustachian tube dysfunction.
• Intranasal vasoconstrictors are often used by patients as symptomatic therapy. Sprays containing oxymetazoline or xylometazoline may provide temporary relief from nasal congestion, but there is no evidence of significant benefit in ARS.

In cases of mild uncomplicated ABRS, there is no indication for systemic antibiotics, treatment is symptomatic, as in cases of viral infection.

Expectant management for 7 days is recommended for ABRS. Systematic reviews and meta-analyses have shown that about 80% of patients with clinically diagnosed ABRS recover without antibiotic therapy within two weeks.

If the state of health does not improve within 7 days or worsens to symptomatic treatment, systemic antibiotic therapy should be added.

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.

Preference for amoxicillin-clavulanate should be given in the following cases.

• The patient lives in an area with a high rate of penicillin-resistant S. pneumoniae strains (greater than 10%).
• Age ≥ 65 years.
• Hospitalization in the last five days.
• Use of antibiotics in the previous month.
• Immunocompromised patients.
• Patients with comorbidities such as diabetes, chronic heart, liver or kidney disease.
• Severe or complicated course of the disease.

In case of allergy to penicillin antibiotics, options for prescribing doxycycline, cephalosporin antibiotics, clindamycin are considered. Another alternative for patients allergic to penicillins are respiratory fluoroquinolones. However, these drugs should only be used when there is no alternative due to serious side effects.

The duration of the course of antibiotic therapy in adults is usually 5-7 days, in children – 10-14 days. There are studies showing that short courses of antibiotic therapy are as effective as long ones.

In the absence of the effect of the first course of antibiotics, the next prescribed drug should have a wider spectrum of activity and / or belong to a different class of drugs.

How is acute rhinosinusitis treated at the Rassvet Clinic?

• We carefully collect anamnesis and conduct an examination.
• We do not prescribe antibiotics unless there is clear evidence of a bacterial infection.
• We do not order x-rays, bacteriological studies or blood tests in a standard situation. It is not necessary.
• We adhere to the principles of evidence-based medicine, which means that when there are indications for antibiotic therapy, we always give preference to systemic antibiotics, usually oral.