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Is gram positive cocci contagious: Contagious, Symptoms, Antibiotics & Rash

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Gram Positive Bacteria – StatPearls

Continuing Education Activity

Gram-positive organisms have highly variable growth and resistance patterns. The SCOPE project (Surveillance and Control of Pathogens of Epidemiologic Importance) found that in those with an underlying malignancy, gram-positive organisms accounted for 62 percent of all bloodstream infections in 1995 and 76 percent in 2000 while gram-negative organisms accounted for 22 percent in 1995 and 14 percent in 2000. This activity reviews the evaluation and management of gram-positive bacterial infections and explains the role of the interprofessional team in improving care for affected patients.

Objectives:

  • Explain how to evaluate for a gram-positive bacterial infection.

  • Identify common infections caused by gram-positive bacteria.

  • Describe treatment strategies for gram-positive bacterial infections.

  • Outline interprofessional team strategies to improve care coordination and communication to provide quality care to patients with gram-positive bacterial infections.

Access free multiple choice questions on this topic.

Introduction

Health professionals need to understand the important difference between gram-positive and gram-negative bacteria. Gram-positive bacteria are bacteria classified by the color they turn in the staining method. Hans Christian Gram developed the staining method in 1884. The staining method uses crystal violet dye, which is retained by the thick peptidoglycan cell wall found in gram-positive organisms. This reaction gives gram-positive organisms a blue color when viewed under a microscope. Although gram-negative organisms classically have an outer membrane, they have a thinner peptidoglycan layer, which does not hold the blue dye used in the initial dying process. Other information used to differentiate bacteria is the shape. Gram-positive bacteria comprise cocci, bacilli, or branching filaments.

Etiology

Gram-positive cocci include Staphylococcus (catalase-positive), which grows clusters, and Streptococcus (catalase-negative), which grows in chains. The staphylococci further subdivide into coagulase-positive (S. aureus) and coagulase-negative (S. epidermidis and S. saprophyticus) species. Streptococcus bacteria subdivide into Strep. pyogenes (Group A), Strep. agalactiae (Group B), enterococci (Group D), Strep viridans, and Strep pneumonia.

Gram-positive bacilli (rods) subdivide according to their ability to produce spores. Bacillus and Clostridia are spore-forming rods while Listeria and Corynebacterium are not. Spore-forming rods that produce spores can survive in environments for many years. Also, the branching filament rods encompass Nocardia and actinomyces. 

Gram-positive organisms have a thicker peptidoglycan cell wall compared with gram-negative bacteria. It is a 20 to 80 nm thick polymer while the peptidoglycan layer of the gram-negative cell wall is 2 to 3 nm thick and covered with an outer lipid bilayer membrane.

Epidemiology

Bloodstream infection mortality rates have increased by 78% in just two decades[1]. Gram-positive organisms have highly variable growth and resistance patterns. The SCOPE project (Surveillance and Control of Pathogens of Epidemiologic Importance) found that gram-positive organisms in those with an underlying malignancy accounted for 62% of all bloodstream infections in 1995 and 76% in 2000 while gram-negative organisms accounted for 22% and 14% of infections for these years.[2]

Pathophysiology

Gram-positive cocci:

Staphylococcus aureus is a gram-positive, catalase-positive, coagulase-positive cocci in clusters. S. aureus can cause inflammatory diseases, including skin infections, pneumonia, endocarditis, septic arthritis, osteomyelitis, and abscesses. S. aureus can also cause toxic shock syndrome (TSST-1), scalded skin syndrome (exfoliative toxin, and food poisoning (enterotoxin). 

Staphylococcus epidermidis is a gram-positive, catalase-positive, coagulase-negative cocci in clusters and is novobiocin sensitive. S. epidermidis commonly infects prosthetic devices and IV catheters producing biofilms. Staphylococcus saprophyticus is novobiocin resistant and is a normal flora of the genital tract and perineum. S. saprophyticus accounts for the second most common cause of uncomplicated urinary tract infection (UTI). 

Streptococcus pneumoniae is a gram-positive, encapsulated, lancet-shaped diplococci, most commonly causing otitis media, pneumonia, sinusitis, and meningitis. Streptococcus viridans consist of Strep. mutans and Strep mitis found in the normal flora of the oropharynx commonly cause dental carries and subacute bacterial endocarditis (Strep. sanguinis).

Streptococcus pyogenes is a gram-positive group A cocci that can cause pyogenic infections (pharyngitis, cellulitis, impetigo, erysipelas), toxigenic infections (scarlet fever, necrotizing fasciitis), and immunologic infections (glomerulonephritis and rheumatic fever). ASO titer detects S. pyogenes infections.

Streptococcus agalactiae is a gram-positive group B cocci that colonize the vagina and is found mainly in babies. Pregnant women need screening for Group-B Strep (GBS) at 35 to 37 weeks of gestation. 

Enterococci is a gram-positive group D cocci found mainly in the colonic flora and can cause biliary tract infections and UTIs. Vancomycin-resistant enterococci (VRE) are an important cause of nosocomial infections. 

Gram-positive rods:

Clostridia is a gram-positive spore-forming rod consisting of C. tetani, C. botulinum, C. perfringens, and C. difficile. C. difficile is often secondary to antibiotic use (clindamycin/ampicillin), PPI use, and recent hospitalization. Treatment involves primarily with oral vancomycin.

Bacillus anthracis is a gram-positive spore-forming rod that produces anthrax toxin resulting in an ulcer with a black eschar. Bacillus cereus is a gram-positive rod that can be acquired from spores surviving under-cooked or reheated rice. Symptoms include nausea, vomiting, and watery non-bloody diarrhea. 

Corynebacterium diphtheria is a gram-positive club-shaped rod that can cause pseudomembranous pharyngitis, myocarditis, and arrhythmias. Toxoid vaccines prevent diphtheria.

Listeria monocytogenes is a gram-positive rod acquired by the ingestion of cold deli meats and unpasteurized dairy products or by vaginal transmission during birth. Listeria can cause neonatal meningitis, meningitis in immunocompromised patients, gastroenteritis, and septicemia. Treatment includes ampicillin. 

History and Physical

It is important to identify patients with sepsis and order necessary blood cultures and labs. 

Physical

Evaluation

Once a gram-positive organism infection is suspected, these laboratory studies are useful:

Treatment / Management

Penicillin was the first antibiotic ever introduced during World War II by Alexander Fleming in 1928. Penicillin does not cover Staph or Enterococcus but used mainly streptococcal infections. The penicillinase-resistant organisms (nafcillin, oxacillin, cloxacillin, dicloxacillin) cover Staph (MSSA) and Strep. Anti-pseudomonal penicillins include piperacillin and ticarcillin effective against gram-positive, gram-negative, pseudomonas, and anaerobes. Carbapenems cover gram-positives, gram negatives, and anaerobes.[3][4][5]

Trimethoprim/sulfamethoxazole, clindamycin, and doxycycline are oral antibiotics used for mild to moderate MRSA infections. It is important to note that trimethoprim/sulfamethoxazole increases warfarin levels leading to increased INR. Vancomycin, linezolid, daptomycin, and tigecycline cover moderate to severe community and hospital-acquired MRSA. Vancomycin requires renal dosing with trough levels between 15 to 20. Linezolid is an option if a patient is allergic to vancomycin. CBC needs to be checked weekly to avoid bone marrow suppression, neutropenia, thrombocytopenia, and anemia. Linezolid, daptomycin, and tigecycline are options to treat vancomycin-resistant enterococci.[6][7][8]

Prognosis

The prognosis following infection with gram-positive organisms is variable. The highest mortality rates are in elderly persons who tend to have suppressed immune systems and less physiologic reserve.

Enhancing Healthcare Team Outcomes

Health professionals, including doctors, nurses, and pharmacists, need to be aware of risk factors to treat patients with selected antibiotics properly. Pharmacists need to accurately monitor vancomycin trough levels to avoid mortality in patients with Staph aureus. They also need to review medication for dose and interactions and counsel patients about finishing all prescribed antibiotics. Infection control nurses evaluate nosocomial infections and implement appropriate policies. An interprofessional approach will produce the best outcomes. [Level 5]

Outcomes: Screening for methicillin-resistant Staphylococcus aureus (MRSA) risk factors enhance infection control. MRSA risk factors include patients who are above age 65, urinary catheter, previous antibiotic treatment past three months, trauma, and those admitted from a long-term facility.[9] [Level 5]

Figure

Gram stain of Staphylococcus aureus. Contributed by Scott Jones, MD

References

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National Nosocomial Infections Surveillance (NNIS) system report, data summary from January 1992-April 2000, issued June 2000. Am J Infect Control. 2000 Dec;28(6):429-48. [PubMed: 11114613]
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Wisplinghoff H, Seifert H, Wenzel RP, Edmond MB. Current trends in the epidemiology of nosocomial bloodstream infections in patients with hematological malignancies and solid neoplasms in hospitals in the United States. Clin Infect Dis. 2003 May 01;36(9):1103-10. [PubMed: 12715303]
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Righi E, Carnelutti A, Bassetti M. Current role of oxazolidinones and lipoglycopeptides in skin and soft tissue infections. Curr Opin Infect Dis. 2019 Apr;32(2):123-129. [PubMed: 30664028]
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Zamoner W, Prado IRS, Balbi AL, Ponce D. Vancomycin dosing, monitoring and toxicity: Critical review of the clinical practice. Clin Exp Pharmacol Physiol. 2019 Apr;46(4):292-301. [PubMed: 30623980]
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Rogalla D, Bomar PA. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 10, 2021. Listeria Monocytogenes. [PubMed: 30521259]
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Rostkowska KA, Szymanek-Pasternak A, Simon KA. Spontaneous bacterial peritonitis – therapeutic challenges in the era of increasing drug resistance of bacteria. Clin Exp Hepatol. 2018 Dec;4(4):224-231. [PMC free article: PMC6311748] [PubMed: 30603669]
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Gashaw M, Berhane M, Bekele S, Kibru G, Teshager L, Yilma Y, Ahmed Y, Fentahun N, Assefa H, Wieser A, Gudina EK, Ali S. Emergence of high drug resistant bacterial isolates from patients with health care associated infections at Jimma University medical center: a cross sectional study. Antimicrob Resist Infect Control. 2018;7:138. [PMC free article: PMC6245755] [PubMed: 30479751]
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Bolia IK, Tsiodras S, Chloros GD, Kaspiris A, Sarlikiotis T, Savvidou OD, Papagelopoulos PJ. A Review of Novel Antibiotic Regimens for the Treatment of Orthopedic Infections. Orthopedics. 2018 Nov 01;41(6):323-328. [PubMed: 30452066]
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Callejo-Torre F, Eiros Bouza JM, Olaechea Astigarraga P, Coma Del Corral MJ, Palomar Martínez M, Alvarez-Lerma F, López-Pueyo MJ. Risk factors for methicillin-resistant Staphylococcus aureus colonisation or infection in intensive care units and their reliability for predicting MRSA on ICU admission. Infez Med. 2016 Sep 01;24(3):201-9. [PubMed: 27668900]

Impetigo: Information For Clinicians | CDC

Impetigo is a superficial bacterial skin infection that is highly contagious. Impetigo can be caused by Streptococcus pyogenes and Staphylococcus aureus. This page focuses on infections caused by S. pyogenes, which are also called group A Streptococcus or group A strep.

Etiology

Impetigo can be bullous or non-bullous. Toxin-producing S. aureus cause bullous impetigo. S. aureus, S. pyogenes, or both cause non-bullous impetigo, which is also called “impetigo contagiosa.”

S. pyogenes are gram-positive cocci that grow in chains (see Figure 1). They exhibit β-hemolysis (complete hemolysis) when grown on blood agar plates. They belong to group A in the Lancefield classification system for β-hemolytic Streptococcus, and thus are also called group A streptococci.

Figure 1. Streptococcus pyogenes (group A Streptococcus) on Gram stain. Source: Public Health Image Library, CDC

Clinical Features

Streptococcal impetigo, or non-bullous impetigo, begins as papules. The papules evolve to pustules and then break down to form thick, adherent crusty lesions (Figure 2). The crusts are typically golden or “honey-colored.” These lesions usually appear on exposed areas of the body, most commonly the face and extremities. Multiple lesions typically develop. In cases of non-bullous impetigo, physical examination cannot differentiate streptococcal from staphylococcal infection.1

Transmission

Streptococcal impetigo is most commonly spread through direct contact with other people with impetigo. People with impetigo are much more likely to transmit the bacteria than asymptomatic carriers. Crowding, such as found in schools and daycare centers, increases the risk of disease spread from person to person.

Lesions can be spread (by fingers and clothing) to other parts of the body.

Humans are the primary reservoir for group A strep. There is no evidence to indicate that pets can transmit the bacteria to humans.

Figure 2. Streptococcus pyogenes caused the lesions on this patient’s left forearm. Source: Public Health Image Library, CDC

Incubation Period

The incubation period of impetigo, from colonization of the skin to development of the characteristic lesions, is about 10 days.1 It is important to note not everyone who becomes colonized will go on to develop impetigo.

Risk Factors

Impetigo can occur in people of all ages, but it is most common among children 2 through 5 years of age. Scabies infections and activities that result in cutaneous cuts or abrasions (e.g., sports such as wrestling and football) increase the risk of impetigo. It is also more common in tropical or subtropical locations and in the summer in temperate climates but can occur anywhere.1

Diagnosis and Testing

Impetigo is usually diagnosed by physical examination, but physical examination cannot reliably differentiate between streptococcal and staphylococcal non-bullous impetigo.1 Gram stain or culture of the exudate or pus from an impetigo lesion can identify the bacterial cause. However, laboratory testing is not necessary nor routinely performed in clinical practice.

Treatment

Antibiotic treatment, whether oral or topical, should be aimed at both bacteria that are associated with impetigo: group A strep and S. aureus. Topical antibiotics, mupirocin or retapamulin, may be used when there are only a few lesions, while oral antibiotics are used for multiple lesions.1,2,3

Prognosis and Complications

Rarely, complications can occur after impetigo. Post-streptococcal glomerulonephritis (PSGN) can occur as a delayed non-suppurative complication of impetigo. It most often occurs one to two weeks after the original infection resolves. PSGN is thought to be the result of an immune response that is triggered by the group A strep infection.

Prevention

The spread of impetigo can be prevented by covering lesions, treating with antibiotics, and practicing good hand hygiene. Clothing, linens, and towels used by an infected person should be washed every day and not shared with others in the household. Persons with impetigo can return to school or work after initiating antibiotic treatment if lesions on exposed skin are covered.

The spread of all types of group A strep infection can be reduced by good hand hygiene, especially after coughing and sneezing and before preparing foods or eating, and respiratory etiquette (e.g., covering your cough or sneeze).

Epidemiology

In the United States, impetigo is more common in the summer.1 The World Health Organization estimates that 111 million children in the developing world have streptococcal impetigo at any one time.4 Higher rates of impetigo are found in crowded and impoverished settings, in warm and humid conditions, and among populations with poor hygiene.

Resources

  1. Bryant AE, Stevens DL. Streptococcus pyogenes. In Bennett J, Dolin R, Blaser M, editors. 8th Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. Philadelphia (PA): Elsevier; 2015:2:2285–300.
  2. Committee on Infectious Diseases. Group A streptococcal infectionsexternal icon. In Kimberlin DW, Brady MT, Jackson MA, Long SS, editors. Red Book: 20182021 Report of the Committee on Infectious Diseases. 31st ed. Itaska (IL): American Academy of Pediatrics; 2018:748–62.
  3. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of Americaexternal icon. Clin Infect Dis. 2014;59(2):147–59.
  4. Carapetis JR. The current evidence for the burden of group A streptococcal diseasesexternal icon. World Health Organization. Geneva. 2005.

Treatment of gram – positive infections in critically ill patients | BMC Infectious Diseases

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    5.53.3.2.1 Protein A-Based Adsorbents for Antibodies Removal

    Staphylococcus protein A (SPA) is a cell wall component that was identified in S. aureus more than 40 years ago. Its capacity to bind the constant regions of antibodies renders it useful as a means for extracting immunoglobulins. The SPA-based products that are mostly used are Immunosorba (Fresenius Medical Care, Germany) and Prosorba (Cypress Bioscience, Inc. USA).13 The Immunosorba column contains purified protein A immobilized within Sepharose beads following cyanogen bromide activation of the beads, and one Immunoadsorba column can bind about 1.2 g of IgG antibodies at saturation. A twin-column system is usually employed, in which two Immunosorba columns are used intermittently during each treatment. A single treatment using Immunosorba columns can cause a considerable reduction in the concentration of IgG antibodies in the patient’s blood, due to the “unlimited” capacity of the columns and the large volume of plasma treated. A set of two Immunosorba columns can be re-used up to 20 times by the same patient. Unlike Immunosorba, Prosorba is a single-column system with limited adsorption capacity. The Prosorba column contains 200 mg of purified protein A immobilized within 123 g of silica bead, and one Prosorba column can bind about 0.6 g of IgG antibody at saturation. Despite the limited volume of processed plasma, which does not allow significant removal of immunoglobulin or circulating immune complexes, this device has been shown to exert immune modulating effects. Its mode of action, however, remains somewhat obscure.

    The columns have been approved by the FDA for the treatment of rheumatoid arthritis and idiopathic thrombocytopenic purpura (Prosorba) and hemophilia with inhibitors (Immunosorba). Apart from these FDA-approved indications, SPA-based immunoadsorption has been tried for several other autoimmune entities.13,14 Some data have supported a possible beneficial effect for nephrology, cardiology, dermatology, hematology, neurology and rheumatology. SPA-based immunoadsorption has been suggested for use in the treatment of patients with life-threatening autoimmune diseases, especially in the case of autoimmune thrombocytopenic purpura patients who do not respond to corticosteroids, and in severe or drug-unresponsive rheumatoid arthritis.

    Apart from the treatment of autoimmune diseases, SPA-based immunoadsorption also has an important application in organ transplantations.15 Many trials have suggested the efficiency of immunoadsorption in reversing severe antibody-mediated rejection, which frequently causes refractory graft dysfunction. In patients with acute vascular rejection after renal transplantation, immunoadsorption can be used to remove donor-specific antibodies in combination with conventional anti-rejection therapy. For human leukocyte antigen (HLA)-pre-sensitized kidney recipients, immunoadsorption could also be successfully used to reduce the anti-HLA antibody titer before transplantation to obtain a negative cross match in highly sensitized patients. Otherwise, it would be difficult for these patients to receive a donated organ.

    Several important issues should be noted during the treatment with SPA-based immunoadsorption. First, immunoadsorption has been proven effective in removing immunoglobulins and circulating immune complex in the blood circulation. However, some inflammatory processes often occur in the tissue and not in the vascular bed. Simple removal of immunoglobulins from the circulation does not necessarily eliminate the autoimmune process. Second, repeated treatment cycles with adequately processed plasma volumes must be used to overcome the redistribution of pathological autoantibodies. Nevertheless, the almost complete elimination of IgG may result in a severe humoral immune deficiency, so that the patients are exposed to the risk of complication resulting from infections. Third, patients suffering from autoimmune diseases may vary in their conditions. Even those may manifest similar symptoms and have different types of pathogenic factors, depending on the diversity of the autoantibodies – their classes and subclasses. Since SPA-based adsorbents show a weak adsorption for IgG3, IgM and IgA, differences in the efficacy of the treatment may exist among different patients.

    Further development of SPA-based adsorbents might lie in the improvement of their manufacture processes and performances. More stable products would reduce their side effects, while cheaper products would widen their applications, making them available for more patients. Moreover, the performance of immunoadsorption would be further improved by integrating into an immunomodulatory treatment for autoimmune disease, through combining with inflammatory cytokine removal, immunosuppression, and selective immune deviation.

    Gram-Positive and Gram-Negative Bacillus: What’s the Difference?

    There are many ways of classifying bacteria. One method is based on the cell membrane. In 1884, a bacteriologist named Christian Gram created a test that could determine if a bacterium had a thick, mesh-like membrane called peptidoglycan. Bacteria with thick peptidoglycan are called gram positive. If the peptidoglycan layer is thin, it’s classified as gram negative.

    Characteristics of Gram-Positive Bacilli

    A gram-positive bacillus doesn’t have an outer cell wall beyond the peptidoglycan membrane. This makes it more absorbent. Its peptidoglycan layer is much thicker than the peptidoglycan layer on gram-negative bacilli.  Gram-positive bacilli are shaped like rods. They can also be characterized based on whether they form spores and whether they need oxygen to survive.  

    Types of Gram-Positive Bacilli

    Resident flora. Most gram-positive bacilli live harmlessly on your body without causing problems. These are called resident flora. The can be found in the following places on your body:

    • Skin
    • Nose
    • Mouth
    • Throat
    • Vagina

    Some types of gram-positive bacilli are pathogenic, which means they cause diseases in people. Some of the major gram-positive bacteria that cause diseases include:

    Anthrax. This is a potentially fatal infection that usually affects the skin or lungs but can rarely infect the gastrointestinal tract as well. Anthrax is a spore-forming type of bacilli. It has the potential to be used as a biological weapon because its spores can be spread in the air and be inhaled. The spores can live for decades and are not easily killed.

    Diphtheria. This is a contagious infection of the upper respiratory tract. Vaccination can prevent this infection. It’s rare in developed countries.

    Enterococcal Infections. These infections can be caused by bacteria known as enterococci. There are over 17 different species. They live in your intestines, where they don’t normally cause problems. If they move to another part of your body, such as your blood, heart valves, or skin, they can cause serious infections.

    Erysipelothricosis. This is a skin infection that usually happens when you get a scrape or puncture wound while handling infected animals. The main symptom is a hard, purplish-red rash.

    Listeriosis. This is an infection caused by eating contaminated food. It causes fever, chills, nausea, vomiting, and diarrhea.

    Treatment of Gram-Positive Bacilli

    Gram-positive bacilli infections are treated with antibiotics. Penicillin, cloxacillin, and erythromycin treat over 90% of gram-positive bacteria.

    However, antibiotic resistance is becoming a serious problem with gram-positive infections. New drugs are being developed to help with this problem. Antibiotics should only be used when you absolutely need them. Infection control standards need to be followed closely to prevent the development and spread of antibiotic-resistant infections. 

    Gram-Negative Bacteria

    Gram-negative bacteria have a hard, protective outer shell. Their peptidoglycan layer is much thinner than that of gram-positive bacilli. Gram-negative bacteria are harder to kill because of their harder cell wall. When their cell wall is disturbed, gram-negative bacteria release endotoxins that can make your symptoms worse. 

    Gram-negative bacteria can cause many serious infections, including:

    Risks for Developing Gram-Negative Bacterial Infections

    Gram-negative infections are most common in hospitals. Your risk increases the longer you stay in the hospital. Other things that increase your risk of developing a gram-negative infection include:

    How Are Gram-Negative Bacteria Treated?

    Gram-negative bacteria have high resistance to antibiotics. They are one of the most serious public health issues in the world. Gram-negative bacteria have the ability to cause a lot of diseases in humans. They can reach almost all of the organ systems. Your doctor may need to try several antibiotics to beat the infection. Older antibiotics may work better. 

    Preventing and Controlling Antibiotic Resistance

    Antibiotic resistance is made worse by the overuse of antibiotics. You can take the following steps to help control and prevent antibiotic resistance:

    • Only use antibiotics prescribed by your healthcare provider.
    • Follow your healthcare provider’s advice about antibiotic use.
    • Don’t use or share leftover antibiotics.
    • Wash your hands.
    • Practice safe sex.
    • Keep your vaccines up to date.
    • Avoid contact with people who are sick when you can.
    • Prepare your food safely.

    Bovine Diagnostics – Mastitis Diagnosis

    When mastitis is identified in a cow’s quarter(s), it is important to identify the pathogen causing the infection because different categories of pathogens require different management strategies. Without a diagnosis, there is no way to know if a given antibiotic will work. However, once you know the infection agent, a dairy farmer can work with his or her veterinarian to target an effective treatment plan. Prudent use of antibiotics reduces the likelihood of resistant pathogens developing and can reduce the duration of treatment a cow may need which decreases operation costs.

    The main bacteria responsible for causing mastitis can be divided into two categories: contagious and environmental.

    Contagious bacteria

    With contagious bacteria, the dairy cow serves as the host and bacteria are transferred from a cow with an infected udder to a healthy cow. The bacteria are often spread cow-to-cow during milking procedures via the milking machine, a milker’s hands or a reused milking towel. Bacterial transfer can also occur from cow-to-cow if milk leakage occurs from the udder into the stall.

    The major contagious pathogens include:

    • Staphylococcus aureus
    • Coagulase-negative staphylococci (CNS)
    • Streptococcus agalactiae
    • Streptococcus dysgalactiae
    • Mycoplasma bovis
    • Mycoplasma spp.
    • Corynebacterium bovis

    Contagious bacteria are mainly Gram-positive mastitis infections. Infected cows usually show abnormal milk and elevated somatic cell count. Gram-positive infections usually respond well to antibiotic treatment.
    However, symptoms caused by Mycoplasma species are unique in that typically multiple quarters of the animal are infected and it is common for cows to show signs of joint swelling and pain. Most Mycoplasma species do not respond to antibiotic treatment. In fact, for M. bovis, the most common mycoplasma mastitis specie in cattle, there is no treatment.

    Prevention involves post-milking teat dip, milk time hygiene, segregation of infected cows and culling of cows with chronic contagious mastitis that are not responsive to treatment.

    Environmental bacteria

    Environmental bacteria are present in the environment including: bedding, soil, walkways, in the pasture or any surface with which the cow or her manure comes in contact. The infection route is from environment to the udder. The environmental bacteria load is highly correlated with the hygiene of the barn and stalls and the cow and udder. Organic materials used for bedding like wood shavings, straw or recycled dry manure solids are common sources of environmental bacteria.

    Environmental pathogens are also categorized as Gram-negative mastitis infections. Infected cows tend to get systemically sick and would be considered a “hotter,” more acute case of mastitis.

    The major environmental pathogens include:

    • Streptococcus uberis
    • Streptococcus dysgalactiae
    • Some Coagulase-negative staphylococci species
    • Escherichia coli
    • Klebsiella spp.
    • Enterococcus spp.
    • Serratia marcescens
    • Trueperella pyogenes/P. indolicus
    • Yeasts
    • Prototheca spp.
    • Bacillus spp.

    Control of environmental mastitis involves the following recommended management from the Cornell University College of Veterinary Medicine:

    1. Cow comfort – Provide well designed stalls that are utilized in a correct manner by cattle.
    2. Provide a clean and dry housing area with adequate bedding that is frequently groomed to remove wet and soiled bedding daily.
    3. Make sure outside cow areas are clean and well drained. Standing water and muddy areas must be eliminated.
    4. Be sure to keep cross-over alleys, walkways and areas around waters where cows may congregate clean and free of manure which might splash up on to the udder.
    5. Make sure barns are well ventilated to limit heat stress and the growth and survivability of bacteria.
    6. Make sure teats are clean, sanitized, well stimulated and dried prior to attachment of the milking unit.
    7. Ensure good claw alignment and support during milking. Inflations need to be in good condition to avoid liner slips.
    8. Be alert to weather conditions (hot and humid) that may initiate an outbreak of environmental mastitis.
    9. Keep good records and culture all clinical cases to identify the early stages of a mastitis outbreak.
    Mastitis-causing Pathogens and Antimicrobial Use

    The basic difference in categories of mastitis is their physiology or cell structure.

    Gram-positive bacteria have a thick cell wall. The cell wall’s membrane is highly selective about how and what move in and out. The cell wall is attacked by penicillin antibiotics, making Gram-positive bacteria more sensitive to these commonly used types of antibiotics.

    Gram-negative bacteria have a thin cell wall sandwiched between two membranes that are somewhat selective, and the outer membrane protects the cell wall. Because they lack a real cell wall, Gram-negative bacteria are more resistant to commonly used antibiotics. A different group of antibiotics is needed for these types of bacteria.

    Mycoplasma spp do not have a cell wall; they only have a cell membrane, and grow very slowly, making them much more resistant to all known antibiotics. Mycoplasmas, specifically Mycoplasma bovis, is a highly contagious pathogen typically introduced when new animals are brought on the farm.

    Selective treatment and selective dry cow therapy

    Blanket dry cow therapy is now generally used in the US and other parts of the world. There is high social pressure on reducing antibiotics. The detection of specific pathogens can help with selective treatment of the animals.

    These are the general recommendations, which vary by region and depend on the somatic cell count (SCC) in the bulk milk:

    • Gram-positive bacteria: to be treated with antibiotics
    • Gram-negative bacteria: not to be treated with antibiotics, because they are mostly cured easily after a few days
    • Mycoplasma spp: separate or cull

    Toxic Shock Syndrome (TSS) | Johns Hopkins Medicine

    What is toxic shock syndrome?

    Toxic shock syndrome (TSS) is a cluster of symptoms that involves many systems of the body. Certain bacterial infections release toxins into the bloodstream, which then spreads the toxins to body organs. This can cause severe damage and illness.

    What causes toxic shock syndrome?

    The following bacteria commonly cause TSS:

    • Staphylococcus aureus
    • Streptococcus pyogenes
    • Clostridium sordellii

    TSS from Staphylococcus infections was identified in the late 1970s and early 1980s when highly absorbent tampons were widely used by menstruating women. Due to changes in how tampons are made, the incidence of tampon-induced TSS has declined.

    TSS from streptococcus infections is most commonly seen in children and the elderly. Other people at risk include those with diabetes, weak immune system, chronic lung disease, or heart disease.

    • Staphylococcus infections. Staphylococcus aureus (or S. aureus) may normally exist on a person’s body and does not cause infection. Because it’s part of the body’s normal bacteria, most people develop antibodies to prevent infection. S. aureus can be spread by direct contact with infected persons. People who develop TSS usually have not developed antibodies against S. aureus. Therefore, it’s not usually considered a contagious infection. S. aureus infections may also develop from another infection, such as pneumonia, sinusitis, osteomyelitis (infection in the bone), or skin wounds, such as a burn or surgical site. If any of these areas are infected, the bacteria can penetrate into the bloodstream.
    • Streptococcus infections. Streptococcus pyogenes (or S. pyogenes) TSS may occur as a secondary infection. Most commonly, this is seen in people who have recently had chickenpox, bacterial cellulitis (infection of the skin and underlying tissue), or who have weak immune systems.
    • Clostridium sordellii infections. Clostridium sordellii (or C. sordellii) normally exists in the vagina and does not cause infection. The bacteria may enter the uterus during normal menstruation, childbirth, or gynecological procedures such as abortion. Intravenous drug use can also cause C. sordellii infections.

    Who is at risk for toxic shock syndrome?

    The following are risk factors for toxic syndrome:

    • History of using super-absorbent tampons
    • Surgical wounds
    • A local infection in the skin or deep tissue
    • History of using the diaphragm or contraceptive sponge
    • History of recent childbirth, miscarriage, or abortion

    What are the symptoms of toxic shock syndrome?

    Symptoms of TSS involve many systems and may look like other infections. While each person may experience symptoms differently, the following are the most common symptoms of staphylococcal TSS:

    • Fever higher than 102°F (38.9°C)
    • Chills
    • Feeling unwell
    • Headache
    • Fatigue
    • Rash that is red and flat and that covers most of the areas of the body
    • Shedding of the skin in large sheets, especially over the palms and soles, seen one to two weeks after the onset of symptoms.
    • Low blood pressure
    • Vomiting
    • Diarrhea
    • Muscle pain
    • Increased blood flow to the mouth, eyes, and vagina, making them appear red
    • Decreased urine output and sediment in urine
    • Decreased liver function
    • Bruising due to low blood platelet count
    • Disorientation and confusion

    The following are the most common symptoms of streptococcal TSS:

    • Dangerously low blood pressure
    • Shock
    • Decreased kidney function
    • Bleeding problems
    • Bruising due to low blood platelet count
    • Rash that is red and flat and that covers most of the areas of the body
    • Liver impairment
    • Shedding of the skin in large sheets, especially over the palms and soles (this does not always occur)
    • Difficulty breathing

    The following are the most common symptoms of C. sordellii TSS:

    • Nausea and/or vomiting
    • Lethargy
    • Flu-like symptoms
    • Abdominal tenderness
    • Generalized swelling from fluid buildup
    • High white blood cell and red blood cell count
    • No fever
    • Low blood pressure
    • Very fast heart rate

    How is toxic shock syndrome diagnosed?

    Ruling out similar illnesses (such as Rocky Mountain spotted fever, among others) is critical in diagnosing TSS. Other diagnostic tests may include:

    • Blood cultures. Tests used to find and identify microorganisms.
    • Blood tests. Tests to measure blood clotting and bleeding times, cell counts, electrolytes, and liver function, among others.
    • Urine tests.
    • Lumbar puncture. A procedure involving the insertion of a needle in between the vertebrae of the spine to draw spinal fluid and check for bacteria.

    How is toxic shock syndrome treated?

    Specific treatment will be determined by your health care provider based on:

    • Your age, health, and medical history
    • Extent of the disease
    • Your tolerance for specific medications, procedures, or therapies
    • Expectations for the course of the disease
    • Your opinion or preference

    Treatment for TSS may include:

    • Giving intravenous (through a vein) antibiotics
    • Giving intravenous fluid to treat shock and prevent organ damage
    • Heart medications in people with very low blood pressure
    • Dialysis may be required in people who develop kidney failure
    • Giving blood products
    • Supplemental oxygen or mechanical ventilation to assist with breathing
    • Deep surgical cleaning of an infected wound

    What are the complications of toxic shock syndrome?

    TSS can result in amputations of fingers, toes, or limbs, or even death.

    Can toxic shock syndrome be prevented?

    • Since reinfection is common, menstruating girls and women should avoid using tampons if they have had TSS.
    • Prompt and thorough wound care is crucial in avoiding TSS.
    • Minimal usage of vaginal foreign body items, such as diaphragms, tampons, and sponges can also help prevent TSS.

    When should I call my health care provider?

    TSS may start like other infections, but it can quickly progress to a seriously life-threatening disease. If a mild illness quickly becomes severe with whole-body symptoms, seek immediate medical attention.

    Key Points about Toxic Shock Syndrome

    • Toxic shock syndrome describes a cluster of symptoms that involve many systems of the body.
    • It can be caused by Staphylococcus aureus, Streptococcus pyogenes, or Clostridium sordellii.
    • Early symptoms are similar to other infections but can progress quickly to become life-threatening.
    • TSS can be life-threatening and requires immediate medical attention.

    Next Steps

    Tips to help you get the most from a visit to your health care provider:

    • Before your visit, write down questions you want answered.
    • Bring someone with you to help you ask questions and remember what your provider tells you.
    • At the visit, write down the names of new medicines, treatments, or tests, and any new instructions your provider gives you.
    • If you have a follow-up appointment, write down the date, time, and purpose for that visit.
    • Know how you can contact your provider if you have questions.

    90,000 Fitness blog. The Mysterious Microbiome, or What Guts Smell

    • Katerina Arkharova
    • BBC Russian Service, London

    Photo author, Getty

    Photo caption,

    For Some people eat a tomato is like ice cream, research has shown

    In addition, if you still manage to bring the conversation to a more specific level, then the “nothing” often hides a whole grocery store: here and half a pack of cornflakes (aka weightless !), and “unsweetened” sweets with a reduced sugar content, and other fantasies.

    So I long ago refused to believe such revelations, but here scientists (and this time not British, but Israeli) proved that every organism

    reacts in its own way to the same food, even healthy.

    Study participants (mostly overweight people) were given the same food for a week and their blood glucose levels were measured. It turned out that even butter did not harm someone, and in one woman in 800, the sugar level skyrocketed from tomatoes like from candy.

    The scientists who conducted the experiment say that this difference in metabolism is largely due to the different composition of the microflora in our stomach or the microbiome, and they recommend completely reconsidering the approach to weight loss and diets, because there is simply no one at all.

    Mention of this mysterious microbiome has begun to appear more and more often (as it has become easier to calculate with the help of the latest technologies), although scientists admit that they know less about it. Take this at least

    the recent “Nobel laureate” – the bacterium Helicobacter pylori.For her ten years ago, two scientists received the Nobel Prize in Medicine; they discovered that it was her presence that caused gastritis and duodenal ulcers.

    Opinion of another specialist

    Photo author, Thinkstock

    Photo caption,

    Ten years ago it turned out that gastritis and ulcers are caused by the bacterium Helicobacter pylori

    Soon after this discovery, everyone who had some kind of stomach problems, began to check for the presence of “helika” in the body.They checked me too. Helik was found, but I was not given the Nobel Prize for it. My family doctor, leaning back in his chair and scrolling a fountain pen in his hands, said the following: “Of course, we can take a course of antibiotics, as they recommend, but I’m afraid not to do a disservice. in itself is far from unambiguous – half of the population has it. ”

    “Healthy microbes”? “Helik is not unambiguous”? Yes, he is delusional, I thought, leaving his office upset without a prescription, but I had nothing to cover, because while the examination was going on, my stomach completely stopped hurting.Helik realized that he was discovered and became a goody. I rushed to get a “second opinion”, that is, the opinion of another specialist – the Internet.

    In general, how we lived for so many millennia without the discovery of Helicobacter, I can roughly imagine, but how without the Internet – it’s just scary to think. You just typed in the word you were looking for and right there – a complete picture of you, who, how many and what, sorry, colors.

    No, I’m serious, it immediately somehow introduces, helps to realize that you are not the only one, terribly unhappy, caught in the clutches of a harmful bacteria on the one hand and a doctor obsessed with the dangers of antibiotics on the other.You understand that there are still a lot of other people, both English and Russian (because the second opinion is usually checked in two languages), who took the course, but did not get rid of the bacteria: she cheerfully waved her tail at the laboratory assistant during the second analysis.

    In short, I decided to postpone the antibiotic bombardment and, it seems, for good reason: this summer, at the Cheltnam Science Festival, professor-gastroenterologist from the University of Oxford Fiona Poury gave a lecture about the fact that some beneficial bacteria that make up the microbiome of Western man on the verge of extinction and it is almost time to put them in the Red Book, like the Amur tiger.

    She cited as an example just Helicobacter pylori, which is now being eliminated from the intestines with antibiotics. “Meanwhile, it has a number of positive properties: it regulates the function of the stomach, which controls the production of acid, so when you do not have H. pylori, there may be severe acid reflux (when stomach acid is thrown into the esophagus, which gives severe heartburn, etc.) etc. – K.A.), which in turn can lead to Barrett’s syndrome and esophageal cancer, “said the professor.

    I am citing this quote here not to scare those who do not have helik, God forbid, but simply to show that not everything is so simple.

    Big Mac Diet

    But antibiotics are not the only reason that the microflora of the population of many developed countries is deteriorating. This is mainly due to poor diet, experts say.

    This was experimentally proved by another British professor, Tim Spector, whose book “The Diet Myth” I have already quoted.He persuaded his son, a geneticist student Tom, for the sake of science to sit on a fast food diet for 10 days in order to understand what would happen to his intestinal microflora. Tom ate big macs, potato chips, chicken nuggets and drank cola.

    Before the start of the experiment, 3,500 bacteria lived peacefully in his intestines, mainly gram-positive firmicuts (for example, bifidobacteria belong to them). However, in the first few days of the experiment, Tom lost 1,300 bacteria, gained almost two kg, and the ratio of bacteria in his intestine changed: gram-negative bacteroids began to take over there, which, in the event of a decrease in immunity and other unfavorable factors, can cause all kinds of nasty things in the body.

    By the way, a similar experience (but, fortunately, without bacteriological analysis) took place in my kitchen when his school friends came to my son: English boys ate only chips and these creepy fish sticks or chicken “nuggets” – I had to, to seem like a “normal mom”, sometimes offer them this nonsense. We still remember one boy who, having come to visit us after school and having thrown around the set dining table, bending his fingers in a boring voice, began to list: “I don’t eat tomatoes, I don’t eat cucumbers, I don’t eat bread, I don’t eat meat , I don’t eat fish … “Those who came from foreign families were much more willing to eat ordinary homemade food, including even a vegetable salad.

    But back to the more scientific experiment of Professor Spector, who confirmed another guess that two-thirds of the British adult population are overweight or obese, not just because they eat too much, but because in their intestines as a result of unreasonable nutrition, beneficial microbes have simply died out, since it is they, in addition to digesting food, also control how we absorb calories and how much.

    Four Ingredients

    Photo Credit, Thinkstock

    Photo Caption,

    People in the West are not diversified enough

    “Most people today consume less than 20 different types of food, the lion’s share of which, if not all, is refined.Most of the pre-processed foods are made, horribly, with just four ingredients: corn, soy, wheat or meat, “lamented Tim Spector.

    It was also found that since the degree of completeness depends on its own microbiota, If a thin person is transplanted with the fecal matter of a fat person, then the thin one is likely to gain weight. something like “Feel with your guts”).He became deeply interested in this question after he and his wife received an acute intestinal infection after a trip to Peru. After recovering, the professor “just like that” lost more than 35 kilograms of his own weight, turning from a very fat man into a man of normal weight. He began to suspect that this was precisely due to the change in his intestinal flora.

    Striking, but true: a very similar thing happened once to me. When I was 11 years old, I spent a whole year in an exotic country and got sick there with some kind of local stomach fever.None of the doctors knew what it was; at first they thought that cholera, then appendicitis, the temperature rose, opinions multiplied. Seeing that equatorial cockroaches joined the consultation of doctors, my mother (not a doctor) took me out of the hospital under her own responsibility, when she felt early signs of the same thing and realized that it was just a virus. She and I successfully recovered from this incomprehensible fever, which, perhaps, was nothing more than a battle between Soviet intestinal bacteria and foreign ones, who knows.

    The main thing is that after that I lost a lot of weight and did not return to my “puffy” state, although my diet did not change, and, returning to Moscow, I continued to indulge in high-calorie buns with raisins for 10 kopecks and other gastronomic pleasures. But in my family there is a tendency to be overweight and, perhaps, if I did not “become friends” then with a foreign microbiome, it would be much more difficult for me to maintain a normal weight all subsequent years, even despite my exercise and fitness.

    Is obesity contagious?

    But I will return to professorial research again. So, Rob Knight discovered that the microbiome varies not only from person to person, but also from country to country – probably due to the peculiarities of the national cuisine. He also found that transplanting bacteria from the intestines of an obese person into the intestines of a slender mouse caused the mouse to gain weight by leaps and bounds.

    Scientists, by the way, have recently begun to lean towards such seditious thought that obesity can be partially contagious: the experiments of Tim Spector proved that if thin mice were transplanted into cages for plump ones, then the first ones also began to gain weight!

    But the most important thing that follows from the research of these two luminaries of gastroenterology is that a healthy (that is, not leading to excess weight) diet is not an exception to some foods, on the contrary, it is a varied diet that will lead to a larger set of bacteria in our intestines.

    In general, this whole “fecal topic” is not so crazy: some scientists predict that it is quite possible that soon the West will have to import “brown gold” mined from the inhabitants of Africa and Latin America, since they have a more diverse microbiome from because they eat natural and varied food. Imagine future newspaper headlines: “Faecal imports have reached unprecedented levels” or something like that.

    In general, it is breathtaking to think that our gastrointestinal bacteria are responsible not only for the state of our body, but also for the state of our spirit: it has already been proven that they control the level of serotonin, on which a good mood depends.The English even have the expression “butterflies in the stomach” – this is when you see a person you are in love with, and you feel as if from somewhere from under the solar plexus all over your body flew, feeling. It is true that these “butterflies” are not yet clear, so there is still a lot of work.

    Maybe a little more deciphering of this intestinal jungle and scientists will come to the conclusion that in fact it is there that all these endless wars are brewed, and not at all in political minds.And they will finally open a peace-loving colony of “butterflies”, which can be packed in the form of a dry capsule and sent to politicians around the world to be swallowed entirely at the stage of the election campaign – for preventive purposes.

    Anthrax

    Siberian ulcer (malignant carbuncle, anthrax) is a particularly dangerous infectious disease of agricultural and wild animals of all types, as well as humans. The disease proceeds with lightning speed, overly acute, acutely and subacutely (in sheep and cattle), acutely, subacutely and anginally (in pigs), mainly in the carbunculosis form in humans.There are also oropharyngeal and gastrointestinal forms [1] . It is characterized by intoxication, the development of serous-hemorrhagic inflammation of the skin, lymph nodes and internal organs; proceeds in the skin or septic form (intestinal and pulmonary forms are also found in animals).

    Origin of the name

    Anthrax, known since ancient times under the names “sacred fire”, “Persian fire”, etc., was repeatedly mentioned in the works of ancient and oriental writers and scientists.A detailed description of the clinic of this disease was made by the French physician Moran in 1766. In pre-revolutionary Russia, in view of the predominant spread in Siberia, this disease was called “anthrax”, when the Russian doctor S.S. the identity of anthrax between animals and humans and proved the possibility of its transmission from animals to humans.

    Exciter

    The causative agent of the disease was almost simultaneously described in 1849-1850 by three researchers at once: A. Pollender, F. Brauell and K. Daven. In 1876, R. Koch singled it out in pure culture. Of all the bacteria pathogenic to humans, the anthrax pathogen was discovered first. The generally accepted name for anthrax is anthrax , from ancient Greek. ἄνθραξ “coal, carbuncle”: this name was given by the characteristic coal-black color of the anthrax scab in the cutaneous form of the disease.The causative agent of anthrax is bacillus Bacillus anthracis . It is a large spore-forming gram-positive rod 5-10 × 1-1.5 microns in size. Anthrax bacilli grow well on mesopatamia media, contain capsular and somatic antigens and are able to secrete exotoxin, which is a protein complex consisting of an edema-causing (increased concentration of cAMP), protective (interacts with cell membranes, mediates the activity of other components) and lethal (cytotoxic effect, pulmonary edema) components.Capsule – antiphagocytic activity. The anthrax bacterium outside the body, when oxygen is available, forms spores, as a result of which it is highly resistant to high temperatures, drying and disinfectants. Anthrax bacteria spores can last for years; pasture contaminated with feces and urine of sick animals can preserve anthrax spores for many years. The vegetative forms of the anthrax bacillus quickly die when boiled and exposed to conventional disinfectants.When autoclaved at 110 ° C, the spores die only after forty minutes. Dry heat at 140 ° C kills spores in two and a half to three hours. Anthrax spores can withstand direct sunlight for ten to fifteen days. Activated solutions of chloramine, hot formaldehyde, and hydrogen peroxide also have a sporicidal effect.

    Epizootology

    Sick farm animals are the source of infection: cattle, horses, donkeys, sheep, goats, deer, camels, in which the disease occurs in a generalized form.Domestic animals – cats, dogs – are not very susceptible.

    Anthrax in animals is characterized by the following features:

    1. short incubation period, usually not exceeding 3-4 days;
    2. pronounced clinic in the form of a severe febrile state, a decline in cardiovascular activity, meningeal phenomena, bloody diarrhea and vomiting;
    3. the rapid development of the infectious process, ending with the death of animals during, as a rule, the first 2-3 days.

    Cattle and horses: Generally acute and subacute. It is characterized by: (septic form) a sharp rise in temperature, apathy, decreased productivity, swelling of the head, neck and dewlap; (intestinal form) apathy, refusal to feed, bloody diarrhea and vomiting, tympania.

    Pigs: (anginal form) occurs only in pigs and is asymptomatic; changes can be detected only during the veterinary and sanitary examination of carcasses for the characteristic catarrhal-hemorrhagic inflammation of the lymph nodes.Anthrax epizootics are geographically tied to soil foci – repositories of pathogens. Primary soil foci are formed as a result of direct soil infection by excretions of sick animals in pastures, in places where animals are kept in stalls, in places of burial of corpses (cattle burial grounds), etc. waters. Infection can occur with the participation of a large number of transmission factors.These include secretions from the skin of sick animals, their internal organs, meat and other food products, soil, water, air, environmental objects, seeded with anthrax spores. Susceptibility to anthrax in humans does not depend on age, sex and other physiological characteristics of the organism; it is associated with routes of infection and the size of the infectious dose.

    Pathogenesis

    Infected skin is usually the gateway to infection for anthrax.In rare cases, the bacillus is introduced through the mucous membranes of the respiratory tract and gastrointestinal tract. At the site of the introduction of the pathogen into the skin, an anthrax carbuncle appears in the form of a focus of serous-hemorrhagic inflammation with necrosis, edema of adjacent tissues and regional lymphadenitis. The local pathological process is due to the action of the anthrax bacillus exotoxin, the individual components of which cause severe microcirculation disorders, tissue edema and coagulation necrosis. Regardless of the entrance gate of the infection, the first stage is a localized lesion of the regional lymph nodes, the second stage is the generalization of the process.Generalization of infection with the breakthrough of anthrax pathogens into the bloodstream and the development of a septic form occurs extremely rarely in the cutaneous form of anthrax. Anthrax sepsis usually develops when the pathogen is introduced through the mucous membranes of the respiratory tract or gastrointestinal tract. In these cases, a violation of the barrier function of the tracheobronchial or mesenteric lymph nodes leads to the generalization of the process. Bacteremia and toxinemia can cause the development of infectious-toxic shock.

    The pathogenesis is based on the action of the pathogen exotoxin, which consists of at least three components or factors:

    • of the first (I), edematous (inflammatory) factor;
    • second (II), protective (protective) factor;
    • third (III) lethal factor. The addition of factor I to factor II increases the immunogenic properties, while factor III reduces them.

    A mixture of factors I and II causes an increase in the inflammatory response and edema due to an increase in capillary permeability.A mixture of II and III factors enhances the effect of the lethal factor and leads to the death of guinea pigs, rats and mice. A mixture of three factors of anthrax toxin (I, II, III) has an inflammatory (edematous) and lethal effect. The morphological essence of anthrax sepsis is acute serous-hemorrhagic, hemorrhagic, less often fibrinous-hemorrhagic inflammation. The leukocyte reaction in the foci of inflammation in sepsis is weak or absent. In the organs of immunogenesis (spleen, lymph nodes, thymus gland) there is a suppression of the body’s immune defense with the replacement of lymphoid tissue by macrophages and the presence of a primitive defense reaction in the form of macrophage incomplete phagocytosis of the pathogen.

    Clinical picture

    The duration of the incubation period ranges from several hours to days, most often 2-3 days. The disease can occur in a localized (skin) or generalized (pulmonary and intestinal) form.

    Cutaneous anthrax

    Occurs in 98-99% of all cases of anthrax. Its most common type is the carbunculous form; edematous, bullous and erysipeloid forms of the disease are less common.Mainly exposed parts of the body are affected; the disease is especially difficult when carbuncles are localized on the head, neck, mucous membranes of the mouth and nose. The clinic of generalization of anthrax infection, regardless of the form – skin or visceral, with an extreme variety of manifestations in the initial period of the disease in the terminal stage is of the same type: it is accompanied by an exit to peripheral blood of anthrax bacteria, the concentration of which reaches hundreds of thousands and millions of bacterial cells in 1 mm³ of blood, which can be considered as anthrax sepsis (see.), and is a clinic of infectious-toxic shock. These are severe disorders of the blood coagulation and anticoagulation systems, acidosis, acute renal failure, drop in body temperature below normal, severe intoxication. Usually there is only one carbuncle, but sometimes their number reaches 10-20 or more. At the site of the entrance gate of the infection, a spot, papule, vesicle, ulcer consistently develops. A painless spot of reddish-blue color and 1-3 mm in diameter, which resembles an insect bite mark, after a few hours turns into a copper-red papule.Itching and burning sensation increases. After 12-24 hours, the papule turns into a bubble with a diameter of 2-3 mm, filled with fluid, which darkens and becomes bloody. When scratching (sometimes spontaneously), the bubble bursts, and in its place an ulcer forms with a dark brown bottom, raised edges and serous-hemorrhagic discharge. In a day, the ulcer reaches 8-15 mm in diameter. As a result of necrosis, the central part of the ulcer in 1-2 weeks turns into a black, painless, dense scab, around which there is a pronounced inflammatory cushion of red color.Outwardly, the scab resembles a coal in a flame, which is the reason for the name of this disease (Antrax – coal). This defeat is called the carbuncle.

    Septic form of anthrax

    The septic form is quite rare. The disease begins acutely with tremendous chills and fever up to 39-40 ° C. Severe tachycardia, shortness of breath, tachypnea, chest pain and cough with frothy bloody sputum are observed. Signs of pneumonia and pleural effusion are determined.With the development of infectious-toxic shock, hemorrhagic pulmonary edema occurs. A large number of anthrax bacteria are found in the blood and sputum. Some patients develop abdominal pains, nausea, bloody vomiting, liquid bloody stools join. Subsequently, intestinal paresis develops, peritonitis is possible. Symptoms of meningoencephalitis are found. Infectious-toxic shock, edema and swelling of the brain, gastrointestinal bleeding and peritonitis can cause death in the first days of the disease.

    Diagnostics

    The diagnosis is made on the basis of clinical, epidemiological and laboratory data. Laboratory diagnostics includes bacterioscopic and bacteriological methods, and for early diagnosis – immunofluorescence. Allergic diagnostics of anthrax is also used by intradermal test with anthraxin, which gives positive results after the 5th day of illness. The material for laboratory research is the contents of vesicles and carbuncles, as well as sputum, blood, feces and vomit in septic form.Anthrax is distinguished with glanders, banal boils and carbuncles, plague, tularemia, erysipelas, pneumonia and sepsis of a different etiology.

    Treatment and prevention

    Etiotropic therapy of anthrax is carried out with antibiotics. Penicillin is prescribed. In pathogenetic therapy, colloidal and crystalloid solutions, plasma, albumin, glucocorticosteroids are used. Surgical interventions for the cutaneous form of the disease are unacceptable: they can lead to the generalization of the infection. Preventive measures are carried out in close contact with the veterinary service.Identified sick animals should be isolated and their corpses burned; infected objects must be disinfected. Chamber disinfection is used to disinfect wool and fur products. Persons who have been in contact with sick animals or infectious material are subject to active medical supervision for 2 weeks. Vaccination of humans and animals with dry live anthrax vaccine is important. The first vaccine was invented and tested by the French microbiologist and chemist Louis Pasteur.

    Forecast

    The prognosis is largely determined by the form of the disease, in general it is conditionally unfavorable and a lethal outcome is possible even with adequate and timely treatment.In the absence of appropriate treatment for the cutaneous form, the mortality rate is 10-20%. With the pulmonary form of the disease, depending on the strain of the pathogen, the lethality can exceed 90-95%, even with appropriate treatment. The intestinal form is about 50%. Anthrax meningitis – 90%.

    Epizootological situation

    Anthrax outbreaks are registered in Russia to this day. So on July 23, 2016, a notification of the veterinary supervision about the death of reindeer in one section of the tundra in the Yamal region appeared.On August 3, 2016, there were reports of an anthrax epidemic in the Yamalo-Nenets Autonomous District. To eliminate the outbreak of anthrax, the Armed Forces of the Russian Federation were involved. On November 9, 2016, in the north of the Volgograd region, in the Nekhaevsky district, bordering the Rostov and Voronezh regions, a case of the death of a cow was established

    90,000 “Bacteria found in urine, what does that mean?” – Yandex.Qu

    A healthy person should not have bacteria in the urine test. If bacteriological examination of urine detects them, this condition is called bacteriuria and requires treatment by a specialist – urologist.

    Escherichia coli most common in urine culture. Bacteriuria in the urine is determined only if the organs of the urinary system (kidneys, bladder, ureters) are infected, and the immune system could not independently cope with the pathogenic bacteria.

    Why bacteria are found in a general urine test in a person, and what this means we will consider in this article.

    How does bacteria get into urine?

    There are several ways of getting the pathogen into the urinary tract:

    1. Ascending – the infectious agent enters the urinary tract through the urethra.This type of infection is more typical for women, due to anatomical features (short and wide urethra). In addition, this mechanism of bacteria penetration into the urine is very likely with such instrumental manipulations as bladder catheterization, ureteroscopy, cystoscopy, urethral bougienage, and transurethral surgical interventions.
    2. Descending – with kidney infection.
    3. Lymphogenous – infection occurs through the lymphatic tract from infectious foci located near the organs of the genitourinary system.
    4. Hematogenous – the pathogen is carried into the urinary tract with blood from distant foci of infection.

    As a rule, in case of pathological changes in the urinary system, in addition to bacteria, an increase in the concentration of other indicators of inflammation – leukocytes and mucus – is detected.

    Forms of bacteriuria

    • True bacteriuria is bacteria that not only enter the urinary tract, but also multiply there, provoking severe inflammation.
    • False bacteriuria – bacteria penetrate the bladder, urinary tract, but do not have time to spread and multiply due to the fact that a person either has an active immune system, or is taking antibiotic therapy for an inflammatory disease.
    • Latent bacteriuria is most often determined during routine clinical examination in people who are not worried about either the bladder, or the kidneys, or impaired urination. Especially often, in that sense, asymptomatic bacteriuria is detected in pregnant women.
    • The fact that a patient has asymptomatic bacteriuria can be said after a positive two-stage urine test. The collection of material should occur at intervals of a day, and the bacterial indicator should be double-confirmed in the range of 100,000 per milliliter of urine.

    The reasons for the appearance of bacteria in the general analysis of urine

    If bacteria are found in large quantities in the urine, this is called bacteriuria, and indicates the likelihood that an infection develops in the urinary system.But before taking any steps, you need to make sure that the analysis was submitted correctly. Perhaps you used a non-sterile jar, and repeated diagnostics will reveal that all indicators are normal. Sometimes you have to retake the tests 2-3 times.

    What diseases can manifest themselves at the initial stages only by changing the above indicator?

    1. Urethritis. If opportunistic microorganisms in the urinary canal begin to multiply actively (as a result of various reasons), inflammation of the urethra occurs.
    2. Pyelonephritis. The second of the most common causes of bacteria in the urine. Inflammation of the kidneys can also be primary or secondary.
    3. Cystitis. One of the two most likely pathologies, accompanied by an increased release of microorganisms.

    When bacteria are found in the urinalysis, it is necessary to determine which bacteria it is in order to find the right treatment. For this, bacteriological sowing of urine is carried out – bacteria are placed in a nutrient medium and grown in favorable conditions for them.With the help of such a study, the type of bacteria is determined, as well as their sensitivity to antibiotics.

    Decoding the results

    The result is estimated in colony-forming units, contained in 1 ml of the test liquid. If indicators are obtained that are less than 1000 CFU / ml, then treatment, as a rule, is not necessary. When the results of the study showed that the number of microorganisms is from 1000 to 100,000 CFU / ml, then this analysis may raise doubts, a urine test will be necessary.

    If the number of microorganisms is equal to or exceeds 100,000 CFU / ml, then we can talk about the connection between inflammation and infection. It is necessary to carry out compulsory treatment.

    Increased white blood cells and bacteria in the urine

    Leukocytes and pathogenic bacteria in urine indicate the possible development of such diseases:

    • pyelonephritis;
    • interstitial nephritis;
    • vasculitis

      ;

    • atheroembolism of the renal arteries;
    • vesiculitis;
    • cystitis;
    • urethritis;
    • nephrosclerosis.

    Epithelial cells are sometimes present in the test material, but in minimal numbers.

    Mucus and bacteria in urine

    If there is mucus and bacteria in the urine in excess of the normal concentration, the causes are usually the following:

    • urolithiasis;
    • jades;
    • inflammation of the ureter, bladder or kidneys.

    Also, microbes, epithelium and leukocytes are often found due to improper collection of body fluid.The external genitals must be thoroughly washed immediately before urination, and it is better to purchase a container for transporting urine at a pharmacy, completely sterile.

    Escherichia coli

    This type of bacteria lives in the lower parts of the digestive system. These are gram-negative bacteria that are secreted during the act of defecation. Once on the genitals, they multiply in the urethra, then reach the bladder.

    Microorganisms multiply very quickly in any part of the urinary system.With the development of these bacteria in the kidneys, pyelonephritis appears, in the urethra – urethritis, in the bladder – cystitis. Escherichia coli is most common in urinary tract infections.

    Enterococcus faecalis

    Enterococcus faecalis is the next most common species after E. coli. Being a gram positive bacterium, it is normally present in the gastrointestinal tract of healthy people, participating in digestion. Entering the urinary tract occurs through feces.Then there is an uncontrolled growth of this bacterium. Infection of the blood, wounds and pelvic area is also possible. Infection caused by Enterococcus faecalis is difficult to treat. This bacterium is very resistant to most antibiotics.

    Causes of bacteria in urine during pregnancy

    There are many reasons for their appearance, because this is a very difficult period for a woman, different conditions are created when urine stagnates and bacteria begin to develop in it.Also, during pregnancy, the uterus constantly grows, which presses on the kidneys and does not allow them to work fully.

    Hormonal changes are often the cause of bacteriuria. It is necessary to take into account the physiological characteristics of the urogenital system of a pregnant woman, the urethra is located near the rectum, while the urethra is too short. In addition, the bladder may be close to the rectum.

    Changes in hormonal levels can also affect the appearance of bacteria in urine during pregnancy.Bacteriuria also occurs with caries or due to a decrease in immunity. In women with diabetes, bacteria can also be found in the urine.

    Pregnant women who lead an irregular sex life, that is, often change sexual partners, are especially at risk of acquiring the bacteria. The same danger lies in wait for women who do not properly follow the rules of personal hygiene. Such diseases of the genitourinary system as cystitis and pyelonephritis carry a certain threat to pregnancy.

    Bacteria in the urine of a child

    Depending on the number of bacteria detected in the child’s urine, the following diseases may occur:

    1. Cystitis and urethritis are more often characterized by dysuric disorders (retention or incontinence of urine, increased frequency of urination at night, urination in small portions), pain and burning sensation during urination, weakness, lethargy, fever up to 37-38 degrees, pain in the lower abdomen with irradiation into the perineum and / or lower back.
    2. Pyelonephritis, in which there is pain in the lumbar region and abdomen, diarrhea, chills, fever, vomiting. In newborns and infants, with the disease, there is a complete refusal to eat and a general anxiety.
    3. Asymptomatic bacteriuria is a condition in which there are no signs of the disease. This phenomenon is benign and does not require treatment, since it does not cause damage to the kidney tissue.
    4. Bacteria in the urine of a child can be detected in infectious and inflammatory diseases of the urinary system, which develop against the background of congenital malformations of the kidneys, ureters and bladder, as well as the genital area (vas deferens, testicles) or with complex congenital inguinal and scrotal hernias.

    Accordingly, the treatment of bacteria in the urine of a child is based on the data of the analysis and the doctor’s prescriptions, individually in each case. The cause should be treated, that is, the disease that made it possible for bacteria to enter the urine.

    Symptoms

    Usually, bacteriuria is accompanied by any clinical manifestations, but in some cases this phenomenon is asymptomatic.

    The most characteristic signs of bacteriuria include:

    • frequent urination

      ;

    • pain and burning sensation when urinating

      ;

    • redness of the external genital organs, accompanied by itching;
    • urinary incontinence;
    • pain in the lower abdomen;
    • urine comes with a pungent, disgusting odor, impurities of blood or mucus are possible;
    • Urine is very cloudy or whitish.

    If the infection affects the bladder or urethra, the body temperature does not rise, but if the infection spreads to the kidneys, fever, dull pain in the lumbar region, nausea and vomiting are possible.

    How to treat bacteria in urine?

    First of all, it is necessary to undergo a detailed examination to detect the nature and cause of bacteriuria. The resistance of bacteria to one or another antibiotic is also experimentally revealed.

    Treatment is aimed at eliminating the focus of the disease and improving the process of urination. Antibiotics, nitrofurans, and sulfa drugs are commonly prescribed.

    In order to prevent the occurrence of bacteriuria, it is imperative to observe personal hygiene, and in case of any suspicion, immediately contact a specialist. Taking tests is not just a whim of doctors, but a way to protect you from dangerous diseases. If the examination reveals doubtful microorganisms, repeat the analysis.

    Material provided

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    Proceedings of scientific conferences

    1 Materials of the scientific student conference “Week of student science” The collection reflects the issues of studying the rational activity of animals, visual diagnostics, physiological characteristics, as well as reproductive function in the field of small-scale animal husbandry. Particular attention is paid to the issues of oncology and biochemistry.The veterinary and sanitary assessment of seasonings and seafood is given. 26 November 2018 Reference to collection
    2 Materials of the scientific student conference “Week of student science” The collection reflects the basic questions of the morphofunctional anatomy of organs and systems of animals. Analyzed the genetic and behavioral diversity of animals by breed and species criteria. Methods for diagnosing animal diseases are presented in detail.Treatment regimens for invasive diseases are presented. Particular attention is paid to the study and increase of productive qualities, a comparative analysis of interior and exterior indicators in domestic breeding. The issues of biotechnology of the food industry, immunology and quantum mechanics, as well as the use of cell cultures are considered. 03 March 2020 Reference to collection
    3 Materials of the scientific student conference “Week of student science” The collection reflects the questions of the pharmacological effectiveness of drugs for the treatment of diseases of the reproductive system of animals, studied the latest morphofunctional features of the somatic, visceral and integrating organ systems in various animal species.The problems of genetic engineering and cloning among productive animals are reflected. A commodity assessment of dairy and fish products, as well as cosmetics, sold in pet stores in the Russian Federation, was carried out. Methods of using immunomodulation by mesenchymal stem cells are presented. Methods of express diagnostics in veterinary practice have been developed. 07 April 2021 Reference to collection

    How Science Fights Antibiotic Resistant Bacteria – Rossiyskaya Gazeta

    We thought that after the discovery of penicillin we would no longer be afraid of germs.But we were wrong. It looks like a real war. Man invents more and more new means of defense against bacterial attacks. In response, microorganisms improve weapons, train fighters, use camouflage and sabotage groups. The problem of antibiotic-resistant infections has become so serious that a special meeting of the UN General Assembly was recently dedicated to it. According to the reported data, at least 700,000 people die each year due to drug-resistant infections. Non-exterminating microbes are on a par with global climate change and other problems of a planetary scale.

    In the winter of 2003, Ricky Lannetti, a successful 21-year-old soccer player, developed a cough followed by nausea. A few days later, Ricky’s mother made her son see a doctor. All the symptoms pointed to a flu virus, so he did not prescribe antibiotics to Ricky, because they kill bacteria, not viruses. But the disease did not go away, and Ricky’s mother took Ricky to a local hospital – by this time, the boy’s kidneys were already failing. He was prescribed two powerful antibiotics: cefepime and vancomycin. But less than a day later, Ricky died.Tests have shown that the killer was methicillin-resistant Staphylococcus aureus (MRSA), a toxic bacterium that is resistant to multiple antibiotics.

    Strains such as MRSA are now called super microbes. Like horror heroes, they mutate and acquire superpowers, allowing them to resist enemies – antibiotics.

    End of the antibiotic era

    In 1928, after returning from vacation, the British biologist Alexander Fleming discovered that the Petri dishes with bacterial cultures left by him inadvertently were overgrown with mold.A normal person would take it and throw it away, but Fleming began to study what happened to the microorganisms. And I found out that in those places where there is mold, there are no staphylococcal bacteria. This is how penicillin was discovered.

    Fleming wrote: “When I woke up on September 28, 1928, I certainly did not plan to revolutionize medicine by discovering the world’s first antibiotic, but I guess that is what I did.” The British biologist received the Nobel Prize in Physiology or Medicine for the discovery of penicillin in 1945 (together with Howard Flory and Ernst Cheyne, who developed the technology for purifying the substance).

    Modern man is accustomed to the fact that antibiotics are affordable and reliable helpers in the fight against infectious diseases. Sore throat or a scratch on the arm does not cause panic in anyone. Although two hundred years ago, this could lead to serious health problems and even death. The 20th century was the era of antibiotics. Together with vaccinations, they saved millions, maybe billions of people who would certainly have died from infections. Vaccines, thank God, are working properly (doctors do not seriously consider the social movement of vaccine fighters).But the era of antibiotics seems to be coming to an end. The enemy is advancing.

    How super microbes are born

    Single-celled creatures were the first to conquer the planet (3.5 billion years ago) – and continuously fought with each other. Then multicellular organisms appeared: plants, arthropods, fish … Those who retained their single-celled status thought: what if we put an end to civil strife and begin to seize new territories? Inside multicellular organisms it is safe and there is a lot of food. Attack! Microbes moved from one creature to another, until they got to a person.True, if some bacteria were “good” and helped the owner, others only caused harm.

    People confronted these “bad” microbes blindly: they introduced quarantine and were engaged in bloodletting (for a long time this was the only way to fight all diseases). It was only in the 19th century that it became clear that the enemy has a face. Hands began to be washed, hospitals and surgical instruments were treated with disinfectants. After the discovery of antibiotics, it seemed that humanity received a reliable means of fighting infections.But bacteria and other unicellular organisms did not want to leave the warm place and began to acquire resistance to drugs.

    Super microbe can resist antibiotics in different ways. For example, it is capable of producing enzymes that degrade the drug. Sometimes he is just lucky: as a result of mutations, his membrane becomes invulnerable – a shell on which drugs used to deal a crushing blow. Resistant bacteria are born in different ways. Sometimes, as a result of horizontal gene transfer, bacteria that are harmful to humans are borrowed from useful defenses against drugs.

    Another more realistic depiction of methicillin-resistant Staphylococcus aureus (MRSA). It spreads more and more every year, especially inside hospitals and among people with weakened immune systems. According to some reports, in the United States, this microbe kills about 18 thousand people annually (the exact number of cases and deaths is still impossible to determine). Photo: “Schrödinger’s cat”

    Sometimes a person himself turns the body into a training center for killer bacteria.Let’s say we treat pneumonia with antibiotics. The doctor prescribed: you need to take the medicine for ten days. But on the fifth, everything goes away and we decide that it’s enough to poison the body with all kinds of nasty things and stop taking it. By this time, we have already killed some of the bacteria that are least resistant to the drug. But the strongest survived and got the opportunity to reproduce. So, under our careful guidance, natural selection began to work.

    “Drug resistance is a natural phenomenon of evolution.Under the influence of antimicrobial drugs, the most sensitive microorganisms die, but the resistant ones remain. And they begin to reproduce, passing on resistance to their offspring, and in some cases to other microorganisms, “explains the World Health Organization.

    – Drug resistance is facilitated by the fact that many antibiotics are available over the counter without a prescription. And doctors themselves are often reinsured and unreasonably prescribe these drugs. Let’s say a person’s temperature rises – they immediately give him antibiotics without doing tests and without figuring out what caused it, – says Yuri Vengerov, professor of MMSU (infectious disease doctor, doctor of medical sciences, co-author of the books “Infectious and Parasitic Diseases”, “Infectious diseases “,” Tropical diseases.Guide for Physicians “,” Lectures on Infectious Diseases “). – The selection of microbes is especially active in hospitals. There people come into contact with various infections, they take many antibiotics. As a result, hospital pneumonia and other nosocomial infections are now widespread. only about bacterial diseases, but also, for example, about fungal. Among fungi, already 30% have acquired resistance to drugs.

    Unicellular attack

    In the fall of 2016, a meeting of the UN General Assembly is taking place in New York, in which representatives of 193 countries participate, that is, in fact, the entire planet.Usually issues of war and peace are discussed here. But now we are not talking about Syria, but about microbes that have developed resistance to drugs.

    “World leaders have shown an unprecedented focus on containing antimicrobial-resistant infections. This refers to the ability of bacteria, viruses, parasites and fungi to resist the drugs that were previously used to kill them and treat the diseases they cause. pledged to take large-scale and coordinated action to tackle the root causes of antimicrobial resistance across a range of areas, primarily health, animal health and agriculture.This is only the fourth time in history that the health issue has been raised by the UN General Assembly, “the WHO website reports.

    The forecast is gloomy. “Patients are finding it increasingly difficult to recover from infections as the level of resistance of pathogens to antibiotics and, even worse, reserve antibiotics is steadily increasing. Combined with the extremely slow development of new antibiotics, this increases the likelihood of respiratory, skin, urinary and urinary infections. pathways, blood flow can become incurable, and therefore fatal, “explains Dr. Nedret Emiroglu from the WHO European Office.

    – I would definitely add malaria and tuberculosis to this list of diseases. In recent years, it has become increasingly difficult to deal with them, since the pathogens have acquired resistance to drugs, says Yuri Vengerov.

    Keiji Fukuda, WHO Assistant Director-General for Health Safety, says roughly the same: “Antibiotics are losing their effectiveness, so common infections and minor injuries that have healed for many decades can now kill again.”

    Model of a bacteriophage that infects a microbe. These viruses invade bacteria and cause them to lysis, that is, dissolution. Although bacteriophages were discovered at the beginning of the 20th century, it is only now that they have begun to be included in official medical reference books. Photo: “Schrödinger’s cat”

    – Bacteria began to resist especially zealously when antibiotics began to be used in huge quantities in hospitals and in agriculture, – assures biochemist Konstantin Miroshnikov (Doctor of Chemistry, Head of the Laboratory of Molecular Bioengineering at the Institute of Bioorganic Chemistry.Academikov M.M. Shemyakin and Yu.A. Ovchinnikov RAS). “For example, to stop diseases in chickens, farmers use tens of thousands of tons of antibiotics. Often for prevention, which allows bacteria to get to know the enemy better, get used to it and develop resistance. Now the use of antibiotics has begun to be limited by law. I believe that public discussion of such issues and further tightening of the law will slow down the growth of resistant bacteria. But they will not stop.

    – The possibilities of creating new antibiotics are almost exhausted, and the old ones are failing.At some point, we will be powerless against infections, – Yuri Vengerov admits. – It is also important to understand that antibiotics turn into a medicine only when there is a dose that can kill microbes, but at the same time not harm a person. The likelihood of finding such substances is less and less.

    Has the enemy won?

    The World Health Organization periodically publishes panicky statements: they say, first-line antibiotics are no longer working, more modern ones are also close to surrender, and fundamentally new drugs have not yet appeared.Is the war lost?

    “There are two ways to fight microbes,” says biologist Denis Kuzmin (candidate of biological sciences, employee of the educational and scientific center of the IBCh RAS). – First, to look for new antibiotics that affect specific organisms and targets, because it is the “large-caliber” antibiotics, which infect a whole bunch of bacteria at once, that cause the accelerated growth of resistance. For example, it is possible to design drugs that begin to act only when bacteria with a certain metabolism enter the interior.Moreover, manufacturers of antibiotics – producing microbes – need to be looked for in new places, more actively to use natural sources, unique geographic and ecological zones of their habitat. Secondly, it is necessary to develop new technologies for the production and cultivation of antibiotic producers.

    These two methods are already being implemented. New methods for finding and testing antibiotics are being developed. Microorganisms that can become a weapon of a new generation are searched for everywhere: in rotting plant and animal remains, silt, lakes and rivers, air … For example, scientists managed to isolate an antimicrobial substance from the mucus that forms on the frog’s skin.Remember the ancient tradition of putting a frog in a jar of milk to keep it from souring? Now this mechanism has been studied and they are trying to bring it to medical technology.

    Another example. More recently, Russian scientists from the N.N. G.F. Gause researched the inhabitants of edible mushrooms and found several potential suppliers of new drugs.

    Scientists from Novosibirsk, working in the Russian-American laboratory of biomedical chemistry of the ICBFM SB RAS, took a different path.They managed to develop a new class of substances – phosphorylguanidines (it is difficult to pronounce, and it is not easy to write it down). These are artificial analogues of nucleic acids (more precisely, their fragments) that easily penetrate the cell and interact with its DNA and RNA. Such fragments can be created for each specific pathogen based on the analysis of its genome. The project is headed by American Sydney Altman (1989 Nobel Prize Laureate in Chemistry (together with Thomas Chek). Professor at Yale University. In 2013 he received a Russian mega-grant and began to work at the Institute of Chemical Biology and Fundamental Medicine of the Siberian Branch of the Russian Academy of Sciences).

    But the most popular directions in the search for anti-infection agents are bacteriophages and antimicrobial peptides.

    Puddle Allies

    From a bird’s eye view, the building of the IBCh RAS looks like a double helix of DNA. And just outside the gate is an incomprehensible sculpture. The plate explains that it is a complex of the antibiotic valinomycin with a potassium ion in the middle. Fifty years ago, employees of the institute understood how metal ions bind to each other and how they then pass through the cell membrane thanks to ionophores.

    Now the IBCh is engaged in another topic – bacteriophages. These are special viruses that selectively attack bacteria. The head of the laboratory of molecular bioengineering, Konstantin Miroshnikov, affectionately calls his wards, bacteriophages, animals.

    – Phages are good and bad at the same time in that they act on a specific pathogen. On the one hand, we aim only at those microbes that interfere with life, and do not bother the rest, and on the other hand, it takes time to find the right phage, which is usually not enough, ”the zavlab smiles.

    There are both bacteria and bacteriophages in every puddle. They are constantly fighting each other, but for millions of years neither side can defeat the other. If a person wants to overcome bacteria that attack his body or potatoes in a warehouse, it is necessary to deliver more corresponding bacteriophages to the breeding site of bacteria. Here is a metaphor, for example: when they were exploring the coast of Golden Sands in Bulgaria, there were many snakes, then they brought many hedgehogs and they quickly shifted the balance of the fauna.

    – Two years ago we began to cooperate with the Rogachevo agricultural park near Dmitrov. The general director of the organization, Alexander Chuenko, is a former electronics engineer and an enlightened capitalist, not alien to the scientific approach, says Konstantin. – The crop of potatoes was eaten up by pectolytic bacteria – soft rot that lives in warehouses. If left untreated, potatoes quickly turn into tons of smelly goo. Phage treatment of potatoes at least dramatically slows down the development of infection – the product retains its taste and presentation longer both in storage and on store shelves.In this case, the phages attacked putrefactive microbes and biodegraded – they disintegrated into DNA particles, proteins and went to feed other microorganisms. After successful tests, the management of several large agricultural complexes became interested in such bio-protection of the crop.

    – How did you manage to find the necessary bacteriophages and turn them into an antidote? I ask, glancing at the toy phage standing on a stack of books.

    – There is a classic double agar method for searching. First, on the first layer of agar in a Petri dish, spread a kind of lawn of bacteria, pour water from a puddle on top and cover with a second layer of agar.After some time, a clean spot appears on this muddy lawn, which means that the phage has devoured the bacterium. We isolate the phage and study it.

    Miroshnikov’s laboratory, together with Russian and foreign colleagues, received a grant from the Russian Science Foundation for research and diagnostics of potato pathogens. There is work to do here: plant bacteria are much less studied than human ones. However, with our body, too, a lot is unclear. According to scientists, doctors do not examine a person this way: all tests and examinations are sharpened for antibiotics, and other methods are needed for phage therapy.

    – Phage therapy is not a medicine in the current sense, but rather a complex service that includes quick diagnosis and selection of the right agent against a specific pathogen. In Russia, phage preparations are included in the list of medicines, but are not mentioned in the guidelines for physicians. So doctors who are in the subject are forced to use phages at their own peril and risk. And in Poland, for example, the legislation states that if a patient cannot be cured by traditional evidence-based medicine, at least dancing with a tambourine, at least homeopathy, at least phage therapy can be used.And at the Hirschfeld Institute in Wroclaw, phages are used as personalized medical care. And with great success, even in the case of advanced purulent infections. The use of phages is a scientifically based and biologically comprehensible, although not a trivial method, sums up Miroshnikov.

    Peptides are a family of substances composed of amino acid residues. Recently, scientists are increasingly considering peptides as the basis for future drugs. It’s not just about antibacterial agents.For example, at Moscow State University. M.V. Lomonosov and the Research Institute of Molecular Genetics of the Russian Academy of Sciences, a peptide drug was created that normalizes brain function, improves memory, attention and resistance to stress. Photo: “Schrödinger’s cat”

    And here is the news from the science city of Pushchino. Scientists from the branch of the IBCh RAS, the Institute of Theoretical and Experimental Biophysics of the Russian Academy of Sciences and the Institute of Biochemistry and Physiology of Microorganisms named after V.I. G.K. Scriabin RAS investigated how the bacteriophage T5 enzyme acts on E. coli. That is, they worked not with the bacteriophages themselves, but with their enzyme proteins.These enzymes destroy the cell walls of bacteria – they begin to dissolve and die. But some microbes have a secure outer membrane, and this method does not work on them. In Pushchino, they decided to attract substances that increase the permeability of the membrane to help the enzyme. As a result of experiments on E. coli cell cultures, scientists have found that together the enzyme and the agent destroy bacteria much more efficiently than separately. The number of surviving cells was reduced by almost a million times compared to the control experiment.Cheap common antiseptics such as chlorhexidine were used as a helper, and in very low concentrations.

    Phages can be used not only as a medicine, but also as a means of increasing the effectiveness of vaccinations.

    – Within the framework of a project supported by the Ministry of Education and Science of Russia, we are going to use bacteriophage proteins to enhance the immunogenic properties of an artificial antigen, says microbiologist Andrei Letarov (Doctor of Biological Sciences, Head of the Laboratory of Microorganism Viruses at the V.I.S.N. Vinogradsky Federal Research Center of Biotechnology RAS). – For this, fragments of the antigen are genetically engineered to link with certain proteins of bacteriophages, which are able to assemble into ordered structures, for example, into tubes or spheres.

    As the scientist explains, such structures with their properties resemble particles of pathogenic viruses, although in fact they do not pose any danger to humans and animals. The immune system is much more willing to recognize such virus-like particles and quickly develops an antibody response.This is the way to create an improved vaccine that, in addition to traditional long-term protection, will provide a quick protective effect to prevent the spread of the disease at the site of infection.

    Worm and pig immunity

    Pavel Panteleev, a junior researcher at the educational and scientific center of the Institute of Bioorganic Chemistry (PhD in Chemistry), likes to ride a bicycle in the mountains. He also loves to study marine invertebrates, more precisely, their antimicrobial peptides, which fight bacteria in living organisms every day.Peptides are the younger brothers of proteins: they also consist of amino acids, only there are no more than fifty of them, and in proteins there are hundreds and thousands.

    – At the beginning of each article about peptides, something like this is written: “There is an urgent need to create new antibiotics, because the old ones no longer work because of resistance. And antimicrobial peptides have a wonderful property – resistance from bacteria is produced with great difficulty to them” … The educational and scientific center where I work is looking for peptides that would allow us to resist pathogenic microorganisms, says Pavel.

    More than 800 such peptides are known today, but none of them work in humans. Medicines based on peptides fail clinical trials over and over again: it is not possible to find stable structures that would enter the right amount in the right place and do not cause side effects. They tend to accumulate in the body: for example, they can kill an infection, but not come out with urine, but remain in the kidneys.

    – We are studying marine annelids, – says Pavel. “Together with colleagues from the Institute of Experimental Medicine, we isolated two peptides from the Arenicola marina worm (sea sandworm) and studied them.When I was a graduate student, we still went to the White Sea for worms, but we never found new peptides in them. Of course, this may be due to the imperfection of the search method, but, most likely, this worm really only has two peptides, and this is enough to defend itself against pathogens.

    – Why worms, are they easier to study?

    The fact is that there is a concept according to which the system of innate immunity in ancient invertebrates must be very strong, because many of them live in unfavorable environmental conditions and still exist.Now one of the objects of my research is horseshoe crabs peptides.

    Pavel pulls out his phone and shows something with a turtle shell and a bunch of disgusting crab legs. This can only be seen in a horror movie or in a bad dream.

    Bacteriophage. Its real height is about 200 nanometers. The bulge at the top is called the head. It contains nucleic acid. Photo: “Schrödinger’s cat”

    “However, it doesn’t matter what you study, worms, horseshoe crabs or pigs,” Paul continues.- In all organisms you will examine the same tissues and cells where the peptides are located. For example, blood cells are neutrophils in mammals or hemocytes in invertebrates. It is not yet known why, one can only put forward hypotheses, including humorous ones. A pig is not a particularly clean animal, so it needs more protectors that will prevent bacteria from its mud bath from infecting the body with anything. But there is also a universal answer: in each specific case, there are as many peptides as necessary to protect the body.

    – Why are peptides better than antibiotics?

    – Peptides are cleverly arranged. Unlike antibiotics, which, as a rule, act on a specific molecular target, peptides are incorporated into the bacterial cell membrane and form special structures in it. In the end, the cell membrane is destroyed under the weight of the peptides, the invaders penetrate inside, and the cell itself explodes and dies. In addition, peptides act quickly, and the evolution of the membrane structure is a very disadvantageous and difficult process for bacteria.Under such conditions, the likelihood of developing resistance to peptides is minimized. By the way, in our laboratory peptides are studied not only from animals, but also from plants, for example, protective compounds of a protein-peptide nature from lentils and dill. On the basis of selected natural samples, we create something interesting. The resulting substance may well be a hybrid – something in between a peptide of a worm and a horseshoe crab, says Pavel.

    P. S.

    Hopefully, in five, ten or twenty years, there will be a new era of germ-fighting.Bacteria are cunning creatures and, perhaps, will create in response even more powerful means of defense and attack. But science will not stand still, so in this arms race, victory will still remain with man.

    Man and bacteria. Metaphors

    Friends

    Staff members are bacteria that live in our body. According to some estimates, their total mass is from one to three kilograms, and their number is greater than that of human cells. They can be employed in manufacturing (production of vitamins), in the processing industry (digestion of food) and in the army (in our intestines, these bacteria suppress the growth of their pathogenic counterparts).

    Invited Food Specialists – Lactic acid and other bacteria are used to make cheese, kefir, yoghurt, bread, sauerkraut and other products.

    Double Agents – Actually, they are enemies. But we managed to recruit them and make them work for the needs of our defense. We are talking about vaccinations, that is, the introduction of weakened versions of bacteria into the body.

    Adopted children are no longer bacteria, but parts of our cells – mitochondria.Once they were independent organisms, but, having penetrated through the cell membrane, they lost their independence and since then they regularly provide us with energy.

    POW laborers – genetically modified bacteria are used for the production of drugs (including antibiotics) and many other useful substances.

    Enemies

    Invaders – all those who invade our body, parasitize on it and lead to angina, tuberculosis, plague, cholera and many other diseases.

    Fifth column – some bacteria that live in our body or on the skin, in normal situations, can be quite harmless. But when the body is weakened, they insidiously rise up and go on the offensive. They are also called opportunistic strains.

    Protective fortresses – colonies of bacteria that cover themselves with mucus and films that protect against the action of drugs.

    Armored Infantry – Among the bacteria resistant to antibiotics, there are those who know how to make their outer shells impervious to drug molecules.The strength of the infantry is hidden in the lipopolysaccharide layer. After bacteria die, this layer of fat and sugar enters the bloodstream and can cause inflammation or even septic shock.

    Training bases – situations in which the most resistant and dangerous strains survive. Such a training base for bacterial special forces can be the human body, which disrupts the course of taking antibiotics.

    Chemical weapons – some bacteria have learned to produce substances that decompose drugs, depriving them of their healing properties.For example, enzymes from the beta-lactamase group block the action of antibiotics from the penicillin and cephalosporin groups.

    Masking – microbes that change the outer shell and protein composition so that the drugs “do not notice” them.

    Trojan Horse – Some bacteria use special techniques to defeat the enemy. For example, the causative agent of tuberculosis (Mycobacterium tuberculosis) is able to get inside macrophages – immune cells that catch and digest wandering pathogenic bacteria.

    Super Soldiers – These omnipotent bacteria are not afraid of almost any medicine.

    WHO recommendation

    Ten Commandments of Antibacterial Behavior

    1. Get vaccinated on time.

    2. Only use antimicrobial drugs when prescribed by a licensed healthcare practitioner.

    3. Once again: do not self-medicate with antibiotics!

    4. Remember that antibiotics do not work against viruses.Treating the flu and many types of “colds” with them is not only useless, but also harmful. It seems that this is done at school, but during a study by VTsIOM to the question “Do you agree with the statement that antibiotics kill viruses as well as bacteria?” 46% of the respondents answered yes.

    5. Take the medicine in exactly those doses and for as many days as prescribed by the doctor. Do not stop taking even when you feel healthy. “If you do not complete the treatment, there is a risk that antibiotics will not kill all the bacteria that caused your illness, that these bacteria mutate and become resistant.This does not happen in every case – the problem is that we do not know who can end the treatment prematurely and without consequences, “admit the WHO experts.