Pathogens of bacterial respiratory infections microbiology. Causative agents of bacterial intestinal and respiratory infections. Fundamentals of private bacteriology
Diphtheria is an acute infectious disease characterized by inflammation of the tonsils, general intoxication and toxic damage to the cardiovascular and nervous systems.
Diphtheria is caused by corynobacteria (diphtheria bacillus, Leffler's bacillus). Corynebacterium diphtheriae is a gram-positive rod-shaped bacteria of the genus Corynebacterium, the causative agent of diphtheria.
· First described by German microbiologist Edwin Klebs. Large, straight, slightly curved polymorphic rod-shaped bacteria. Metachromatic volutin grains (Babesch-Ernst grains) are localized at the cell poles, giving the cells a characteristic “club” shape. Volutin grains are stained with methylene blue or Neisser. On micropreparations they are located singly or, due to the peculiarities of cell division, they are arranged in the shape of the Latin letter V or Y. In many strains, microcapsules are isolated. Facultative anaerobe. They grow on complex nutrient media containing whey, for example, coagulated horse whey according to Roux, a mixture of bovine whey with sugar broth according to Leffler. On blood agar with tellurite (Klauber's medium), the colonies become black due to the reduction of tellurite.
The cause of the disease can be both toxigenic and non-toxigenic strains of diphtheria bacillus, but only the first of them cause complications such as myocarditis and neuritis. The pathogen is resistant to high and low temperatures and drying. It dies quickly when boiled and exposed to disinfectants. During the reproduction process, it produces a toxin that plays a major role in the pathogenesis of the disease. C. diphtheriae can cause not only diphtheria of the pharynx, but also skin lesions.
The source of the disease is a sick person or a bacteria carrier.
The patient is contagious from the last day of the incubation period until complete sanitization of the body, which can occur at different times.
Diphtheria is transmitted primarily by airborne droplets, but contact and food transmission are possible.
The incubation period lasts 1 – 6 days. Clinically, diphtheria is divided into several types depending on the location of the virus:
pharynx disease (90% of cases),
· larynx,
· respiratory tract (trachea, bronchi).
More rare localizations: eyes, skin, wounds, genitals. According to the nature of the course, typical (membranous) and atypical (catarrhal, hypertoxic, hemorrhagic) diphtheria are distinguished. Depending on the severity, there are mild, moderate and severe forms.
Possible complications of diphtheria: in young children, due to the lumen of the larynx or trachea being closed by a detached film, sudden death may occur. A complication of the disease is myocarditis, which can develop after both severe and mild forms of diphtheria, but more often with widespread lesions and delayed diagnosis. Neurological complications are expressed by motor disorders and usually disappear after recovery. The most characteristic complication is paralysis of the soft palate, which develops in the 3rd week of the disease. The voice becomes nasal, and when swallowing, liquid food pours out through the nose. Sometimes oculomotor nerve palsy occurs. Tendon reflexes decrease, muscle weakness and coordination loss appear. If the muscles of the neck and torso are affected, the patient cannot walk or hold his head up. Gastritis, nephritis, and hepatitis may develop.
Prevention of diphtheria mainly consists of immunization, as well as isolating patients and suppressing the spread of infection. A patient is considered infectious as long as the pathogen is detected at the site of infection. Isolation is stopped after receiving three negative bacteriological test results.
The medical worker should conduct a conversation with the patient’s relatives about infectious safety. He must tell them that they must allocate separate dishes for the patient and disinfect them; the dishes should not come into contact with the common ones. Also, people in contact with the sick person must wear a hygienic mask, carry out daily wet cleaning of the house with a disinfectant solution, regularly ventilate the room, and maintain personal hygiene.
WHOOPING COUGH
Whooping cough is an acute infectious disease of children with a cyclical course and characteristic attacks of convulsive cough.
The causative agent of whooping cough is Bordetella pertussis - small coccoid gram-negative rods with rounded ends (0.2-0.5 x 0.5-2 µm), bipolar colored. Motionless. There is no dispute. They have a microcapsule and drank. obligate aerobes. They have O-antigen and capsular antigens.
The infection is transmitted by airborne droplets. The pertussis bacillus, found in droplets of sputum and mucus of a patient, enters the air when coughing and then penetrates through the respiratory tract into the body of a healthy person. Infection is only possible through contact with sick people, since Bordetella pertussis quickly dies outside the body. The danger of infection through surrounding objects is practically eliminated.
Children from 1 to 5 years of age are most often affected, sometimes children under 1 year of age. The disease is rare in adults. Whooping cough leaves lasting immunity, recurrent illnesses are very rare.
The incubation period lasts from 2 to 15 days (average 5-9 days).
Clinic. At first there is a slight cough, which gets worse every day. The temperature rises, the child becomes irritable, sleep and appetite worsen, this period is called catarrhal, lasts up to 2 weeks. All manifestations of the disease continue to increase; gradually the child’s well-being worsens, the cough becomes longer and more severe, and at the end of the second - beginning of the third week it becomes paroxysmal in nature: the disease passes into the third period - spasmodic, which lasts 1-5 weeks. Attacks of convulsive coughing are the main and constant symptom of the disease. The cough begins with two or three deep coughing impulses, followed by a series of short impulses, they follow one another and end with a deep whistling breath due to convulsive narrowing of the larynx. Then the coughing starts again. The severity of the disease depends on the duration and frequency of attacks. In young children, coughing attacks are long-lasting (up to 2-3 minutes) and consist of short exhalation impulses without whistling breaths. During an attack, the patient's face turns red, then acquires a bluish tint. Tears appear in the eyes, sometimes hemorrhages form in the white membrane of the eyes, the tongue sticks out of the mouth, the neck veins swell, and involuntary separation of feces and urine is possible. The attack ends with the discharge of viscous sputum and often vomiting. Cough attacks are repeated from 5 to 30 or more times a day. The face becomes puffy, the eyelids swell, and hemorrhages may appear on the skin of the face. In the intervals between coughing attacks, children feel quite satisfactory. Gradually, the cough weakens, attacks become less frequent - a period of recovery begins, which lasts on average 1-3 weeks.
The total duration of the disease is from 5 to 12 weeks. A child is considered contagious within 30 days from the onset of the disease. Mass vaccinations have led to the emergence of so-called erased forms of whooping cough, when the spasmodic period can be very mild or completely absent.
Pathogenesis. Bordetella pertussis reproduces mainly on the mucous membrane of the respiratory tract. Their epithelium undergoes dystrophic changes and desquamates, and signs of catarrhal inflammation are revealed. The decay products of the pathogen (endotoxins) cause irritation of the nerve receptors of the larynx, impulses appear that go to the brain and lead to the formation of a persistent focus of irritation in it. Due to the lowering of the threshold of excitation of nerve centers and receptors, an insignificant nonspecific irritation is enough to cause an attack of spasmodic cough. “Respiratory tract neurosis” develops, which is clinically manifested by successive jerky exhalations, followed by convulsive deep inhalations, repeated many times and ending with the discharge of viscous sputum or vomiting. Whooping cough in infants is especially severe; they do not have spastic coughing attacks; their equivalent is attacks of apnea with loss of consciousness and asphyxia.
Currently, thanks to seroprophylaxis and mass vaccination, the severity and morbidity have decreased significantly, the mortality rate does not exceed tenths of a percent.
Complications: pneumonia (especially in children from 1 to 3 years), nosebleeds, respiratory arrest. In infants and weakened children, whooping cough can be very difficult: the catarrhal period is short, sometimes a spasmodic period immediately sets in, and often coughing attacks lead to respiratory arrest.
Death is now rare, mainly in infants from asphyxia, pneumonia, and in rare cases from spontaneous pneumothorax.
Causative agents of intestinal infections
Bacteria
family of enterobacteriaceae
vibrios
Viruses
Rotaviruses, Enteroviruses
Noroviruses, Astroviruses
Caliciviruses and others
Protozoa
Mushrooms
CAUSES OF BACTERIAL INTESTINAL INFECTIONS
Enterobacteriaceae family
40 genera, more than 100 species
Childbirth is the most important thing for a person.
· Escherichia,
· Salmonella,
· Shigella,
· Yersinia (Yersinia),
· Proteus (Proteus),
· Klebsiella, etc.
Infectious dose UPB-10⁶- 10⁷ microbial cells
Infectious dose of PEB - 10²- 10³ microbial cells
The genus Shigella − Shigella
Enterobacteria family, genus Shigella − Shigella "-" G, motionless sticks highlights endotoxin, some types of shigella produce exotoxins (shigella Grigorieva-Shiga)
There are 4 types of Shigella:
1. Sh. dysenteriae
Pathogen modern shigellosis are Sh. Sonnei - Shigella Sonne
Sustainability
Are preserved in the external environment
up to 30 −45 days or more
They are well preserved on food products. They multiply and accumulate in dairy products (Sh. Sonnei)
The most persistent are Shigella Sonne
They die when boiled under the influence of 1% chlorine soda. solutions, ultraviolet irradiation, antibiotics.
Epidemiology
Source (anthroponosis): Patient and Carrier
Transmission routes: 1) Aquatic (Shigella Flexner) 2) food often Shigella Sonne Main!!! 3) contact-household indirect
Entrance gate - mouth
The tropism of Shigella is the distal part of the large intestine (rectum and sigma)
Shigella never gets into the blood
Shigella is excreted into the external environment in feces
CLINIC
Fever
phenomena of general intoxication
colitis syndrome
Colitis syndrome m
pain in the left iliac region + loose stools (frequent and scanty) + tenesmus - these are nagging pains in the area of the sacrum and rectum, appear during the act of defecation, last 5-10 minutes after and are accompanied by a false urge to go down
Laboratory diagnostics
Feces for culture in the intestinal group
Blood for RNGA with shigella diagnosticums.
Treatment: Antibiotics, Nitrofurans, hydroxyquinolines
Escherichia genus - escherichia
Escherichia coli - E. coli was discovered by T. Escherich in 1885. A normal representative of the colon microflora
Performs a number of useful functions
antagonist of pathogenic intestinal bacteria, putrefactive bacteria, fungi of the genus Candida
takes part in the synthesis of vitamins B, E, K
partially breaks down fiber.
E. coli can cause harm to humans. Opportunistic strains, living in the large intestine, with ID cause purulent-inflammatory diseases outside the gastrointestinal tract cystitis, otitis, meningitis and coli-sepsis. These diseases are called parenteral escherichiosis. Exist definitely pathogenic strains of E. coli- CAUSE DIARRHEA (entering the body from the outside) cause outbreaks of diseases, intestinal escherichiosis.
Causative agents of escherichiosis: 1) intestinal escherichiosis = acute infectious diseases characterized by lesions of the gastrointestinal tract (absolutely pathogenic E. coli) 2) parenteral escherichiosis = acute infectious diseases in ID, characterized by lesions of any organs (opportunistic strains of E. coli)
Etiology Enterobacteriaceae family Escherichia
E. coli“−”Gram Escherichia coli has a complex antigenic structure
Escherichias are divided into 5 categories
enteropathogenic - EPKP
enterotoxigenic - ETC
entroinvasive - EICP
enteroadhesive - EAKP
enterohemorrhagic – EHEC
Transmission mechanism− fecal-oral
Transmission routes: 1) food 2) water 3) contact and household indirect
Clinical picture: fever, vomiting, diarrhea , dehydration, signs of kidney damage. Colienteritis is one of the causes of early childhood mortality.
Laboratory diagnostics
culture of vomit
stool culture for intestinal group
blood for RNGA with Escherichia diagnosticums
culture of blood, cerebrospinal fluid, urine (for generalized forms)
Treatment: antibiotics
Prevention: sanitary and hygienic measures.
Salmonella genus
Enterobacteriaceae family Genus Salmonella It has > 2.5 thousand species (serovar). The most pathogenic for humans are >100 . They are divided into groups A, B, C 1, C 2, D.
genus salmonella: Typhoid fever, Paratyphoid A, Paratyphoid B, Paratyphoid C, salmonellosis
Etiology Salmonella typhi Enterobacteria family, genus Salmonella group D, Gram "−", motile aerobic bacillus, has a complex antigenic structure, secretes endotoxin
Highly resistant: In water - up to 1-5 months , in feces - up to 25 days, on food products - several days
Dies at: 100˚C after 3-4 minutes, drying, UV , 3% solution of chlorine-containing preparations
Transmission mechanism - fecal-oral
tropism - lymphoid apparatus of the ileum of the small intestine (Peyer's patches and solitary follicles)
Salmonella typhi multiply, secrete endotoxin, toxinemia - phenomena of general intoxication and Bacteremia is always
80% settles in the liver, since it accumulates well on bile acids) S. typhi can be fixed in the lungs, in the heart, in the membranes of the brain With bile, S. typhi enters the intestines and is excreted by the body in feces, urine and always in the blood
Clinic: fever 40−41˚C prolonged, CNS damage (typhoid status), CVD damage, skin rash
CNS: typhoid status The patient is lethargic, lies with his eyes closed, is indifferent, answers questions poorly or does not answer, and makes almost no complaints. There may be hallucinations, quiet delirium
Laboratory diagnostics: 1) Blood for culture for blood culture in bile broth (Rappoport's medium), 2) feces for culture for coproculture, 3) urine for culture for urine culture, 4) blood for RNGA with a combined salmonellosis diagnosticum
Treatment: All patients must be hospitalized, Regimen, Diet, antibiotics
Salmonella genus -salmonella
Etiology: Family Enterobacteriaceae Genus Salmonella has > 2.5 thousand species (serovar). The most pathogenic for humans are> 100. They are divided into groups A, B, C 1, C 2, D. Small mobile "-" Gram stick.
Lives In meat and dairy products, eggs actively reproduces, withstands freezing
At boiling is dying instantly, sensitive to 1% chlorine solutions, antibiotics
Mechanism− fecal-oral
Clinic: Fever + symptoms of intoxication, dyspeptic syndrome, abdominal pain, nausea, repeated vomiting, profuse watery stools, flatulence, dehydration
Blood may appear in: SEPTIC FORM and TYFOLIKE FORM
Diagnostics: sowing of vomit and rinsing water; feces for culture; blood for RNGA with a combined salmonella diagnosticum; blood for culture (for generalized forms)
Vibrio cholerae Vibrio cholerae
Cholera (Form 30) This is an acute anthroponotic bacterial especially dangerous infectious disease that is caused by Vibrio cholerae. Characterized by damage to the small intestine
Etiology: "−" Gr. Bacteria - a small, slightly curved, comma-shaped rod, mobile, with a flagellum. Releases exotoxin - cholerogens (determines the clinic)
Stable. In water - up to 1 month, On fresh vegetables and fruits - up to 2 weeks, In the body of crustaceans, mollusks and the like, it accumulates and persists for several months.
Transmission mechanism: fecal-oral
Clinic: Profuse diarrhea (up to 10 liters per day) , Vomiting fountain , Rapidly developing dehydration
Bacterial food poisoning – BPO is a group of diseases that occur when eating food contaminated with microbes and their toxins.
BPO polyetiological
Up to 500 species of opportunistic microbes are known
Staphylococcus
Streptococci
Klebsiella
Enterococci
Serations
Hafnii et al.
The route of spread of BPO is nutritional.
Transmission factors- solid (sausages, jellies, eggs, canned meat, fish, etc.) and liquid (soups, milk, juices, jelly, kvass, lemonade, beer, cocktails, etc.) food products that are a breeding ground for bacteria.
BPO CLINIC: Dyspeptic syndrome: Repeated vomiting associated with food intake, Heaviness in the epigastric region
Exicosis
Dry skin, mucous membranes, tongue
decreased skin turgor
· painful cramps in the calf muscles, abdominal muscles
decreased diuresis
tachycardia, hypotension
Intoxication
Botulism− this food poisoning occurs when eating products containing botulinum toxin, characterized by damage to the nervous system
Etiology of Clostridium botulinum
Rod, has flagella, spore-forming, there are 7 types: A, B, C, D, E, F, G
Types A, B, E are dangerous to humans
Strict anaerobe
The optimal growth temperature is 36 C (A, B, C, D, G) or 28-30 C (E, F).
Produces exotoxin - the most powerful poison. For an adult, the lethal dose of type B toxin is 0.005-0.008 mg. Toxins are thermolabile proteins (destroyed at 80 C after 30 minutes, at 100 C - 10-20 minutes). Spores are thermostable (when boiled, they die after 6-8 hours; when autoclaved at a temperature of 120 C, they die after 20-30 minutes). Spores tolerate high salt concentrations (up to 14%).
Transmission mechanism: fecal-oral
Human infection occurs more often when consuming products home canning (mushrooms, vegetables, fish, meat)
MAIN TRANSMISSION FACTORS
Sausage, ham, other smoked meats, canned meat;
Salted, smoked, dried fish, canned fish and preserves, especially home-made;
Vegetable and fruit juices, canned peas, squash caviar, canned vegetables, compotes, etc.
Mushrooms, pickled, salted, fried, especially in hermetically sealed jars
BOTULOTOXIN - NEUROTOXIN
MEDULLA(CARDIAC AND BREATHING STOP)
CRANIAL NERVES(VISUAL IMPAIRMENT, ETC.)
PARESIS AND PARALYSIS OF MUSCLES pharynx and larynx, heart, intercostal muscles and diaphragm
CLINIC OF BOTULISM
NAUSEA, VOMITING
VISION IMPAIRMENT
difficulty swallowing
hoarseness of swallowing
slurred speech
violation of external respiration
Defeat SSS
CAUSES OF RESPIRATORY TRACT INFECTIONS (RESPIRATORY INFECTIONS)
CAUSE OF DIPHTHERIA
Pathogen resistance
Sensitivity to
– 10% solutions of H 2 O 2
– boiling, dies after 1 minute
– antibiotics
Epidemiology
Source: sick; bacteria carrier (after illness); bacteria carrier* (healthy)
Transmission routes: airborne; airborne dust; food (via milk)
Antitoxic immunity
Entrance gate
mucous membrane of the upper respiratory tract (nose, pharynx, oropharynx, trachea)
skin, genitals
mucous membrane of the eye
Specific prevention
V1 – 3 months DTP 0.5 ml i/m
V2 – 4.5 months. DTP 0.5 ml i/m
V3 – 6 months. DTP 0.5 ml i/m
R1 – 18 months DPT 0.5 ml i/m
R2 – 7 years ADS-M 0.5 ml s/c under the shoulder blade
R3 – 14 years ADS-M 0.5 ml s/c under the shoulder blade
Then every 10 years until age 54 ADS-M
0,5 ml s/c under the shoulder blade.
WHOOPING COUGH
Whooping cough- spicy ANTHROPONOTIC BACTERIAL infectious disease, characterized by paroxysmal spasmodic cough.
Bordetella pertussis
Prevention
The main measure for the prevention of pertussis infection is specific prophylactic (DTP).
Non-immunized children in contact with the patient are injected with normal anti-pertussis human immunoglobulin.
The causative agent of pulmonary tuberculosis is a tubercle bacillus (Koch's bacillus, mycobacterium tuberculosis, mycobacterium tuberculosis, AFB, TB, BC) - an extremely aggressive and resistant microbe.
Distinguish between mycobacterium tuberculosis human, bull And bird types. For humans, they are pathogenic.
In organs affected by tuberculosis (lungs, genitourinary system, lymph nodes, skin,
bones, intestines, etc.)
A specific “cold” tuberculous inflammation develops and leads to the formation of multiple tubercles with a tendency to decay.
Respiratory chlamydia
Chlamydia psittaci. This type of chlamydia is found in birds, which can transmit the infection to humans.
This type of chlamydia can provoke diseases such as atypical pneumonia, arthritis, encephalomyocarditis and pyelonephritis.
Chlamydia is transmitted by airborne droplets or airborne dust.
Chlamydia pneumoniae is a type of chlamydia that is transmitted from person to person, which can occur through airborne droplets.
· Chlamydophila felis, affects animals, from which infection can occur to humans. This type of chlamydia is characterized by frequent manifestations of conjunctivitis, both in humans and animals.
Super unstable
· Destroys at temperatures below +25⁰С
Therefore, sampling and sowing of material immediately near the patient’s bedside
Meningococcus tropen nasopharynx
· Inoculation is carried out on serum agar
Sources of infection: patient and carrier
Path: Airborne
Clinical forms:
Localized
· carrier status
nasopharyngitis
Generalized
meningococcemia
meningitis
meningoencephalitis
· mixed forms
Rare
endocarditis
· pneumonia
iridocyclitis
Laboratory diagnostics
Microbiological method (nasopharyngeal swab, cerebrospinal fluid, blood)
Serological method
· Express diagnostics RIF
· Microscopy of cerebrospinal fluid
Treatment: Antibiotics
Meningococcal meningitis
Meningococcal infection. Generalized form. Meningococcemia. ITS II – III
Hemorrhagic rash 2nd day from the onset of the disease
Prevention
Identification of patients and carriers, their sanitation
Sanitation of chronic lesions in the nasopharynx and pharynx
Healthy lifestyle
Compliance with sanitary and epidemiological regulations
Specific prevention
MENINGO A+C vaccine from 18 months of age required just one dose of vaccine. The duration of immunity is 3-5 years. Immunity is developed within 5 days, reaching a maximum by the 10th day.
Meningococcal group A vaccine, dry polysaccharide Vaccination scheme: once. The vaccination dose for children from 1 year to 8 years is 0.25 ml; aged 9 years and older – 0.5 ml. Revaccination after three years
STREPTOCOCCI
Etiology
gram-positive cocci of the genus Streptococcus of the family Streptococcaceae.
according to antigenic properties they are divided into 20 groups: A, B, C, D, etc.
Group A streptococci, i.e. Str. pyogenes dominate in human pathology form chains of different lengths (Greek Streptos - twisted in the form of a chain).
Streptococci are resistant in the external environment.
They can withstand drying and last for months.
under the influence of disinfectants they die within 15 minutes.
They die when boiled.
Epidemiology
Reservoir and source of infection –
patients with various clinical forms of acute streptococcal diseases
carriers of pathogenic streptococci
Mechanism of transmission of infection - aerosol, Transmission routes –
airborne
nutritional
contact-household
Transmission factors
care items
contaminated food
HUMAN DISEASES: Suppurative diseases of the skin, subcutaneous tissue (abscesses, phlegmon, etc.); Otitis; Sinusitis; Pneumonia; Tonsillitis; Scarlet fever; Rheumatism; Erysipelas
Suppuration of wounds as a result of infection in the wound with an instrument, dressing, or infection from the carrier.
Symptoms of sepsis
prolonged fever with chills and sweat
recurrent fever
pronounced symptoms of intoxication
hemorrhagic rash on the skin
abscesses in various organs and tissues
Causative agents of bacterial intestinal and respiratory infections
ADD THE PHRASE
1. The drug for the Mantoux reaction - ______.
2. Main biovars of C. diphtheriae: ________ and _______.
3. Planned specific prevention of diphtheria is carried out with diphtheria ______.
4. The causative agent of diphtheria - _________ ___________
5. Drug for planned specific prophylaxis of tuberculosis: _____________.
6. The causative agent of whooping cough - ______ __________.
7. In the treatment of toxic forms of diphtheria, in addition to antibiotics, _________ ________ must be used.
8. The Mantoux test, performed for the diagnosis of ________, determines the ____ type of hypersensitivity.
9. Bordet-Gengou medium is used to isolate the pathogen __________.
10. To create artificial active immunity against diphtheria, drugs containing __________ __________ are used.
11. For routine specific prevention of whooping cough, the vaccine used is _________.
12. Micropreparations for bacterioscopic examination of tuberculosis are stained using the _______ method.
13. The causative agent of leprosy is _____________.
CHOOSE ONE OR MORE CORRECT ANSWERS
14. The causative agent of diphtheria:
1. Gram-positive rod
2. Polymorphic
3. Movable
4. Contains volutin grains
15. Morphological structures of the causative agent of diphtheria:
2. Fimbriae
3. Flagella
4. Volutin grains
16. Typical location of diphtheria bacilli in pure culture:
1. In bunches
2. In the form of chains
3. In the form of a “picket fence”
4. At an angle to each other
17. Basic differential biochemical properties of the causative agent of diphtheria:
1. Does not break down urea
2. Breaks down lactose
3. Breaks down cysteine
4. Breaks down sucrose
18. Biovar gravis differs from biovar mitis in the following properties:
1. Morphological
2. Cultural
3. Antigenic
4. Biochemical
19. C. diphtheriae is distinguished from opportunistic corynebacteria by the following properties:
1. Morphological
2. Cultural
3. Biochemical
4. Toxigenic
20.. C. diphtheriae is distinguished from opportunistic corynebacteria by:
1. Polymorphism
2. The presence of bipolar grains of volutin
3. Arrangement of cells in the form of V, X
4. Biochemical properties
21. The significance of opportunistic corynebacteria:
1. They can cause osteomyelitis
2. Overdiagnosis of diphtheria may be associated with them
3. They Can Cause Meningitis
4. They can cause diphtheria (if the tox gene is present)
22. Nutrient media for cultivating the causative agent of diphtheria:
2. Blood tellurite agar
3. Yolk salt agar
4. Curdled whey
23. Factors of pathogenicity of diphtheria bacillus:
1. Exotoxin
2. Cord factor
3. Adhesins
4. Neuraminidase
24. The main pathogenicity factor of C.diphtheriae:
1. Cord factor
2. Endotoxin
3. Exotoxin
4. Neuraminidase
25. Diphtheria toxin has a pathological effect on:
1. Heart muscle
3. Adrenal glands
4. Nerve ganglia
26. Mechanism of action of diphtheria exotoxin:
1. Impaired respiration of body cells
2. Inactivation of transferase II enzyme
3. Impaired transmission of impulses through neuromuscular synapses
4. Suppression of protein synthesis in the cells of the macroorganism
27. Localization of genes regulating the synthesis of diphtheria exotoxin:
1. In the bacterial chromosome
2. In a plasmid
3. Associated with transposons
4. In Prophage
28. Entrance gate for the causative agent of diphtheria:
1. Mucosa of the upper respiratory tract
2. Genitals
3. Eyes, ears
4. Wound surface
29. Sources of infection for diphtheria:
1. Sick people
2. Pets
3. Bacteria carriers
30. Routes of transmission of diphtheria:
1. Airborne
2. Contact
3. Nutritional
4. Transmission
31. Immunity for diphtheria:
1. Antibacterial
2. Antitoxic
3. Non-sterile
4. Humoral
32. Methods for microbiological diagnosis of diphtheria:
1. Microscopic
2. Biological
3. Bacteriological
4. Allergic
33. Material for microbiological examination for suspected diphtheria:
1. Mucus from the throat
2. Film from the throat
3. Nasal mucus
34. Serological reactions to determine antitoxic immunity in diphtheria:
3. Agglutination reaction
35. Drugs for planned specific prevention of diphtheria:
1. Tetraanatoxin
3. Antitoxic anti-diphtheria serum
36. Planned specific prevention of diphtheria is postponed until the child is 3-4 months old due to:
1. Receipt of secretory Ig A with mother’s milk
2. Lack of formed normal microflora
3. Production of high titers of own antibodies
4. The presence of Ig G received from the mother through the placenta
37. Drugs for specific emergency prevention of diphtheria:
2. Killed vaccine
3. Bacteriophage
4. Anatoxin
38. The phenomenon due to which diphtheria toxoid is effective for emergency prevention of diphtheria:
3. Immunological tolerance
4. Immunological memory
39. Pathogens of tuberculosis:
1. M. tuberculosis
40. Pathogens of mycobacteriosis:
1. M. tuberculosis
42. Diseases caused by mycobacteria:
1. Actinomycosis
2. Tuberculosis
3. Deep mycoses
43. Morphological transformations of tuberculosis pathogens, contributing to the chronicization of the inflammatory process, the persistence of the microbe, and the diversity of the clinical picture of the disease:
1. Non-acid-resistant forms
3. Filterable forms
4. Bacillary forms
44. The main sources of tuberculosis:
1. Patients with open form of tuberculosis
2. Patients with closed form of tuberculosis
3. Sick farm animals with destructive processes
4. Guinea pigs
45. Basic methods of microbiological diagnosis of tuberculosis:
1. Microscopic
2. Bacteriological
3. Allergic
46. Material for research in pulmonary forms of tuberculosis:
1. Sputum
2. Pleural fluid
3. Bronchial lavage water
4. Ascitic fluid
47. Microscopic examination methods for tuberculosis allow:
1. Detect acid-fast bacteria
2. Identify microbes to species
3. Tentatively suggest a diagnosis
4. Determine the type of microbe
48. Method of accelerated bacteriological diagnosis of tuberculosis:
1. Homogenization
2. Microcultivation
3. Precipitation
4. Price method
49. Methods of “enrichment” of the test material for microscopic diagnosis of tuberculosis:
1. Homogenization and precipitation
2. Price method
3. Flotation method
50. Laboratory animals used in the microbiological diagnosis of tuberculosis:
1. White mice
2. Rabbits
4. Guinea pigs
51. The Mantoux test allows:
1. Identify those infected
2. Assess the strength of anti-tuberculosis immunity
3. Select persons for revaccination
4. Detect class M immunoglobulins
52. Mantoux reaction:
1. Belongs to type IV according to Jell and Coombs
2. Belongs to type III according to Jell and Coombs
3. Indicates that a person is infected
4. Reliably indicates the presence of the disease
53. Drugs for specific prevention of tuberculosis:
54. Vaccine for specific prevention of tuberculosis:
3. Anatoxin
55. Epidemiological features of leprosy:
1. The source is a sick person
2. Contact transmission path
3. Airborne transmission
4. Source - rodents
56. Biological models for cultivating the causative agent of leprosy:
1. Guinea pigs
2. Rabbits
3. Golden hamsters
4. Armadillos
57. Characteristic location of the causative agent of leprosy in the affected tissues:
1. In intercellular spaces
2. Intracellular
3. In the form of long chains
4. Forms clusters of cells in the form of balls
58. You can distinguish the causative agent of tuberculosis from the causative agent of leprosy during microbiological diagnostics by:
1. Acid resistance
2. Growth on artificial nutrient media
3. PCR results
4. Bioassay results
59. Antigen for staging the Mitsuda reaction:
1. Autoclaved suspension of the causative agent of leprosy, obtained by homogenizing the contents of leprosy
2. Lepromin-A
3. Integral lepromin
4. Dry purified tuberculin
60. To prevent leprosy, use:
1. Dry purified tuberculin
2. Integral lepromin
61. Properties of the causative agent of whooping cough:
1. Gram-negative rod
2. Forms exotoxin
3. Biochemically inactive
4. Produces spores
62. Properties of the causative agent of whooping cough:
1. Demanding on nutrient media
2. Biochemically little active
3. Highly sensitive to environmental factors
4. Grows on simple media
63. Nutrient media for the cultivation of the pertussis pathogen:
2. Casein charcoal agar
3. Clauberg environment
4. Bordet-Gengou medium
64. Factors of pathogenicity of the causative agent of whooping cough:
1. Filamentous hemagglutinin
2. Pertussis toxin
3. Extracellular adenylate cyclase
4. Endotoxin
65. Methods for microbiological diagnosis of whooping cough:
1. Bacterioscopic
2. Bacteriological
3. Allergic
4. Serological
66. The causative agent of legionellosis:
1. L. pneumophila
67. Properties of Legionella:
1. They form spores
2. Free-living bacteria
3. Have endotoxin
4. Gram-negative rods
68. Main forms of legionellosis:
1. Philadelphia fever
2. Fort Bragg Fever
3. Pontiac Fever
4. Legionnaires' disease
69. Material for microbiological diagnosis of legionellosis:
1. Pleural fluid
2. Phlegm
3. Pieces of lungs
4. Blood serum
70. Serological tests for the diagnosis of legionellosis:
1. Hemagglutination reaction
3. Precipitation reaction
71. Methods for microbiological diagnosis of legionellosis:
2. Serological
3. Allergic
4. Bacteriological
MAKE LOGICAL PAIRS: QUESTION-ANSWER
72. Biovar gravis
73. Biovar mitis
A. Forms large, smooth, red colonies
B. Forms small black colonies
B. Forms large, rough, gray colonies
74. Breaks down urea
75. Does not have cystinase
76. Does not have urease
77. Produces cystinase
A. The causative agent of diphtheria
B. Opportunistic corynebacteria
G. Neither one nor the other
79. Produce urease
A. Toxigenic strains of diphtheria bacillus
B. Non-toxigenic strains of diphtheria bacillus
G. Neither one nor the other
80. Release the pathogen into the environment
81. Can be detected during an allergy test
82. Can be detected by bacteriological examination
83. Can be a source of infection for diphtheria
A. Patients with diphtheria
B. Bacterial carriers of the causative agent of diphtheria
G. Neither one nor the other
Describe the course of bacteriological examination for diphtheria
A. Subculture of suspicious colonies with coagulated serum
B. Inoculation of the test material on Clauberg’s medium
B. Identification of the isolated pure culture
B. Mycobacteriosis
B. Tuberculosis
91. M.1ergae
93. M. tuberculosis
A. Located intracellularly, forming clusters in the form of balls
B. Gram-negative cocci
B. Long thin sticks
G. Short thick sticks
95. L.pneumophila
96. B.parapertussis
A. Parawhooping cough
B. Whooping cough
V. Paratyphoid
G. Legionellosis
100. M. tuberculosis
A. Guinea pigs
B. Rabbits
B. Nine-banded armadillos
D. Rapid growth on nutrient media
ESTABLISH IF STATEMENT I IS TRUE, IF STATEMENT II IS TRUE AND IS THERE A CONNECTION BETWEEN THEM?
101. Myocarditis is often a complication of diphtheria, because
Diphtheria exotoxin disrupts protein synthesis in myocardial cells.
102. C.pseudodiphtheriticum causes diphtheria because
The pseudodiphtheria bacillus lives in the pharynx.
103. For specific emergency prevention of diphtheria, diphtheria toxoid can be used because
· People vaccinated against diphtheria have an immunological memory.
104. Anti-diphtheria serum is administered according to Bezredka, because
After administration of anti-diphtheria serum, serum sickness may develop.
105. M.tuberculosis causes tuberculosis only in humans, because
·M. tuberculosis is not capable of infecting laboratory and farm animals.
106. The main route of transmission of M. bovis is alimentary, because
·M.bovis from sick animals is more often transmitted through milk.
107. The most reliable method of microbiological diagnosis of tuberculosis is microscopic, because
· tuberculosis pathogens grow slowly on nutrient media.
108. The microscopic method for diagnosing tuberculosis is indicative because
The microscopic method for diagnosing tuberculosis does not allow determining the type of pathogen.
109. The detection of tuberculosis pathogens in pathological material reliably indicates the activity of the infectious process, because
detection of antibodies in the blood serum allows only an indirect assessment of the nature of the activity of tuberculosis.
110. The microscopic method is a mandatory method for diagnosing tuberculosis, because
Ziehl-Nelsen staining makes it possible to distinguish acid-resistant causative agents of tuberculosis from opportunistic mycobacteria.
111. When diagnosing mycobacteriosis, pathogens are identified to the species and sensitivity to antibiotics is determined, because
Conditionally pathogenic mycobacteria are similar in some biological properties to the causative agents of tuberculosis, but are resistant to anti-tuberculosis drugs.
112. Pasteurization of milk is aimed at preventing tuberculosis because
· tuberculosis pathogens are transmitted through milk and dairy products.
113. Bacteriological research is important in differentiating the causative agents of tuberculosis and leprosy, because
The causative agent of leprosy does not grow on artificial nutrient media.
114. The tuberculoid form of leprosy belongs to prognostically favorable forms, because
The Mitsuda reaction for tuberculoid leprosy is negative.
115. The causative agent of whooping cough and other representatives of this genus differ in biochemical properties, because
The causative agent of whooping cough has a pronounced saccharolytic and proteolytic activity.
116. Filamentous hemagglutinin is one of the main factors of whooping cough pathogenicity, because
· due to hemagglutinin, B.pertussis adheres to the epithelium of the respiratory tract.
117. Pertussis endotoxin is the main factor in the pathogenicity of the whooping cough pathogen, because
thanks to pertussis endotoxin, the pathogen attaches to the epithelium of the respiratory tract.
118. Extracellular adenylate cyclase is one of the main pathogenicity factors of the pertussis pathogen, because
· B. pertussis adenylate cyclase suppresses the phagocytic activity of macrophages.
119. Whooping cough has a long course because
· in the patient’s body the virulence of the whooping cough pathogen increases.
120. The pathogenesis of whooping cough includes adhesion of the pathogen to the surface epithelium of the trachea, bronchi and the action of toxic substances, because
· in the patient’s body, the microbe can move from phase I (virulent) to phase IV (non-virulent).
121. Blue-green algae are important in the spread of Legionella because
· mucous secretions of algae retain the pathogen in aerosols and provide a high infectious dose.
122. In the spread of the causative agent of legionellosis, the leading role belongs to the water factor, because
Legionella's natural habitat is warm water bodies, where they are in symbiotic association with blue-green algae and amoebae.
123. To diagnose legionellosis, a bacterioscopic method for examining sputum and blood is used, because
Legionella is not cultivated on nutrient media.
124. Legionellosis is classified as a sapronotic infection because
Legionellosis is easily transmitted from person to person.
125. When diagnosing legionellosis, the microscopic method is not used because
· sputum and pleural fluid contain few microbes
126. Tuberculin is used to treat tuberculosis because
· Tuberculin is an anti-tuberculosis chemotherapy drug.
Pathogentuberculosis
The causative agents of tuberculosis are mycobacteria (Mycobacterium tuberculosis, Mucobacteriuin bovis) - Gr+ thin curved rods without spores, capsules and flagella; due to the characteristics of the chemical composition (increased lipid content), the tuberculosis bacillus is stained as spores (according to Ziehl-Neelsen, it is stained burgundy , background - blue). The pathogen does not grow on simple media; it is grown, for example, on an egg medium with starch, glycerin and malachite greens to suppress the growth of accompanying microflora (Levenshtein-Jensen medium).
Two types of mycobacteria are pathogenic for humans:
M. tuberculosis are thin, slightly curved rods that grow better on media containing glycerol; Guinea pigs are more sensitive to them; source of infection- Human, infection- by airborne droplets or airborne dust; pulmonary tuberculosis develops more often;
M-bovis - thick short sticks; rabbits are more sensitive to them; source of infection- farm animals; infection- more often in the alimentary (food) way; observed tuberculosis of the mesenteric lymph nodes.
The virulence of mycobacteria is associated with endotoxin and cord factor (cell wall glycolipids); allergenic properties are associated with cellular proteins. The incubation period is from several weeks to several years.
Disease occurs in various forms and can be generalized with damage to the organs of the genitourinary system, bones, meninges, eyes, and skin. Features of immunity in tuberculosis:
marked natural predisposition l people to tuberculosis, due to the genotype;
immunity non-sterile(to superinfection) - while there are tuberculosis bacilli in the body, newly entering mycobacterium tuberculosis is inactivated (die or encapsulated);
antibodies do not play a protective role, and their high titer only indicates the severity of the process (protection is mainly due to immune T-lymphocytes);
immunity is accompanied by the development allergies;
Nonsterile immunity after the body is freed from the pathogen becomes sterile.
Microbiological diagnostics carried out by microscopy of stained smears from the material, by the microbiological method, by infection with material from a sick guinea pig (biological method); Allergy diagnostics are also carried out (Mantoux test with tuberculin).
Specific treatment: in accordance with the sensitivity of the isolated strain is prescribed antibiotics(streptomycin, kanamycin, rifampicin, etc.), drugsPACK(para-aminosalicylic acid), GINK preparations(isonicotinic acid hydrazides - ftivazide, etc.)
Specific prevention: at 5-7 days of age it is administered intradermally live vaccine BJ (BCG - attenuated strain of M. bovis, obtained by Calmette and Guerin); revaccination is carried out for persons under 30 years of age with a negative Mantoux test. This test is done
annually by intradermal injection tuberculin(specific extractable protein allergen of Mycobacterium tuberculosis). In adults, the Mantoux test is usually positive; in the absence of clinical manifestations, this indicates infection of the body with tubercle bacilli and, therefore, the presence of immunity to tuberculosis. In children, the test is either negative or positive with a swelling diameter at the injection site of 5-10 mm (vaccination allergy). If the diameter is more than 10 mm or the intensity of the reaction increases by 6 mm or more per year, the child needs an additional examination in order to exclude or confirm tuberculosis.
Pathogendiphtheria
Corynebacterium diphtheria (Corynebacterium diphtheriae) - Gr + thin, slightly curved rods, located at an angle to each other in preparations. There are no spores or capsules (they form a microcapsule in the body), they are immobile. Volutin grains are located in the thickenings at the ends of the sticks, which are revealed using special staining methods. They do not grow on simple media, they are grown on clotted horse serum, blood-tellurite and other media. Diphtheria is more often caused by C. diphtheriae biovar gravis, less often - other biovars (mitis or intennedius). Biovars are distinguished by cultural and biochemical properties. As part of the normal microflora of the human body, there are non-pathogenic corynebacteria (false diphtheria bacilli, diphtheroids), which are distinguished by morphological and physiological characteristics.
Diphtheria bacilli are relatively stable in the external environment; can be stored on toys for up to 2 months; they are stored for a long time in diphtheritic films. Sensitive to drying, heating, sunlight and conventional disinfectants. Based on their ability to produce exotoxin, diphtheria bacilli are divided into toxigenic and nontoxigenic. Non-toxigenic ones can acquire the ability to produce exotoxin under the influence of a moderate bacteriophage that carries toxigenic genes (tox genes). C. diphtheriac exotoxin has general And local action. Locally, it causes necrosis (death) of tissues and increased vascular permeability: a dense gray film is formed, “fused” to the underlying tissues. In addition, the exotoxin is absorbed into the blood and circulating in the body, affecting its tissues, especially the myocardium, adrenal glands, and nervous system (general effect).
Source of infection- a sick person or microbial carrier.
Infection More often it occurs by airborne droplets, less often by household contact (through toys, dishes) or alimentary route.
Disease characterized by severe intoxication and local symptoms. There are diphtheria of the pharynx, nose, larynx, and wounds. eyes, other locations. Immunity is mainly antitoxic and unstable.
diphtheria and diphtheria microbial carriage is carried out by examining material from the source of inflammation (microscopy of stained smears, isolation of a pure culture with identification and mandatory determination of its toxicity).
Specific treatment. At the first suspicion of diphtheria, an antitoxic antidiphtheria drug is administered. whey(heterologous). For antimicrobial therapy, antibiotics are prescribed; They are also used for the sanitation of microbial carriers.
Specific prevention held diphtheria toxoid(from the 1st year of life). It is part of the associated DPT vaccines. ADS (the drug ADS-M with a reduced dose of antigen is administered to weakened individuals and children with allergic status).
Pathogenwhooping cough
Whooping cough is caused by Bordetella pertussis - Gr is a polymorphic rod without spores and flagella. Forms a capsule in the body. Does not grow on simple media; it is grown on a potato-glycerin medium with blood, on casein-charcoal agar. It forms small, smooth, shiny (like droplets of mercury) colonies, which are studied with side lighting (they cast a cone-shaped beam of light onto the medium). Biochemically inactive. Identification is carried out based on a complex of morpho-physiological characteristics and antigenic structure. The causative agent of whooping cough has endotoxin and produces substances such as exotoxins. Unstable in the external environment. Sensitive to heat, sunlight, and common disinfectants.
Source of infection- a microbe carrier or a sick person who is contagious in the last days of the incubation and catarrhal periods of the infection. Infection- by airborne droplets. Children get sick more often. Disease accompanied by allergization and proceeds in several periods: 1) catarrhal(characterized by symptoms of acute respiratory infections); 2) spasmodic(convulsive), when Bordetella toxins irritate the endings of the vagus nerve and a focus of excitation is created in the brain: attacks of indomitable coughing are noted, which often ends in vomiting; 3) period recovery. Immunity is cellular and humoral, persistent.
Microbiological diagnostics in the early period of the disease it is carried out by isolating a pure culture of B. pertussis from sputum, in a later period - by serodiagnosis in the RSC, etc.).
Specific treatment: antibiotics, human immunoglobulin.
Specific prevention: killed vaccine (part of the DTP vaccine).
Pathogenmeningococcalinfections
Meningococci, or Neisseria meningitidis (Neisseria meningitidis) - Gr-cocci that look like coffee beans and are located in pairs with concavities towards each other. There are no spores or flagella; form a capsule in the body. They do not grow on simple media; They are grown on serum media, where they form medium-sized, round, transparent colonies. Biochemically inactive. They have a complex antigenic structure. Meningococci serogroup A usually cause epidemic outbreaks and the most severe diseases. The pathogen is very sensitive to cooling and dies quickly at room temperature; therefore, the material being tested (cerebrospinal fluid, swabs from the back of the throat, blood) is sent to the laboratory warm, for example, after covering it with heating pads. Disinfectants destroy instantly.
Pathogenicity factors meningococci - fimbriae(provide adhesion of the microbe to the epithelium of the nasopharynx), capsule(invasive and antiphagocytic properties), enzymes hyaluronidase and neuraminidase (distribution in tissues). Bacteremia that occurs during infection is accompanied by the breakdown of microbial cells and the release of endotoxin, a large amount of which can cause endotoxic shock(with damage to blood vessels, coagulation of blood in them and the development of acidosis).
Source of infection:- a carrier or a sick person. Infection- by airborne droplets (in close contact). The incubation period is 5-7 days. The following types are distinguished: rmy meningococcal infection: epidemic cerebrospinal meningitis(inflammation of the soft meninges), epidemic nasopharyngitis(proceeds like an acute respiratory infection), meningococcal sepsis (meningococemia). Generalization of infection occurs, as a rule, in persons with immunodeficiency. Allergic reactions are involved in the pathogenesis of severe forms of infection. Immunity is persistent, type-specific, cellular and humoral; recurrent illnesses are possible.
Microbiological diagnosis is carried out using the microbiological method; in case of meningitis, microscopy of stained preparations from cerebrospinal fluid sediment is also carried out.
Specific treatment: antibiotics (in large doses); human immunoglobulin.
Specific prevention: chemical vaccine(from polysaccharide antigens of the causative agent of meningococcal infection A and C)
Lecture 11. Particular bacteriology. Features of immunity in bacterial infections.
1. Fundamentals of private bacteriology. The concept of PTI.
2. General characteristics of microorganisms:
I. General characteristics of pathogens of bacterial intestinal infections. Family of intestinal bacteria.
1) Genus Escherichia - Escherichia.
2) Genus Shigella - Shigella.
3) Genus Salmonella – salmonella.
4) Pathogens of typhoid fever, paratyphoid fever A and B.
5) Pathogens of particularly dangerous infections. Genus Vibrio – vibrio.
6) Spore-forming anaerobic bacteria. The causative agent of botulism.
II. Causative agents of bacterial respiratory infections:
1) Diphtheria.
2) Scarlet fever.
3) Whooping cough.
4) Tuberculosis.
III. Causative agents of bacterial blood infections: plague, tularemia, borreliosis.
IV. Causative agents of bacterial infections of the external integument: anthrax, tetanus, gas gangrene, syphilis, gonorrhea.
V. Infectious diseases caused by opportunistic bacteria (cocci, pseudomonads, non-spore-forming anaerobes).
D.z. according to account Prozorkina pp. 143-152,158-165, 189-193; 148-153, 99-101; 162-167, 195-203, 207-210, 215-218; 2007 – pp. 145-154, 164-218.
Cherkess s. 235-305, 315-332, 337-411, 415-418.
1. Taxonomy.
2. Morphology.
3. Cultivation.
4. Enzymatic properties.
5. Toxin formation.
6. Antigenic structure.
7. Resistance.
8. Epidemiology.
9. Pathogenesis.
10. Clinical picture.
11. Identification methods.
12. Treatment and prevention.
Fundamentals of private bacteriology.
Medical microbiology - studies the microorganisms that cause diseases in humans, and the processes that occur in the body when pathogens are introduced.
Foodborne illnesses (FTI)- an extensive group of acute intestinal infections that develop after eating foods infected with pathogens and their toxins.
Clinically, these diseases are characterized by a sudden onset, a combination of intoxication syndromes, gastroenteritis, and the frequent development of dehydration.
General characteristics of microorganisms.
General characteristics of pathogens of bacterial intestinal infections.
I. Family Enterobacteriaceae.
All intestinal bacteria are “-” rods, facultative anaerobes. They grow well on simple nutrient media. They differ in enzymatic activity.
Genus Escherichia - Escherichia.
Escherichiosis– diseases caused by Escherichia coli. There are:
1) enteral (intestinal, epidemic) escherichiosis - acute infectious diseases characterized by a predominant lesion of the alimentary tract;
2) parenteral proceed with damage to any organs (caused by opportunistic strains of Escherichia coli).
Escherichia genus.
1) Taxonomy.
Escherichia coli was discovered by T. Escherich (1885). Significance: it is a normal representative of the microflora of the large intestine (its absence is dysbacteriosis), has an antagonistic effect against pathogenic and putrefactive bacteria and fungi of the genus Candida.
“+”: takes part in the synthesis of vitamins B, E, K, partially breaks down fiber, is a universal genetic model in biotechnology, is used as a sanitary indicator microorganism to detect fecal contamination of environmental objects (coli index).
“-”: when the body’s immune system is weakened, it causes purulent inflammation - purulent-inflammatory diseases outside the gastrointestinal tract (otitis, cystitis).
2) Morphology.
These are small gram “-” rods with rounded ends, they do not form spores, they are peritrichous, sometimes they eat pili.
3) Cultivation. A facultative anaerobe, E. coli is not demanding on the nutrient medium.
4) Enzymatic properties.
High saccharolyticity. Proteolytic properties: form indole.
Biochemical properties: ferment glucose with the formation of acid and gas; ferment lactate.
5) Toxin formation.
They have endotoxin (thermolabile and thermostable effects). Pyrogenic, enterotropic, neutrotropic actions. Produce exotoxins.
6) Antigenic structure.
Has O-Ag (somatic), H-Ag (flagellar), K-Ag (surface) antigens A, B, L, M. The structure of the O-antigen determines belonging to the serogroup.
7) Resistance. More resistant to environmental influences (in soil for 2-3 months, in disinfectant solutions for 15-20 minutes). Sensitive to dyes.
8) Epidemiology.
The sources of enteric escherichiosis are human and living, the transmission mechanism is fecal-oral, the route is food, contact and household.
9) Pathogenesis.
The development of escherichiosis depends on the route of introduction of the pathogen into the body and on the serogroup. The entrance gate is the oral cavity. The main pathogenicity factors of Escherichia coli facilitate adhesion and tropism to the epithelium and promote colonization of the lower parts of the small intestine. When the bacterium dies, heat-labile endotoxin is released, which enhances intestinal motility, causes diarrhea, and signs of general intoxication. In addition, an exotoxin is released, causing more severe diarrhea, vomiting, and impaired water-salt metabolism.
10) Clinical picture.
1. Enteral intestinal infections:
group I: causative agent of coenteritis in young children.
group II: causative agent of dysentery-like conditions in children and adults
group III: causative agent of cholera-like diseases.
2. Urinary tract infections: asymptomatic bacteriuria, cystitis, pyelonephritis are clinically manifested by frequent urge to urinate (dysuria), fever.
3. Bacteremia (20-35%) in children and adults. Risk factors during childbirth.
4. Meningitis (in newborns). Develops as a complication of bacteremia.
Pathogenic E. coli are divided into four main classes.
A. ETEC – enterotoxigenic Escherichia coli.
They have tropism for the epithelium of the small intestine. They produce exoenterotoxin. Clinically, the disease occurs as a mild form of cholera.
B. EIEC – enteroinvasive Escherichia coli.
They have tropism for epithelial cells of the large intestine. In place of dead cells, ulcers and erosion are formed, surrounded by inflammation.
C. EPEC – enteropathogenic Escherichia coli. Causes enterocolitis in children under one year of age. The epithelium of the small intestine is affected.
D. EHEC – enterohemorrhagic Escherichia coli. They have tropism for epithelial cells of the large intestine. Cause hemocolitis.
11) Identification methods. Microbiological diagnostics - using the bacteriological method, an antibiogram must be determined.
12) Treatment and prevention.
Treatment: antibiotics: (ampicillin, tetracycline), coliproteus bacteriophage.
Prevention: compliance with the rules of personal hygiene and sanitary regime.
The genus Shigella is a shigella.
Taxonomy. The first pathogen was discovered by Grigoriev and described by Shiga.
1) According to the international classification, united in honor of Shiga:
group A: Grigorieva-Shiga (Sh. dysenteriae)
group B: Flexera (Sh. flexneri)
group C: Boyd (Sh. boydii)
group D: Sonne (Sh. sonnei)
2) Morphology.
Small rods with rounded ends, do not have spores or capsules, lack flagella, are immobile, gram “-”.
3) Cultivation.
Facultative anaerobes, unpretentious to nutrient media.
4) Enzymatic properties.
Shigella has less enzymatic activity. The attitude towards mannitol is important for differentiation: groups B, C, D splitting and non-splitting mannitol (mannitone-negative).
5) Toxin formation.
They have endotoxin, Shigella Grigoriev - Shigi also secrete exotoxin. Pathogenicity factors:
a) outer membrane proteins;
b) contact hemolysin (promotes lysis of cell vacuole membranes);
c) exotoxin (has enterotropic, cyto- and neurotoxic effects);
d) endotoxin (has a general toxic effect on the body).
6) Antigenic structure: O-Ag.
7) Resistance. Low resistance to various factors, except for Shigella Sonne.
8) Epidemiology. Dysentery is an anthroponotic infection: sources - sick people and carriers, transmission mechanism - fecal-oral, transmission routes: food with Sonne's dysentery, water with dysentery Flexner, contact-household with dysentery Grigoriev-Shiga.
9) Pathogenesis.
They enter the gastrointestinal tract through the mouth and reach the colon. Thanks to the invasive factor, they penetrate into cells, where they multiply and form ulcers. When they die, they release endotoxin. As a result of the action of the exotoxin, water-salt metabolism is disrupted and the kidneys and central nervous system are affected.
10) Clinical manifestations.
The incubation period is 1-7 days, it can begin asymptomatically or very severely: t = + 38-39 ° C, in the loose stool there is an admixture of blood, mucus (a type of grated potato), and later pus. Immunity is short-lived.
11) Diagnostic methods.
The basis of microbiological diagnostics is the bacteriological method.
12) Treatment. Complex: fluoroquinolones, sulfonamides with broad-spectrum antibiotics with mandatory consideration of the antibiogram.
Specific prevention: IRS19 vaccine. Prevention: general sanitary and anti-epidemic measures (isolation of patients, early diagnosis, disinfection).
Specialist. emergency prevention: polyvalent dysentery bacteriophage in foci.
The causative agent of salmonellosis.
8. Epidemiology.
The source of infection is animals and birds, usually domestic animals, less often sick people. Mechanism: fecal-oral, route - food: meat, eggs, milk.
9. Pathogenesis. Once in the small intestine, endotoxin is released and causes diarrhea.
10. Clinic. The incubation period is up to 3 days. Characteristic symptoms: nausea, vomiting, diarrhea for more than 7 days. Im-tet is short-lived.
Bacteriological and serological method.
12. Treatment. Detoxification of the body: gastric lavage, administration of large amounts of fluid, diet, a/b are not prescribed.
Prevention: compliance with the sanitary regime and personal hygiene in public catering establishments, constant strict veterinary and sanitary control (over livestock, slaughter and cutting of carcasses, storage and processing of meat and meat products).
Genus Vibrio.
1) View - Vibrio cholerae.
Vibrio cholerae with 2 biovars: classic Vibrio cholerae and El Tor biovar; more biovars: V.cholerae proteus – common causes diarrhea in birds, gastroenteritis in humans.
2) Morphology.
A small gram “-” curved stick, comma-shaped, monotrichous, does not form spores or capsules.
3) Cultivation.
Facultative anaerobe (but better with O2), grows quickly in liquid media, forms a film in 6-8 hours.
4) Enzymatic properties. High saccharolytic activity.
5) Antigenic structure.
O-Ag, H-Ag (heat labile). O-Ag has components: A, B, C, D, E, depending on which the serovars Ogawa (AB), Inaba (AS), Gikoshima-Hikojima (ABC) are distinguished.
6) The formation of endotoxin, the release of exotoxin (cholerogen).
7) Very sensitive to ↓t (in water for up to 5 days, soil for 2 months), sensitive to t, disinfectants, especially acids.
8) Epidemiology. The source of the disease is a sick person or a carrier, the transmission mechanism is fecal-oral, contact-household, less often.
9) Pathogenesis of lesions.
Vibrios that enter the stomach through the mouth can die as a result of the action of hydrochloric acid. But some reach the small intestine, where they multiply and secrete an exotoxin. The latter leads to disruption of water-salt metabolism and severe dehydration of the body.
10) Clinical picture.
The incubation period is 1-6 days. Most people have mild symptoms of oblivion, in severe cases, abdominal pain, vomiting, diarrhea in the form of “rice water” and a “fishy” smell. Severe form - IV degree of dehydration - cholera algid, ends in death.
11) Identification methods - bacterial method and express diagnostics using RIF.
12) Treatment with antibiotics and the introduction of plasma-substituting fluids.
Professional: non-specific sanitary and hygienic measures and quarantine. For a specific profession, a vaccine is used.
Diphtheria.
1. Taxonomy. Corynebacterium diphtheria.
This is an infectious disease caused by corynebacteria diphtheria, characterized by fibrinous inflammation in the pharynx, larynx, trachea and intoxication.
2. Morphology.
Pathogens are bacteria characterized by polymorphism. These are thin, slightly curved, gr+ rods, in smears they are located at an angle to each other, motionless, do not form spores, have a microcapsule, and are characterized by the presence of club-shaped thickenings at the ends - grains of Babesch-Ernst volutin.
3. Cultivation.
Aerobes or facultative anaerobes grow well on media containing protein, on blood agar, form small black round colonies, on potassium tellurite - large gray rough ones.
4. Enzymatic properties.
Biochemical activity is quite high.
5. Toxigenicity.
They produce a very strong exotoxin and affect the heart muscle, adrenal gland, and nerve ganglia. Capable of toxigenicity, which is associated with lysogenicity, diphtheria pathogens produce aggression enzymes: hyalorunidase, neuraminidase and cord factors.
6. Antigenic structure. O and H antigens distinguish 11 serovars.
Resistance. Resistant to low temperatures and drying, can be stored for 1 - 2 months, in water for up to 20 days, sensitive to increased temperatures and disinfectant solutions.
8. Epidemiology.
Sources: sick people and carriers. The main route of transmission is airborne droplets, contact and household contact, the susceptibility is high.
9. Pathogenesis of lesions.
The entrance gates are the mucous membranes of the pharynx, nose, eyes, respiratory tract, and less commonly the skin. At the site of entry of the pathogen, fibrinous inflammation is observed, the formation of a diphtheritic film of a grayish-yellow color, which is difficult to separate from the underlying tissue. The exotoxin released by bacteria enters the blood and toxinemia develops. The toxin affects the myocardium, kidneys, and adrenals.
10. Clinical manifestations.
According to localization, forms are distinguished: diphtheria of the pharynx (85 - 90%), diphtheria of the nose, eyes, skin, external genitalia.
The incubation period is 10 days, the disease begins with fever, pain when swallowing, films appear on the tonsils, and lymph nodes become enlarged. In children, the larynx becomes inflamed, as a result of which swelling develops diphtheria croup, leading to asphyxia, the cause of death is complications (paralysis of the respiratory muscles).
Immunity is long-lasting, up to 3-5 years post-vaccination, antitoxic (Chick reaction).
After the illness, unstable and short-lived antibacterial immunity and persistent antitoxic immunity are formed.
Children aged 1 to 4 years are most susceptible to diphtheria.
11. Microbiological diagnostics.
For bacterial diagnosis of diphtheria, material is taken from the throat and nose, the bacterioscopic method is used for a preliminary diagnosis.
12. Treatment. The main method of treatment is the immediate administration of antitoxic diphtheria serum. Antibiotic therapy is administered.
Etiotropic therapy: antitoxic antidiphtheria serum; is administered in a dose of 10,000-50,000 AE (depending on age and severity of the disease). 1 AU is the minimum amount of serum that will neutralize 100 DLF of diphtheria toxin.
Serotherapy is effective in the early period of the disease, until the toxin is fixed in the cells of the body and the tissues are not significantly damaged.
13. Prevention: early diagnosis and hospitalization, detection of bacteriocarrier.
Special prophylaxis: administration of diphtheria toxoid. Immunization is carried out from 3 months of age, then revaccination every 10 years.
Scarlet fever.
Scarlet fever- an acute exanthemic disease caused by the action of streptococcal toxin and characterized by the appearance of skin punctate rashes or small spots of intense red color, appearing first on the neck and upper chest, and then taking a generalized form. Characteristic are tonsillitis and lymphadenitis. An interesting clinical feature is erythema of the tongue (“crimson tongue”).
Tuberculosis.
Tuberculosis - This is an infectious disease caused by mycobacteria, characterized by lesions of various organs and organ systems.
1. Taxonomy. Pathogenic: Mycobacterium tuberculosis (human), M.bovis (bovine), M.avium (avian), M.murium (mouse).
2. Morphology. These are long, thin, motionless, slightly curved sticks, sometimes with swellings at the ends. Gr “+”, they do not form spores or capsules, they are stained according to Ziehl – Nielsen.
Mycobacterium tuberculosis is characterized by pronounced polymorphism. Their cytoplasmic membrane contains characteristic inclusions - Fly grains. Mycobacteria in the human body can transform into L-forms.
The cell wall is surrounded by a layer of glycopeptides called mycosides (microcapsules). Tuberculosis bacillus is difficult to perceive conventional dyes (Gram stained for 24-30 hours).
3. Cultivation.
Tuberculosis bacillus grows slowly, is demanding on nutrient media, and is glycerin-dependent. Aerobe, less often facultative anaerobe. On liquid media, Koch sticks form a wrinkled film after 1–2 weeks, and on dense media, after 2–4 weeks, they form a warty coating in the form of dry cottage cheese or cauliflower.
Their reproduction occurs very slowly, generation time is 14–16 hours. This is due to pronounced hydrophobicity, which is due to the high lipid content. Visible growth on media is 21–28 days.
4. Enzymatic properties. Enzymatic activity is low.
5. Antigenic structure. The antigenic structure is complex.
6. Toxin formation.
Tuberculin is considered an antigen that causes a local allergic reaction (Mantoux test). Virulent strains contain a cord factor.
7. Resistance.
Mycobacteria are very resistant to the environment: they persist in water for 5–12 months, in soil for 6 months, on objects for 3 months, in dried pus and sputum for up to 10 months. When boiled they die within 5 minutes. For disinfection, an active solution of chloramine and bleach is used.
8. Epidemiology.
Tuberculosis is pandemic in nature and is a social problem, especially in underdeveloped countries. The source of infection is a sick person, transmission routes: airborne droplets, contact and household contact. Only patients with an open form of tuberculosis pose an epidemic danger.
9. Pathogenesis of lesions.
In case of aerogenic infection, the primary infectious focus develops in the lungs (with good infection - a closed “Gon focus”), and in case of alimentary infection – in the lymph nodes. In the development of the disease, primary, disseminated and secondary tuberculosis are distinguished. At the site of pathogen penetration, a primary tuberculosis complex is formed, which can spread throughout the body. The lungs are most often affected, and a primary focus of Gon is formed.
10. Clinical manifestations.
The incubation period is from 3 – 8 weeks to 5 years. The disease can begin acutely with chest pain and severe shortness of breath. Reactive tuberculosis manifests itself as a cough, sometimes with hemoptysis, loss of body weight, and night sweats.
11. Microbiological diagnostics. Typically, sputum, bronchial lavage water, and urine are examined. Bacterioscopy of smears stained according to Ziehl-Nielson is effective only with a high concentration of microbacteria.
Tuberculin diagnostics (Mantoux test) is required. For early detection, a radiological diagnostic method is used, and from the age of 15, fluorography.
12. Treatment: antibacterial drugs are prescribed - isoniazid, rifampicin, ethambutol, pyrazinamide, PAS.
13. Prevention.
Carrying out a complex of sanitary, hygienic and anti-epidemic measures. Special prophylaxis: administration of BCG. Vaccination is carried out in the maternity hospital on the 4th-7th days of life using the intradermal method.
The causative agent of plague.
1. Taxonomy. Genus Yersinia pestis - Yersinia.
2. Morphology. Small, polymorphic, ovoid, gr “-” rod, has a capsule, is immobile, does not form spores.
3. Cultivation. A facultative anaerobe, young colonies have uneven edges - a “lace handkerchief”, mature ones - in the form of a “daisy”.
- Enzymatic properties.
It has biochemical activity and saccharolytic properties.
- Antigenic structure. Plague bacteria are highly virulent and have K- and O-antigens.
- Toxigenicity. They produce exotoxin and endotoxin.
- Resistance. Very resistant to low temperatures, sensitive to high temperatures, drying, and disinfectants.
- Epidemiology. The source is sick rodents, transmitted through flea bites, transmissible, nutritional, contact, airborne droplets. This is a natural focal disease. Patients are quarantined.
The main hosts of Yersinia plague in nature are rodents (gophers, tarbagans, etc.). Human infection occurs through transmissible (carriers - fleas), contact and nutritional routes. Patients with pneumonic plague infect others through aerogenic means.
9. Pathogenesis of lesions.
Forms of plague: cutaneous, bubonic, intestinal, pneumonic, primary septic.
The main place of reproduction of the pathogen is the lymph nodes. Insufficient barrier function of the lymph nodes leads to the development of the primary septic form of plague.
The secondary septic form develops against the background of bubonic or pulmonary forms.
10. Clinical manifestations. It begins suddenly with chills, fever, and headache. Immunity is strong.
11. Microbiological diagnostics.
Research is carried out in special laboratories in protective suits. Plague is a particularly dangerous infection. Work with materials containing the causative agent of the disease is carried out in special laboratories, trained personnel, subject to established safety measures.
12. Treatment. Antibiotics (tetracyclines), anti-plague immunoglobulins and specific bacteriophages are used for treatment.
13. Prevention.
Preventive measures prevent the introduction of infection from abroad and the occurrence of diseases in plague-endemic areas (South-East Asia). Specialist. prevention: administration of a live vaccine.
The causative agent of tularemia.
1. Tularemia is a naturally occurring zoonotic infectious disease caused by Francisella tularensis, characterized by fever and lymph node involvement.
2. Morphology.
These are small gr “-” polymorphic bacteria, immobile, and do not have spores.
3. Cultivation.
Facultative anaerobes grow on media supplemented with yolk or cystine.
4. Enzymatic properties are little expressed. Biochemical properties are unstable. Produce hydrogen sulfide.
5. Toxigenicity. Pathogenic and immunogenic properties are associated with toxic substances such as endotoxin.
6. Antigenic structure. Francisella contains shell Vi- and somatic O-AG.
7. Resistance.
The pathogen is resistant to low temperatures. Not resistant to temperature increases, disinfectants, UV rays, and many antibiotics. Low resistance to high temp.
8. Epidemiology.
The source of infection is all types of rodents, transmission through blood-sucking arthropods (ticks, mosquitoes). The transmission route is transmission, contact - household, food, air. The pathogen is not transmitted from person to person. The natural hosts of the pathogen are rodents (water rats, voles, mice, hamsters, hares).
Human infection occurs through direct contact with sick animals or dead bodies, through contaminated water and food products. The disease can be transmitted by ticks, mosquitoes, and horseflies. The pathogen enters the human body through the skin and mucous membranes of the eyes, mouth, nose, respiratory tract and digestive tract. Then the pathogen ends up in the lymphatic tract, where it multiplies intensively and appears in the blood.
9. Pathogenesis of lesions.
Penetrates through the skin and mucous membranes, even undamaged ones. A primary focus develops at the site of penetration. The pathogen and its toxins, penetrating into the blood, cause damage to the lymph nodes and form buboes.
10. Clinical manifestations.
The incubation period is 3 – 7 days, the disease begins suddenly with a rise in temperature, symptoms depend on the route of transmission of the infection.
Forms: bubonic, oculobubonic, angio-bubonic, septic.
Immunity is long lasting.
11. Microbiological diagnostics. Serological, biological and bacteriological examination of materials taken from the patient.
12. Treatment. Not sensitive to penicillin and sulfonamides. Aminoglycosides (streptomycin, kanamycin), erythromycin, chloramphenicol, tetracycline are used.
13. Prevention. Control of rodents and insects. Specialist. prevention: immunization of people living in areas of natural outbreaks with a live vaccine.
Borreliosis.
Genus Borrelia belong to the Gracilicutes department of the order Spirochaetales of the Spirochaetaceae family. It is formed by motile spiral bacteria; spirals have 3-10 irregular large curls. Gram "-".
Borrelia are strict anaerobes and grow at 20-37 °C. They are fastidious to cultivation conditions - they grow on media enriched with animal proteins and on chicken embryos.
Borrelia recurrentis ( Obermeyer's spirochete) - filamentous spiral bacterium; the spiral has uneven turns.
Borrelia recurrentis reproduces by transverse division and does not form spores. Can be dyed well with basic aniline dyes.
According to Romanovsky-Giemsa and methylene blue, Borrelia recurrentis are colored blue-violet (but not pink, like pale spirochetes).
Epidemiology of tetanus.
The natural reservoir and source of tetanus is soil. Human infection is a consequence of domestic and industrial injuries, most often superficial, when the patient does not seek medical help. An increased incidence is noted in regions with a warm climate, which creates conditions not only for the long-term preservation of spores in the soil, but also for their germination.
The main risk group in peacetime is agricultural workers (accounting for 80-86% of cases). The annual death rate from tetanus exceeds 100,000 people.
Vegetative cells of tetanus. Gram-positive rods with rounded ends. Motile (contain 20 flagella or more, located along the periphery of the cell). In smears they are located singly or in chains.
Tetanus spores. Round, less often oval, located terminally. Their diameter is 2-3 times greater than the thickness of bacteria, as a result of which they resemble “tennis rackets” or “drumsticks”. The spores are resistant to chemical and physical influences.
Clostridium tetani is a strict anaerobe, highly sensitive to 0 2. On MPA and terminal spores of gelatin, the tetanus pathogen grows slowly and forms thin transparent colonies of two types: smooth, transparent S-tetanus colonies and greyish-yellow, rough R-tetanus colonies. S-colonies of tetanus form shoots that give them a spider-like shape.
Later, the processes merge, forming a “mesh” on the surface of the medium. When sown in a column in semi-liquid agar after 24-48 hours, S-colonies of tetanus look like fluff with a dense brown center; R-colonies of tetanus have the appearance of lentils.
Tetanus clinic.
The leading manifestations of tetanus are a convulsive syndrome, including painful muscle contractions (tetanus) and prolonged muscle tension. Characteristic signs of tetanus include opisthotonus - tetanic spasm, when the spine and limbs are bent, the patient lies on his back and leans on the back of his head and heels and risus sardonkus (risus caninus) - a kind of grin caused by spasm of the facial muscles.
A mild form of tetanus (localized tetanus) is characterized by periodic spasms in the affected area.
For analysis, blood (10 ml) and pieces of liver and spleen (20-30 g) are taken.
Material from a patient or corpse, dressing and suture surgical material, as well as soil, dust and air are subject to research.
Prevention of tetanus. Carry out planned and emergency activities.
For specific treatment of tetanus, human tetanus immunoglobulin is used. At the same time, antibiotic therapy is carried out.
Gas gangrene.
Gas gangrene [from Greek. gangraina, corrosive ulcer] is a wound infection characterized by crepitus of surrounding tissues due to gas bubbles (a product of the enzymatic action of clostridia), tissue necrosis as a result of a decrease or complete absence of blood supply and general septic manifestations.
It is most often caused by Clostridium perfringens, C. novyi and C. septicum; less commonly - C. histolyticum, C. bifermentans, C. ramosum, C. sporogews, C.fallax, C. sordelli, etc.
One of the most common pathogenic Clostridium species. Based on their ability to produce the four main toxins (a-, p-, e- and i-), Clostridium perfringens microorganisms are divided into six serovars - A, B, C, D, E and F. The main causative agent of human diseases is type A bacteria. In necrotic In enteritis, microorganisms of types C and F are sometimes isolated; Type D pathogens cause infectious enterotoxemia. C. perfringens type A was discovered by American pathologists W. Welch and G. Nuttell (1892). A pure culture was obtained by the French bacteriologists A. Veillon and J. Joubert (1893), who gave it the name perfringens [from lat. perfringo, break through].
Syphilis clinic.
Syphilis occurs in several stages, but their strict sequence is not always observed. Duration incubation period of syphilis varies from 10-11 to 90 days. (on average 21-24 days).
Typical presentation late form of syphilis - Hutchinson's triad- parenchymal keratitis, “barrel teeth” and deafness (due to damage to the labyrinth); Changes in the tibias (“saber shins”) are often observed.
Immunofluorescent methods are used for early diagnosis of syphilis.
The main methods for diagnosing syphilis are RSC, proposed by A. Wassermann.
Infectious diseases caused by opportunistic bacteria(cocci, pseudomonads, non-spore-forming anaerobes).
Classification of cocci.
Bergi classification:
Pathogenic cocci belong to 3 families:
1) micrococci Micrococcaceae – staphylococcus genus Staphylococcus;
2) streptococci Streptococcaceae – genus Streptococcus streptococci and pneumococci;
3) Neisseriaceae – genus of Neisseria Neisseria (meningo- and gonococci).
II. Streptococci
1. Types of streptococci – Streptococcus pyogenes (hemolytic) and Streptococcus pneumonia (pneumococcus).
2. They are small spherical cells, characterized by polymorphism: in smears they are arranged in chains or pairs. They do not form spores, are motionless, gram “+”. Freshly isolated strains form a microcapsule.
3. Streptococci are facultative anaerobes. Optimal media containing blood or serum. On dense media, small gray colonies form (on liquid har-ren, bottom growth).
4. Based on biochemical properties, 21 species are distinguished. Most of them are opportunistic.
By Brown classification groups of streptococci are divided into:
a) α-greening - give a greening zone of hemolysis of Streptococcus pneumonia
b) β-hemolytic - give complete hemolysis on blood agar
c) γ-non-hemolytic – do not form a hemolysis zone.
5. Exotoxins form: streptolysins, leukocidins, erythrogenic - scarlet fever, cytotoxins.
1) hemolysins
2) erythrogenin has a pyrogenic effect.
6. Typical antigens are located on the surface, specific antigens are located in the cytoplasm, and PS (polysaccharide) is located in the cell wall.
Antigens of streptococci.
1. Extracellular – proteins and exoenzymes. This is a variant of specific antigens.
2. Cellular.
Landsfield classification streptococcal serogroups based on PS AG – “substance C”:
group A - has antigen M on the surface of cells, which produces pathogenicity enzymes. They are permanent inhabitants of the oral mucosa and pharynx, carriers of 20-25% of the population;
group B - includes opportunistic pathogens that live on the mucous membrane of the nasopharynx, in the gastrointestinal tract, and in the vagina;
group C – pathogenic microorganisms;
group D – non-pathogenic (except enterococci).
7. Around environment are preserved for a long time. In dried pus and sputum, they persist for months. They die during pasteurization. Sensitive to disinfection. solutions.
8. Sources of infection: sick people, bacteria carriers, less often animals.
9. Diseases in humans are most often caused by β-hemolytic streptococci of serological group A.
10. Hemolytic streptococci cause pharyngitis, scarlet fever, erysipelas, rheumatic carditis and puerperal sepsis. Immunity is unstable.
11. Microbiological diagnostics - serological reactions.
12. A/B are most often used: penicillin, erythromycin and tetracycline.
Prevention – sanitary and hygienic measures, strengthening the general resistance of the body.
Viridans streptococci
1.Str. Mitis is localized in the crevices between the gum and the surface of the tooth, which causes inflammation of the dental pulp.
2.Str. Salivarius live in saliva and on the back of the tongue, causing caries of the tooth root surface.
3.Str. Sanguis causes dental caries and periodontitis. Living in the oral cavity, microbes break down carbohydrates or nitrogenous substances in food to form acid, which contributes to the dissolution of tooth enamel and leads to dental caries.
III. Pneumococci.
1. Streptococcus pneumoniae
2. They belong to diplococci, usually lanceolate in shape. Motile, do not have spores, form a capsule, gram-positive. In old cultures, gr “-” bacteria were found.
3. Facultative anaerobes and demanding media with the addition of protein (blood).
4. Exhibit saccharolytic properties.
5. Endotoxins are formed by: streptolysins, leukocyphins, erythrogenic cytotoxins.
6. There is a protein antigen in the cytoplasm, and polysaccharides in the capsule.
7. Resistant to low temperatures. Sensitive to increased temperatures, des-r-rams.
8. The owner is a person. White mice are highly sensitive; lambs, calves, and piglets get sick. The source is a sick person and a bacteria carrier.
9. GVD (purulent-inflammatory diseases) – lobar pneumonia, creeping corneal ulcer, otitis media.
10. Clinic: with lobar pneumonia, a lobe or the entire lung is affected.
11. Microbiological research is used - serological reactions.
12. Treatment with antibiotics: penicillin, tetracycline. Prof: sanitary measures.
IV. Neisseria.
Meningococci
1. Neisseria meningitides is the causative agent of meningococcal infection. Healthy carriage of meningococci is widespread.
2. Meningococci - small diplococci, located in the form of a pair of coffee beans, facing each other with concave surfaces.
They are immobile (have pili), do not form spores, and have a capsule. Gr "-".
3. Obligate aerobes are cultivated on media containing native protein or selective media with ristomycin. They grow well in nutrient media supplemented with blood, milk or egg yolk.
4. Biochemically little active. They exhibit saccharolytic properties.
5. They form a strong endotoxin – cell wall lipopolysaccharide.
6. According to capsulnum (polysaccharide) antigen serogroups: main A; B, S, D.
7. Meningococci are poorly resistant in the environment. environment (proper transportation from the patient). Resistant to ristomycin and sulfonamides. Sensitive to drying and cooling, UV irradiation, disinfectants, a/b: penicillin.
8. Sources of infection: a sick person and a bacteria carrier (anthroponoses).
