Lecture No. 8. Infections caused by pathogens of the Pseudomonas group

1. Pseudomonas infection

Representatives of Pseudomonas - numerous gram-negative bacteria that live in soil and in water, are a common flora of wet rooms, including hospitals. They cause diseases mainly in newborns and children with insufficient protective mechanisms, for example, with cystic fibrosis, immunodeficiency states, malignant neoplasms, other chronic diseases, burns, dystrophy, and also after treatment with immunosuppressive drugs.

Etiology. Among the many well-identified strains of Pseudomonas, only a few are pathogenic to humans. The most common is P. aeruginosa. Others are incidental pathogens: P. cepatica, P. roaltophilia, P. putrefacies. P. mallet causes glanders in horses. All species of the Pseudomonas group are strict aerobes, capable of utilizing various carbon sources and reproducing in a humid environment containing minimal amounts of organic matter.

Pseudomonas aeruginosa is a Gram-negative bacterium that causes hemolysis on blood agar. More than 90% of bacterial strains produce a bluish-green phenazine pigment (blue pus), as well as fluorescein, which is yellowish-green, diffusing into the nutrient medium, which stains around the colonies. The strains of the pathogen differ in epidemiological significance, serological, phage characteristics, and the ability to produce pyocin.

Epidemiology. Pseudomonas is often found in medical institutions on the skin, clothing and shoes of patients and staff. It can grow in any moist environment, is often isolated even from distilled water, and is present in hospital laundries and kitchens, antiseptic solutions and on equipment used for inhalation and respiratory therapy. In some healthy individuals, Pseudomonas is found in the intestines.

Pathogenesis. For its development, Pseudomonas requires oxygen, the lack of which reduces the virulence of the microorganism. The endotoxin produced by it is significantly inferior in activity to the endotoxins of other gram-negative bacteria, but can cause diarrhea.

Pseudomonas aeruginosa releases large amounts of exotoxins, including lecithinase, collagenase, lipase, and hemolysins, causing necrotic lesions on the skin. One of the hemolytic factors is a heat-resistant glycolipid capable of destroying lecithin, which is part of the pulmonary surfactant. This leads to the development of atelectasis of the lung. The pathogenicity of Pseudomonas aeruginosa also depends on its ability to resist phagocytosis, which, in turn, depends on the production of protein toxins by it. The patient's body reacts to infection by the formation of antibodies to exotoxins (exotoxin A) and lipopolysaccharides of the macroorganism.

Clinical manifestations. In healthy people, Pseudomonas aeruginosa, which gets into small wounds, causes suppuration and local abscesses, which contain green or blue pus. Skin lesions that develop as a result of septicemia or direct inoculation of the pathogen into the skin initially appear as pink spots, which, as the infection progresses, turn into hemorrhagic nodules and undergo necrosis. In their place, scabs form, surrounded by a red rim (ecthyma gangrenosum). Bacteria multiply in affected areas.

Occasionally, healthy children may develop septicemia, meningitis, mastoiditis, folliculitis, pneumonia, and a urinary tract infection. Rarely, Pseudomonas causes gastroenteritis.

Otitis externa caused by P. aeruginosa develops in swimmers who repeatedly use polluted water bodies. Dermatitis and outbreaks of urinary tract infections are possible when using shared baths and showers. Skin lesions appear several hours (up to 2 days) after contact with these water sources, manifesting as erythema, macules, papules, and pustules. Skin lesions may be limited or widespread. Some children have fever, conjunctivitis, rhinitis, and sore throat at the same time.

Other members of the Pseudomonas family rarely cause disease in healthy children. Cases of pneumonia and abscesses in children caused by P. cepacia, otitis media - with P. stutzeri infection, suppuration and septicemia caused by P. maltophila are described.

Shunts, catheters. Septicemia most often develops in children after the introduction of intravenous or urinary catheters. Pneumonia and septicemia are more common in children who are on artificial or assisted breathing. Peritonitis and septicemia develop when instruments used for peritoneal dialysis are contaminated. Pseudomonas can cause abscessing or meningitis in children with dermoid fistulas and malformations of the meningeal membranes, particularly meningomanoceles. These bacteria can cause acute or subacute endocarditis in children with congenital heart disease, both before and after surgery.

Burns and wound infection. Pseuomonas and other gram-negative bacteria are often found on wound and burn surfaces, but their presence does not always lead to the development of an infectious process. Septicemia may be due to the multiplication of the pathogen in necrotic tissues or prolonged use of intravenous or urinary catheters.

Antibiotics that can suppress the microflora sensitive to them do not prevent the reproduction of some strains of Pseudomonas aeruginosa.

cystic fibrosis. Pseudomonas aeruginosa is excreted in sputum in most children with cystic fibrosis, but does not prove an infectious lesion with its characteristic destructive process in the lungs, but may reflect changes in the composition of the microflora due to previous treatment with broad-spectrum antibiotics. Antibiotics sometimes contribute to the elimination of this microflora, sometimes it disappears spontaneously.

Pseudomonas aeruginosa infection in patients with cystic fibrosis is most often limited to the lungs; septicemia develops very rarely.

Malignant neoplasms. Children with leukemia and especially those treated with immunosuppressive drugs are most susceptible to Pseudomonas aeruginosa infection. The leukopenia that develops against the background of such treatment contributes to the activation of the pathogen, usually saprophytic in the gastrointestinal tract, its penetration into the general bloodstream and the development of septicemia. Clinical manifestations of the disease are anorexia, fatigue, nausea, vomiting, fever and diarrhea. Generalized vasculitis develops.

Hemorrhagic necrosis can appear in all organs, including the skin in the form of purple nodules or areas of ecchymosis, rapidly undergoing necrosis. Inflammatory changes are usually hemorrhagic and necrotic in nature, abscesses often develop in the perirectal tissue. Sometimes there may be a picture of ileus and a sharp decrease in blood pressure.

Diagnosis and differential diagnosis. The diagnosis of Pseudomonas infection depends on culture of the pathogen from blood, urine, CSF, or pus obtained from abscesses or areas of inflammation. Specific pneumonia is diagnosed based on the results of a puncture biopsy of the lung or data from a bacteriological examination of sputum.

Bluish nodular skin lesions and ulcerations with an ecchymotic and gangrenous center and a bright halo are pathognomonic of this infection. In rare cases, a similar picture of skin changes is observed with septicemia caused by Aeromonas hydrophila.

Prevention. Of primary importance is the fight against nosocomial infection, timely identification and elimination of its sources, careful adherence to aseptic requirements in the preparation of solutions for parenteral administration, in the disinfection of catheters and the daily replacement of all devices used for prolonged intravenous infusions. Burn patients should be actively immunized with a Pseudomonas polyvaccine to reduce the incidence of septicemia and mortality. The administration of hyperimmune specific globulin prevents the development of septicemia. Timely diagnosis and surgical interventions for dermoid anomalies communicating with the spinal canal can prevent the development of infection with Pseudomonas aeruginosa.

Treatment. In case of infection caused by Pseudomonas aeruginosa, it is necessary to immediately begin treatment with antibiotics to which the pathogen is sensitive in vitro. Antibiotic therapy should be especially intensive and prolonged in patients with impaired immunological reactivity. Many of the new beta-lactam antibiotics have varying degrees of activity against Pseudomonas. Patients with meningitis caused by Pseudomonas aeruginosa infection are treated with intravenous antibacterial drugs. Sometimes it is additionally recommended to administer gentamicin into the ventricles of the brain or under the dura mater.

Abscesses should be opened and drained, without which even long-term antibiotic treatment remains ineffective.

Forecast. The outcome largely depends on the nature of the underlying disease. The immediate cause of death in children with leukemia is sepsis, in half of all cases caused by Pseudomonas. These pathogens are isolated from the lung tissue of most children with cystic fibrosis and in many cases can be the main cause of death. The prognosis for patients who have had specific meningitis is unfavorable.

2. Diseases caused by other strains of Pseudomonas

Sap is a severe infectious disease of horses caused by P. mallet, sometimes transmitted to humans. The disease is most common in Asia, Africa, and the Middle East, but is extremely rare in the United States. Manifestations of infection are acute or chronic pneumonitis, hemorrhagic necrosis of the skin, mucous membranes of the nose and lymph nodes.

Melioidosis is a very rare disease found in Southeast Asia. The causative agent is P. pseudomallei, which lives in the soil and water of tropical countries. Infection occurs by inhalation of dust or contamination of wounds and scratches.

Pulmonary infection in melioidosis can be subacute and mimic tuberculosis. In some cases, septicemia develops, multiple abscesses form in all organs.

Often there is the development of myocarditis, endocarditis, pericarditis, intestinal abscesses, cholecystitis, acute gastroenteritis, septic arthritis, osteomyelitis, paraspinal abscesses, urinary tract infections and generalized lymphadenopathy. Melioidosis may be accompanied by symptoms of encephalitis, high body temperature and convulsions. Antibiotic therapy is usually effective.

The disease can be latent for a long time and manifest clinical symptoms only with a decrease in the resistance of the macroorganism years after the initial infection. Patients with both glanders and melioidosis are treated with tetracycline or chloramphenicol in combination with sulfonamides for several months. Aminoglycosides and penicillins are ineffective. You can prescribe trimethoprim with sulfamethoxazole.

Author: Muradova E.O.

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