Symptoms of streptococcal infection

Clinical symptoms of streptococcal infection are varied and depend on the type of pathogen, localization of the pathological process and the condition of the infected organism. Diseases caused by group A streptococci can be divided into primary, secondary and rare forms. Primary forms include streptococcal lesions of the ENT organs (tonsillitis, pharyngitis, acute respiratory infections, otitis, etc.), skin (impetigo, ecthyma), scarlet fever, erysipelas. Secondary forms include diseases with an autoimmune mechanism of development (non-purulent) and toxic-septic diseases. Secondary forms of the disease with an autoimmune mechanism of development include rheumatism, glomerulonephritis, vasculitis, and toxic-septic diseases include metatonsillar and peritonsillar abscesses, necrotic lesions of soft tissues, septic complications. Rare forms include necrotic fasciitis and myositis; enteritis; focal lesions of internal organs, TSS, sepsis, etc.

Clinical and laboratory symptoms of streptococcal infection with signs of invasion:

• A drop in systolic blood pressure to 90 mmHg or below.
• Multiorgan lesions involving two or more organs:
  • kidney damage: creatinine levels in adults are equal to or exceed 2 mg/dl, and in children twice the age norm;
  • coagulopathy: platelet count less than 100x10 ⁶ /l; increased intravascular blood coagulation; low fibrinogen content and the presence of its decay products;
  • liver damage: age-related norms for transaminase and total bilirubin levels are exceeded by two times or more:
  • acute RDS: acute onset of diffuse pulmonary infiltration and hypoxemia (with no signs of cardiac damage); increased capillary permeability; widespread edema (fluid in the pleural or peritoneal area); decreased albumin levels in the blood;
  • widespread erythematous macular rash with epithelial desquamation;
  • soft tissue necrosis (necrotizing fasciitis or myositis).
• Laboratory criterion - isolation of group A streptococcus.

Cases of streptococcal infection are divided into:

• probable - the presence of clinical signs of the disease in the absence of laboratory confirmation or when another pathogen is isolated; isolation of group A streptococcus from non-sterile environments of the body;
• confirmed - the presence of the listed signs of the disease with the isolation of group A streptococcus from normally sterile body fluids (blood, cerebrospinal fluid, pleural or pericardial fluid).

There are four stages of development of the invasive form of streptococcal infection:

• Stage I - the presence of a localized lesion and bacteremia (in severe forms of tonsillopharyngitis and streptoderma, blood cultures are recommended);
• Stage II - circulation of bacterial toxins in the blood;
• Stage III - pronounced cytokine response of the macroorganism:
• Stage IV - damage to internal organs and toxic shock or comatose state.

Young people are more likely to get sick. The invasive form of streptococcal infection is characterized by a rapid increase in hypotension, multi-organ damage, RDS, coagulopathy, shock and high mortality. Predisposing factors: diabetes mellitus, immunodeficiency states, vascular diseases, use of glucocorticoids, alcoholism, chickenpox (in children). A provoking moment can be a minor superficial injury, hemorrhage into soft tissues, etc.

Necrotizing fasciitis (streptococcal gangrene)

• Confirmed (established) case:
  • soft tissue necrosis involving the fascia;
  • a systemic disease that includes one or more of the following symptoms: shock (a drop in blood pressure below 90 mm Hg), disseminated intravascular coagulation, damage to internal organs (lungs, liver, kidneys);
  • isolation of group A streptococcus from normally sterile body fluids.
• Probable case:
  • the presence of the first and second signs, as well as serological confirmation of streptococcal (group A) infection (4-fold increase in antibodies to streptolysin O and DNase B);
  • the presence of the first and second signs, as well as histological confirmation of soft tissue necrosis caused by gram-positive pathogens.

Necrotic fasciitis can be provoked by minor damage to the skin. External signs: swelling; red and then bluish erythema; formation of quickly opening vesicles with yellowish fluid. The process affects not only the fascia, but also the skin and muscles. On the 4th-5th day, signs of gangrene appear; on the 7th-10th day - a sharp outline of the affected area and tissue detachment. Symptoms of streptococcal infection rapidly increase, early multi-organ (kidneys, liver, lungs) and systemic lesions, acute RDS, coagulopathy, bacteremia, shock (especially in the elderly and people with concomitant diabetes mellitus, thrombophlebitis, immunodeficiency state) develop. A similar course of the process is possible in practically healthy people.

Streptococcal gangrene differs from fasciitis of other etiologies. It is characterized by transparent serous exudate, diffusely impregnating the flabby whitish fascia without signs of purulent melting. Necrotic fasciitis differs from clostridial infection by the absence of crepitus and gas release.

Streptococcal myositis is a rare form of invasive streptococcal infection. The main symptoms of streptococcal infection are severe pain that does not correspond to the severity of external signs of the disease (swelling, erythema, fever, feeling of muscle stretching). Characterized by a rapid increase in signs of local necrosis of muscle tissue, multiorgan damage, acute distress syndrome, coagulopathy, bacteremia, shock. Mortality is 80-100%.

Toxic shock syndrome is a disease that poses a direct threat to life. In 41% of cases, the entry point for infection is a localized soft tissue infection; mortality is 13%. Pneumonia is the second most common primary source of pathogen entry into the blood (18%); mortality is 36%. Invasive streptococcal infection leads to the development of toxic shock syndrome in 8-14% of cases (mortality is 33-81%). Toxic shock syndrome caused by group A streptococcus is superior to toxic shock syndrome of other etiologies in the severity of the clinical picture, the rate of increase in hypotension and organ damage, and the mortality rate. Rapid development of intoxication is characteristic. Symptoms of shock appear after 4-8 hours and depend on the localization of the primary infection. For example, when toxic shock syndrome develops against the background of a deep skin infection involving soft tissues, the most common initial symptom is sudden intense pain (the main reason for seeking medical help). At the same time, objective symptoms (swelling, soreness) may be absent at the initial stages of the disease, which causes erroneous diagnoses (flu, muscle or ligament rupture, acute arthritis, gout attack, deep vein thrombophlebitis, etc.). Cases of the disease with a fatal outcome in apparently healthy young people have been described.

Severe pain, depending on its location, may be associated with peritonitis, myocardial infarction, pericarditis, pelvic inflammatory disease. Pain is preceded by the development of a flu-like syndrome: fever, chills, muscle pain, diarrhea (20% of cases). Fever is detected in approximately 90% of patients; soft tissue infection leading to the development of necrotic fasciitis - in 80% of patients. In 20% of hospitalized patients, endophthalmitis, myositis, perihepatitis, peritonitis, myocarditis and sepsis may develop. Hypothermia is likely in 10% of cases, tachycardia, hypotension in 80%. Progressive renal dysfunction is detected in all patients, and acute respiratory distress syndrome is found in half of the patients. As a rule, it occurs against the background of hypotension and is characterized by severe dyspnea, pronounced hypoxemia with the development of diffuse pulmonary infiltrates and pulmonary edema. In 90% of cases, tracheal intubation and artificial ventilation are necessary. More than 50% of patients experience disorientation in time and space; in some cases, coma may develop. Half of the patients who had normal blood pressure at the time of hospitalization experience progressive hypotension over the next 4 hours. DIC syndrome often occurs.

Extensive necrotic changes in soft tissues require surgical debridement, fasciotomy and, in some cases, amputation of the limbs. The clinical picture of shock of streptococcal genesis is characterized by a certain torpidity and a tendency to persistence, resistant to the treatment measures (antibiotic therapy, administration of albumin, dopamine, saline solutions, etc.).

Kidney damage precedes the development of hypotension, which is characteristic only of streptococcal or staphylococcal toxic shock. Characteristic are hemoglobinuria, an increase in creatinine levels by 2.5-3 times, a decrease in the concentration of albumin and calcium in the blood serum, leukocytosis with a shift to the left, an increase in ESR, a decrease in hematocrit by almost two times.

Lesions caused by group B streptococci occur in all age categories, but neonatal pathology dominates among them. Bacteremia (without a specific focus of primary infection) is detected in 30% of children, pneumonia in 32-35%, and meningitis in the rest, which often occurs during the first 24 hours of life. Diseases in newborns are severe, with mortality reaching 37%. Meningitis and bacteremia are often observed in children, with 10-20% of children dying, and residual disorders are noted in 50% of survivors. In women in labor, group B streptococci cause postpartum infections: endometritis, urinary tract lesions, and complications of surgical wounds during cesarean section. In addition, group B streptococci can cause lesions of the skin and soft tissues, pneumonia, endocarditis, and meningitis in adults. Bacteremia is observed in elderly people suffering from diabetes mellitus, peripheral vascular diseases and malignant neoplasms. Of particular note are streptococcal pneumonias that occur against the background of acute respiratory viral infections.

Streptococci of serological groups C and G are known as causative agents of zoonoses, although in some cases they can lead to local and systemic inflammatory processes in humans. Viridans streptococci can cause bacterial endocarditis. Less significant, but incomparably more frequent symptoms of streptococcal infection are dental caries caused by streptococci of the mutans biogroup (S. mutans, S. mitior, S. salivarius, etc.).

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