NAME OF DISEASE:
1. Invasive (cellulitis)
b. Puerperal fever
c. Surgical scarlet fever
e. Necrotizing fasciitis
b. Ecthyma - hardbase
The above may be antecedent to acute glomerulonephritis.
ETIOLOGICAL AGENT: Streptococcus pyogenes
NOTE: All beta-hemolytic
streptococci are grouped from A to U based on the C-antigen
(Lancefield classification). Most human diseases are due to group A organisms but a
few can be caused by members of group B, C and G also.
A pus-generating infection of the skin or mucous membranes. Surgical wounds are often infected by this organism as well as the uterus after childbirth.
Pathology is the result of toxin production:
1. Streptolysin - two types
(S and O). They kill leukocytes, lyse RBC's and destroy heart
2. Streptokinase - a plasma activator that initiates the fibrinolytic dissolution of fibrin clots.
4. Erythrogenic toxin - produces the generalized erythematous rash of scarlet fever.
5. Streptodornase - DNAase
7. Exotoxin A - a super antigen which causes over production of cytokines
8. Cysteine protease (Exotoxin B)
Pyoderma strains of S. pyogenes can colonize or survive on normal skin surfaces for extended periods. Epidermal carriage or acquisition appears to be the initial event predisposing to the development of impetigo in some patients. Following acquisition on the normal skin, minor trauma may be a prerequisite for initiating infection. Pyoderma strains of S. pyogenes produce the gamut of extracellular substances considered in relation to virulence and infectivity.
The initial lesion of streptococcal impetigo is a vesicle in the superficial epidermis; capillary dilation and infiltration with leukocytes occurs in the upper cutis. Older lesions are frankly purulent and ecthyma is characterized by an ulcer crater with thickened margins. Lymphatic channels and regional lymph nodes are involved; lymphangitis is more common in cellulitis and deeper wound infections. Bacteremia may result from pyoderma, but it is more likely in erysipelas or deeper, suppurative infection.
Immunopathologic studies in man have revealed glomerular deposition of IgG, complement, fibrin, and occasionally in early, acute lesions, products and components of streptococcal cells. A decrease in complement occurs prior to or in the absence of hematuria in patients infected with nephritogenic streptococci, including persons who go on to develop clinical nephritis. A hyperimmune response to streptococcal antigens has also been demonstrated in patients with pyoderma-nephritis.
Differences in the pathology and natural history of poststreptococcal nephritis in children and adults have been described and progressive changes are more often observed in the adult. Nephritis after pyoderma is infrequent in adults.
1. Invasive infections (cellulitis)
Erysipelas - portal of entry is the skin or outer mucous membrane. Erysipelas
characterized by acute toxicity; the typical lesion is a raised, demarcated, bright red
area of dermal and subcutaneous inflammation which advances as the disease
B. Puerperal fever - uterus is infected
C. Surgical scarlet fever - surgical wound is infected
D. Myositis - muscle is destroyed
E. Necrotizing fasciitis - muscle sheath is destroyed
2. Local infections (pyodermas)
Impetigo - infection of superficial layer of skin in small children. Brown
crust on skin is
major symptom. The typical lesions of impetigo are crusted and vesicular. Systemic
manifestations are minimal or absent. The lesions begin as vesicles with little erythema.
They rapidly progress to pustules that are subsequently covered with thickened, yellow
crusts, with thin pus beneath. Such lesions commonly occur over exposed areas,
especially on the extremities. Itching is frequent. Satellite impetigo lesions may develop
along scratch lines. Urticaria or erythema multiform occasionally develops. Scarlet
fever may accompany streptococcal pyoderma or wound infection (surgical scarlet
fever). Transient lymphadenitis occurs, and significant regional lymphadenopathy is
characteristic of streptococcal impetigo.
Secondary infection or dermatoses, such as eczema and seborrheic dermatitis,
in the development of confluent, purulent, crusted lesions with concomitant lymphatic
Redness, heat, edema, and streaking lymphangitis are hallmarks of the more
toxic forms of streptococcal skin and wound infections. Chills and fever commonly
accompany such illnesses.
The etiologic diagnosis of streptococcal pyoderma is confirmed by the isolation of S. pyogenes in cultures of material from typical lesions. Underlying skin diseases that predispose to streptococcal pyoderma, such as tinea capitis and eczema, may become more apparent.
The major clinical and laboratory manifestations
of acute post-streptococcal glomerulonephritis are:
|Abrupt onset||Hematuria, cylindruria|
|Edema, oliguria, dark urine||Azotemia|
|Hypertension, congestive failure, encephalopathy||Low serum complement (acute)|
|Diuresis, weight loss, clinical recovery||Elevated streptococcal antibody titer|
|Positive streptococcal culture|
Acute nephritis encompasses a broad clinical spectrum, ranging from minimal disease to death. Acute nephritis with normal urinary findings has been documented by biopsy. The finding of a low beta 1-C/beta 1-A complement not only confirms the clinical diagnosis of acute glomerulonephritis, but also it is of value in the detection of subclinical or asymptomatic cases of nephritis. The usual self-limited course of poststreptococcal nephritis, with the return of urine abnormalities - proteinuria, hematuria, and cylindruria - and complement to normal within days to weeks after onset of the disease, distinguishes AGN from other nephritides. The triad of documented streptococcal infection, self-limited illness, and transient low complement is diagnostic of acute poststreptococcal nephritis.
Penicillin G for 7 days.