Antibiotics for skin infection amoxicillin

S carlet Fever: Scarlet fever has its highest prevalence in children 4 - 8 years of age and is very uncommon in adults.

The primary infection most commonly associated with scarlet fever is pharyngitis, though soft tissue infection at a surgical site has been described (surgical scarlet fever). A cute Rheumatic Fever: Large epidemics of scarlet fever have been reported in the literature since the 12 and 13th centuries in association with childbed fever, non-pasteurized milk,

surgical

from

Reductions in incidence and mortality rates of ARF in the United States had begun prior to the discovery of penicillin, primarily because of improved housing, sanitation, and delivery of health care.

The recent

increase

However, the use of penicillin in the treatment of GAS pharyngitis dramatically reduced the incidence of ARF.

Mucoid colonies of group A streptococci have been associated with cases of rheumatic fever in North America but not in de­veloping countries. Five

serotypes

StrepTSS

prevalence

It has been estimated that the risk of secondary cases may be approximately 200 times greater than the risk among the general population (23) There is ample data from studies conducted over several decades that Group A streptococcus is quickly and efficiently transmitted from amoxicillin & clavulanic acid index cases to susceptible individuals and that transmission may result in colonization, pharyngitis, scarlet fever, rheumatic fever or invasive Group A streptococcal infections.

The risk for secondary cases is likely related to close or intimate contact and crowding as well as host factors such as 1.

active viral infections such as varicella or influenza; 2. recent surgical wounds and childbirth (author's unpublished observations); 3. absence of type specific opsonic antibody against the

Group

Interestingly, a specific portal cannot be defined in the remaining 50% (87). Rarely, patients with symptomatic pharyngitis develop StrepTSS. Surgical procedures such as suction lipectomy, hysterectomy, amoxicillin 875 mg pink vaginal delivery, bunionectomy and bone pinning provide a portal of entry in some cases. Numerous cases have developed within 24 - 72 hours of minor non-penetrating trauma resulting in hematoma, deep bruise to the calf or even following muscle strain (87). Virus infections such as varicella and influenza have provided portals in other cases (87). In some cases the use of non-steroidal anti-inflammatory agents may have either masked the presenting symptoms or predisposed to more severe streptococcal infection and shock (87).

Most cases of StrepTSS occur sporadically, though outbreaks of severe Group A streptococcal infections have been described in closed environments such as nursing homes (2,42), and hospital environments (25,31). Each type of streptococcal infection presents with its own unique set of clinical manifestations. Thus, each type of infections will be described below in the section on specific antimicrobial treatment.

The diagnosis of GAS infection may be suspected on clinical grounds, but rests on

the

An antecedent streptococcal infection may be diagnosed by a 4-fold increase in antibody against streptolysin O (ASO), hyaluronidase, or DNAse B (56).

Anti-Phagocytic Properties: M-protein contributes to invasiveness through its ability to impede phagocytosis of streptococci by human polymorphonuclear leukocytes (PMNL) (52).

Conversely, type specific antibody against the M-protein enhances phagocytosis (52).

Following infection with a particular M-type, specific antibody confers resistance to challenge with viable GAS of that M-type (52). Recently, Boyle has shown that GAS protease cleaves the terminal portion of the M-protein, rendering the organism more susceptible to phagocytosis by normal serum but more resistant to phagocytosis in the presence of type specific antibody (72). While M types 1 and 3 strains have accounted for the vast majority of strains isolated from cases of StrepTSS, many other M types, including some non-typeable strains, have also been isolated from such cases. M types 1 and 3 are also commonly isolated from asymptomatic carriers, and patients with pharyngitis or mild scarlet fever (45,48). M echanisms of Fever Induction: Pyrogenic exotoxins induce fever in humans and animals and also participate in shock by lowering the threshold to exogenous endotoxin (77). Streptococcal pyrogenic exotoxin A (SPEA) and SPEB induce human mononuclear cells amoxicillin 300 mg to synthesize not only tumor necrosis factor- ? (TNF?) (28) but also interleukin-1? (IL-1?) (38) and interleukin-6 (IL-6) (38,62,68) suggesting that TNF could mediate the fever, shock and organ failure observed in patients with StrepTSS (87). Pyrogenic exotoxin C has been associated with mild cases of scarlet fever in the United States (author's observations) and in England (41).

The roles of two newly described pyrogenic exotoxins, SSA (60) and MF (67), in the pathogenesis of Strep TSS have not been elucidated. Cytokine Induction: There is strong evidence suggesting that SPEA, SPEB

and

concomitant

Recently, Hackett and Stevens demonstrated that SPEA induced amoxicillin prescribing information both TNF? and TNF? from mixed cultures of monocytes and lymphocytes (39), supporting the role of lymphokines (TNF?) in shock associated with strains producing SPEA. Kotb (49) has shown that a digest of M-protein type 6 can also stimulate T cell responses by this mechanism.

Interestingly, quantitation of such V? T-cell subsets in patients with acute StrepTSS demonstrated deletion rather than expansion, suggesting that perhaps the life-span of the expanded subset was shortened by a process of apoptosis (91). In addition, the subsets deleted were not specific for SPEA, SPEB, SPEC, or MF suggesting that perhaps an as yet undefined superantigen may play a role in StrepTSS (91).

Cytokine production by less exotic mechanisms may also contribute to the genesis of shock and organ failure.

Peptidoglycan, lipoteichoic acid (84) and killed organisms (37,63) are capable of inducing TNF? production by mononuclear cells in vitro (40,63,77). Exotoxins such as SLO are also potent inducers of TNF? and IL-1?. SPEB, a proteinase precursor, has the ability to cleave pre-IL-1? to release preformed IL-1? (46).

Finally, SLO and SPEA together have additive

effects

Finally, a cysteine protease formed from cleavage of SPEB may play an important role in

pathogenesis

release

The mere presence of virulence factors, such as M-protein or pyrogenic exotoxins, may be less important in Strep TSS than the dynamics of their production in vivo.

For example, Chaussee et al (11) have demonstrated that among strains from patients with necrotizing fasciitis and StrepTSS, 40% and 75% produced SPEA or SPEB, respectively. In addition, the quantity of SPEA but not SPEB was higher for strains from Strep TSS patients compared to non invasive cases (11). Recently,

Cleary

Multi-locus enzyme electrophoresis demonstrates two patterns that correspond to M-1 and M-3 type organisms which produce pyrogenic exotoxin A, a finding that fits epidemiologic studies implicating these strains in invasive GAS infections (64) in the United States.

P athogenic Mechanisms in Acute Rheumatic Fever: The pathogenesis of acute rheumatic fever involves an intimate interplay between streptococcal virulence factors and the susceptible host.

That T cells play an integral role was demonstrated by obtaining T-cell clones from valvular tissue of patients with rheumatic fever and then showing that these clones were responsive to specific epitopes of type 5 M-protein (35).

That B-lymphocytes play an important role is suggested by the demonstration that antibodies raised against particular M-protein digests cross react with cardiac tissue including myosin and endothelium (71). Interestingly anti-myosin antibodies also react strongly to cardiac endothelium (36). Thus, as antibody against M-protein develops in a patient with antecedent Group A streptococcal pharyngitis, antibody could fix complement, thereby damaging and activating the endothelium yielding cytokines and chemokines which attract and activate T-lymphocytes.

Thus, molecular mimicry between specific epitopes on M-protein and cardiac tissue results in damage to endothelium on the heart valve mediated by specific B and T-lymphocytes.

P ost Streptococcal Glomerulonephritis: It is clear that only certain strains of streptococci are capable of causing post-streptococcal glomerulonephritis. The best hypothesis at the present time is that proteins with unique antigenic determinants produced only by Anephritogenic strains, intercalate into the lipid bilayer of the glomerular basement membrane during the course of pharyngitis or impetigo. Recent studies suggest that streptokinase, which has certain lipophilic regions may be the streptococcal virulence factor responsible. Once streptokinase is membrane bound, complement is activated directly. Further glomerulus-bound streptokinase interacts with circulating anti-streptococcal antibodies, resulting in further complement fixation and glomerular damage (66). Susceptibilities for commonly used antibiotics in the treatment of GAS are presented in Table 1. Susceptibilities from Coonan and Kaplan's study were obtained from 282 pharyn­geal isolates along with 43 isolates from severe or invasive group A streptococcal disease (18).

No in vitro susceptibility testing has been undertaken to investigate whether combinations of antibiotic may exert an additive, synergistic or antagonistic effect against GAS. Despite possible changes in virulence, group A streptococci have universally remained susceptible to penicillin since its introduction. This is of considerable interest, since other strep­tococci have developed multiple antibiotic resistance, and higher concentrations of penicillin are currently required to in­hibit pneumococcus. Penicillin is still considered first-line therapy in the treatment of most GAS infections despite a recognized increase in microbiologic failure rates.

Eryth­romycin has been the antibiotic of choice in the penicillin-­allergic child for most GAS infections, yet impressive emergence of resistance has been documented on three continents during the last 30 years (57,58,75). Thus, antibiotic treatment of GAS infections in general will likely become much more complex. G AS Pharyngitis: GAS infections of the pharynx are the most common bacterial infections of childhood. Treatment of GAS pharyngitis is primarily aimed at preventing non-suppurative (in particular, rheumatic fever) and suppurative complications.

The drug of choice remains penicillin VK , 25 to 50 mg/kg/day in 4 divided doses for children, or 250 to 500 mg per dose, 4 times/day for adults.

demonstrated that twice-a-day dosing of penicillin was as effective as three-times-a-day dosing (34). Treatment with penicillin should be continued for 10 days since shorter courses of penicillin have shown decreased efficacy.

A clinical response is generally obtained within 24 h of beginning therapy, and most children have a negative throat culture by 48 h and can return to school at that time. Persistence of symptoms beyond this period suggests development of a suppurative complication of GAS, a lack of compliance, or the presence of another underlying disease. A single injection of 1.2 million units of penicillin G benzathine given intramuscularly is as effective as enteral penicillin (4) and was the long-time gold standard in treatment of GAS pharyngitis. It can provide bactericidal levels against GAS for as long as 28 days. Children who weigh less than 140 pounds (64 kg) should receive an intramuscular injection composed of 900,000 units of benzathine penicillin G and 300,000 units of procaine penicillin G.