Amoxicillin for gastroenteritis

In 1994, an epidemic of related invasive infections occurred in Wannamingo, Minnesota (16) with an annualized prevalence of 24 cases per 100,000 population.

In Missoula, Montana in 1999, the incidence of invasive infections reached 30 cases per 100,000 population.

In addition to community-based infections, invasive Group A streptococcal infections have also been described in hospitals, convalescent centers and among hospital employees and family contacts of patients with invasive infections (11,25,31). Some of these studies have documented the same M-type and identical RFLP patterns in strains from primary and index cases (11,25,31,44).

In addition, carriage of Group A streptococcus by healthcare personnel has been associated with the spread of life threatening Group A streptococcal infections in the obstetrics/gynecology and ear-nose-throat wards of American hospitals (1). Such infections have also originated in outpatient surgical settings and within the home environment.

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 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recent surgical wounds and childbirth (author's unpublished observations); 3.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 A streptococcus causing the index case; and 4.

absence of neutralizing antibody against pyrogenic exotoxin A or B (59).

The

portals

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, 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

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 demonstration of the organism in samples of pharyngeal exudates, blood, tissue, or body fluids using criteria described under Microbiology above. Rapid strep tests have proven useful for the office diagnosis of streptococcal pharyngitis, though the specificity and sensitivity vary widely (reviewed in (76)).

A negative rapid strep test should be followed with a pharyngeal culture.

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 to synthesize not only tumor necrosis factor- ? (TNF?) (28) but also interleukin-1? (IL-1?) (38)

and