Exposure to air pollution and scarlet fever resurgence in China: a six-year surveillance study.

Scarlet fever has resurged in China starting in 2011, and the environment is one of the potential reasons. Nationwide data on 655,039 scarlet fever cases and six air pollutants were retrieved. Exposure risks were evaluated by multivariate distributed lag nonlinear models and a meta-regression model. We show that the average incidence in 2011-2018 was twice that in 2004-2010 [RR = 2.30 (4.40 vs. 1.91), 95% CI: 2.29-2.31; p < 0.001] and generally lower in the summer and winter holiday (p = 0.005). A low to moderate correlation was seen between scarlet fever and monthly NO2 (r = 0.21) and O3 (r = 0.11). A 10 µg/m3 increase of NO2 and O3 was significantly associated with scarlet fever, with a cumulative RR of 1.06 (95% CI: 1.02-1.10) and 1.04 (95% CI: 1.01-1.07), respectively, at a lag of 0 to 15 months. In conclusion, long-term exposure to ambient NO2 and O3 may be associated with an increased risk of scarlet fever incidence, but direct causality is not established.

The Association between Environmental Factors and Scarlet Fever Incidence in Beijing Region: Using GIS and Spatial Regression Models.

(1) Background: Evidence regarding scarlet fever and its relationship with meteorological, including air pollution factors, is not very available. This study aimed to examine the relationship between ambient air pollutants and meteorological factors with scarlet fever occurrence in Beijing, China. (2) Methods: A retrospective ecological study was carried out to distinguish the epidemic characteristics of scarlet fever incidence in Beijing districts from 2013 to 2014. Daily incidence and corresponding air pollutant and meteorological data were used to develop the model. Global Moran's I statistic and Anselin's local Moran's I (LISA) were applied to detect the spatial autocorrelation (spatial dependency) and clusters of scarlet fever incidence. The spatial lag model (SLM) and spatial error model (SEM) including ordinary least squares (OLS) models were then applied to probe the association between scarlet fever incidence and meteorological including air pollution factors. (3) Results: Among the 5491 cases, more than half (62%) were male, and more than one-third (37.8%) were female, with the annual average incidence rate 14.64 per 100,000 population. Spatial autocorrelation analysis exhibited the existence of spatial dependence; therefore, we applied spatial regression models. After comparing the values of R-square, log-likelihood and the Akaike information criterion (AIC) among the three models, the OLS model (R² = 0.0741, log likelihood = -1819.69, AIC = 3665.38), SLM (R² = 0.0786, log likelihood = -1819.04, AIC = 3665.08) and SEM (R² = 0.0743, log likelihood = -1819.67, AIC = 3665.36), identified that the spatial lag model (SLM) was best for model fit for the regression model. There was a positive significant association between nitrogen oxide (p = 0.027), rainfall (p = 0.036) and sunshine hour (p = 0.048), while the relative humidity (p = 0.034) had an adverse association with scarlet fever incidence in SLM. (4) Conclusions: Our findings indicated that meteorological, as well as air pollutant factors may increase the incidence of scarlet fever; these findings may help to guide scarlet fever control programs and targeting the intervention.

Snippets from the past: is Flint, Michigan, the birthplace of the case-control study?

In the summer of 1924, an outbreak of scarlet fever occurred in Flint, Michigan. Unable to trace it to the usual causes, particularly fresh milk, the Michigan Department of Health used a novel approach to disentangle the enigma: The 116 cases of scarlet fever were compared with 117 "controls" selected from neighbors of the quarantined cases and from patients at the City Health Center who had been treated for ailments unrelated to scarlet fever. The extraordinary culprit was ice cream, which had a frequent/occasional/none consumption prevalence of 60%, 34%, and 6% among the cases and 24%, 51%, and 25% among the controls, respectively. The 1925 report reads, "Detailed epidemiological investigation, by means of case histories and control histories on well persons, confirmed early suspicions and established the fact that the epidemic was spread by ice cream" (Am J Hyg. 1925;5(5):669-681). This forgotten epidemiologic study is the oldest study using the case-control design to have been resurrected thus far. The case-control study design may have been conceived simultaneously, but independently and for different purposes, in England (Janet Lane-Claypon's 1926 report on the determinants of breast cancer) and the United States.

Patrón de resistencia del staphylococcus aureus a oxacilina en cultivos de muestras de secreción de partes blandas en el Hospital Patrocinio Peñuela Ruíz, San Cristóbal-estado Táchira desde 1998-2006 / Resistance pattern of the staphylococcus aureus to oxacilina in cultures of samples of secretion of soft tissue: Hospital Patrocinio Peñuela Ruíz San Cristóbal, state-Táchira 1998-2006

El Staphylococcus aureus es una bacteria ampliamente difundida que ha emergido en las últimas cuatro décadascausante de una gran variedad de enfermedades que van desde leves infecciones en piel pasando por casos de Escarlatina y Síndrome de Piel Escarlatina hasta llegar al terrible Síndrome de Shock Toxico Stafilococico (SSTS). Existe un rápido aumento a nivel mundial en el número de bacterias resistentes a antibióticos; debido al uso excesivo o mal uso de antibióticos. El objetivo de este trabajo fue estudiar la resistencia del Staphylococcus aureus (SA) a algunos antimicrobianos; provenientes de cultivos obtenidos durante el período 1998-2006. Los datos se obtuvieron del Departamento de Microbiología del Hospital Patrocinio Peñuela Ruíz de San Cristóbal Estado Táchira; sólo se tomaron aquellos cultivos realizados en secreciones de lesiones de partes blandas, independientemente de la condición de base del paciente. Mediante disco de difusión se evaluó la resistencia de la bacteria a los siguientes antibióticos: oxacilina, clindamicina y vancomicina. Los resultados fueron consignados en una ficha organizada por año y edad. Analizamos 216 muestras y cada año se evidenció la resistencia a la oxacilina con un aumento progresivo d ela misma, paralelamente se evidencio un incremento de la resistencia a la clindamicina usando como medicamento alterno en caso de resistencia axacilina. se observó que un 75 por ciento se debió a abscesos en piel, en lo que respecta a la edad es relevante la resistencia a oxacilina con 20,83 por ciento en emnores de 15 años. Su importancia clínica radica no sólo en la multiresistencia sino en el potencial patogénico, favorecido por factores tales como hacinamiento, mala higiene y presencia de abrasiones en piel.

Tonsillopharyngitis: clinical highlights.

Tonsillopharyngitis is an extremely common infection seen in adults and children. Although the symptoms and signs of this disease are usually sufficient to make a diagnosis, it is often difficult to make a distinction between bacterial and viral etiology on clinical grounds alone. The complications of tonsillopharyngitis may be classified into suppurative and nonsuppurative complications. The nonsuppurative complications include scarlet fever, acute rheumatic fever, and post-streptococcal glomerulonephritis. Suppurative complications include peritonsillar, parapharyngeal, and retropharyngeal cellulites and/or abscess. Features suggestive of viral bacterial (GABHS) etiologies, the medical and surgical guidelines for managing tonsillopharyngitis, and its complications are highlighted in this article.

Penicillin for acute sore throat in children: randomised, double blind trial.

OBJECTIVE: To assess the effectiveness of penicillin for three days and treatment for seven days compared with placebo in resolving symptoms in children with sore throat. DESIGN: Randomised, double blind, placebo controlled trial. SETTING: 43 family practices in the Netherlands. PARTICIPANTS: 156 children aged 4-15 who had a sore throat for less than seven days and at least two of the four Centor criteria (history of fever, absence of cough, swollen tender anterior cervical lymph nodes, and tonsillar exudate). Interventions Patients were randomly assigned to penicillin for seven days, penicillin for three days followed by placebo for four days, or placebo for seven days. MAIN OUTCOME MEASURES: Duration of symptoms, mean consumption of analgesics, number of days of absence from school, occurrence of streptococcal sequelae, eradication of the initial pathogen, and recurrences of sore throat after six months. RESULTS: Penicillin treatment was not more beneficial than placebo in resolving symptoms of sore throat, neither in the total group nor in the 96 children with group A streptococci. In the groups randomised to seven days of penicillin, three days of penicillin, or placebo, one, two, and eight children, respectively, experienced a streptococcal sequela. CONCLUSION: Penicillin treatment had no beneficial effect in children with sore throat on the average duration of symptoms. Penicillin may, however, reduce streptococcal sequelae.

Reactivity of rheumatic fever and scarlet fever patients' sera with group A streptococcal M protein, cardiac myosin, and cardiac tropomyosin: a retrospective study.

Archived sera (collected in 1946) from acute rheumatic fever (ARF) and untreated scarlet fever and/or pharyngitis patients were reacted with streptococcal M protein, cardiac myosin, and cardiac tropomyosin. Except for very low levels to tropomyosin, antibodies to other antigens were not elevated in the sera of ARF patients relative to those of non-ARF patients, even though there was roughly equivalent exposure to group A streptococci. This suggests that antibodies to these molecules may not play a central role in the induction of ARF.

Immunohistochemical and serological evidence for the role of streptococcal proteinase in acute post-streptococcal glomerulonephritis.

BACKGROUND: We have previously demonstrated the preferential secretion of streptococcal proteinase or streptococcal pyrogenic exotoxin B (SPEB) by nephritic strains of Group A streptococci isolated from the skin or throat of patients with acute poststreptococcal glomerulonephritis (APSGN). METHODS: To further explore the possible role of SPEB in APSGN, we performed ELISA studies to detect anti-SPEB antibodies in the sera of patients with APSGN, acute rheumatic fever (ARF), scarlet fever (SF) and normal children. Using ELISA, anti-SPEB titers on acute and convalescent APSGN sera were measured to determine immunity to APSGN. We also performed immunofluorescence studies on APSGN and non-APSGN kidney biopsies to probe for the presence and localization of SPEB. RESULTS: Our data show that anti-SPEB antibodies are present in APSGN sera and antibody titers are significantly higher than in ARF, SF and normal sera. Anti-SPEB titers tend to rise acutely and decrease with time but do not reach baseline after one year. When kidney biopsies were probed with rabbit anti-SPEB antibody, 12 of 18 (67%) of the APSGN cases were positive while only 4 of 25 (16%) of the non-APSGN cases were positive. CONCLUSIONS: In summary, we were able to demonstrate unique reactivity to SPEB in human sera and kidney biopsies of APSGN suggesting a significant role of this toxin in the pathogenesis of acute post-streptococcal glomerulonephritis.

Epidemic streptococcal disease among Army trainees, July 1989 through June 1991.

Outbreaks of group A streptococcal infection occurred at four of seven US Army basic training installations between 1 July 1989 and 30 June 1991. Study data were collected through a respiratory disease surveillance program and on-site epidemiologic investigations. Although hospitalizations were frequent (range, 191-334) during each outbreak, average rates of hospitalization were low (2.4-4.8 hospitalizations/1000 trainees/week). Outbreak-associated morbidity included streptococcal toxic shock syndrome (2 cases, 1 fatal), acute rheumatic fever (6), acute glomerulonephritis (1), scarlet fever (1), and numerous other invasive sequelae. Four serotypes of Streptococcus pyogenes (M-1, -3, -5, and -18) were identified; M-18 caused significant disease at 2 installations. Disease control was rapidly achieved through prophylaxis programs using benzathine penicillin G in nonallergic trainees. These outbreaks extend other reports that document an evolution of the nature and severity of circulating S. pyogenes in the United States.

Hypothesis--the natural selection of psoriasis.

The high genetic frequency of some inherited disorders may in part be related to a survival advantage conferred against an environmental hazard. Psoriasis is an inherited disorder which is common amongst populations of northern latitudes. Cutaneous delayed-type hypersensitivity response to streptococcal antigen is altered in such patients with a decrease in induration and erythema. Scarlet fever has until recently been associated with a high childhood mortality, the pathogenesis of which is related to interdependent primary toxicity and secondary toxicity (including delayed-type hypersensitivity) to streptococcal antigen (erythrogenic toxin), leading to cellular damage and potentially lethal shock. Streptococcal infection, usually presenting as pharyngitis, is a classical trigger for both scarlet fever and psoriasis. Individual susceptibility to scarlet fever has been clinically assessed in the past by the Dick test--an intradermal injection of the filtrate of a broth culture of scarlatina-producing strains of Streptococcus giving an erythematous reaction at 24-48 h (Dick-positive). The degree of reaction is directly related to susceptibility to scarlet fever. The severity of and mortality from scarlet fever may be ameliorated by immunological mechanisms also found in psoriatic patients. The high prevalence of psoriasis amongst some populations today may be related to such a protective factor.

Group C beta-hemolytic streptococci causing pharyngitis and scarlet fever.

After a young woman had scarlet fever associated with group C beta-hemolytic streptococcal pharyngitis, we reviewed all cases of pharyngitis treated at a student health clinic during that semester. From 541 cases of pharyngitis, 34 cultures yielded group C Streptococcus. The patients who harbored group C organisms were similar to the patients with group A streptococcal pharyngitis in the presence of fever, exudate, and cervical adenopathy. The severity of symptoms and the demonstration of scarlet fever developing from infection with this organism supports antibiotic treatment of patients with group C streptococcal pharyngitis.

Cutaneous manifestations of bacterial sepsis.

In short, bacterial sepsis is associated with a number of peripheral manifestations involving the skin and soft tissues. The pathogenesis of the lesions observed is not fully understood and is almost certainly multifactorial. In ecthyma gangrenosum, the presence of large numbers of gram-negative bacilli in the walls of small blood vessels without a substantial inflammatory response suggests that either the bacteria themselves or bacterial products are responsible for tissue damage. Endotoxin probably plays a prominent role in producing these lesions. That Pseudomonas and Aeromonas species seem to cause ecthyma out of proportion to their prevalence as a cause of bacteremia might suggest that the endotoxin of these organisms has a special predilection for skin and subcutaneous structures. More likely, it indicates that other bacterial substances, such as exotoxins or proteases, are involved. The absence of PMN leukocytes is thought to play a permissive role, allowing unopposed bacterial proliferation. Lesions of symmetric peripheral gangrene characteristically do not have bacteria present. The presence of intravascular fibrin accumulation probably resembles the generalized Shwartzman phenomenon. However, the gangrenous lesions themselves more likely result from systemic hypotension and the resulting hypoperfusion of the tissues than from vessel obstruction. In lesions associated with vigorous inflammatory response, bacterial products may damage tissue either directly or by attracting leukocytes that, in turn, release substances that cause further tissue damage. An etiologic role for endotoxin or the gram-positive bacterial cell wall is likely, since endotoxin is known to produce similar lesions in the localized Shwartzman reaction. Favoring a role for other bacterial substances is the predisposition of V. vulnificus to cause cellulitis or of C. fetus to cause inflammation of the major vessels during sepsis; the mechanisms for these reactions are entirely unknown. It is interesting that in most instances in which peripheral lesions are caused by sepsis, either a large number of bacteria or an intense inflammatory response by PMNs is present, but not both. In both kinds of lesion, the tendency to involve blood vessels by different pathogenetic mechanisms contributes to the evolution of the disease process. In intensely inflamed lesions, veins and arteries can be shown histologically to be occluded. In the absence of inflammation, bacterial invasion of vessel walls or simply the presence of bacterial products adjacent to the vessel may produce spasm. As noted, the pathogenetic significance of thrombosis observed in the lesions of DIC remains unclear.(ABSTRACT TRUNCATED AT 400 WORDS)

Septic scarlet fever due to Streptococcus pyogenes cellulitis.

We report three cases of septic scarlet fever due to Streptococcus pyogenes Group A (serotype M1/T1/OF-) cellulitis in healthy young adults. Despite prompt treatment two of the patients died. Such cases of cellulitis associated with scarlet fever, severe toxaemia and septicaemia have not been reported in the post-antibiotic era.