This property (model is completely agnostic about further extensions) makes our model extremely flexible in dealing with diverse customer behaviors observed across multiple contexts and platforms

How to delete all files before a certain date in Linux

If you have a list of files, but you only want to delete files older the a certain date, for example, a maildir folder with 5 years worth of email, and you want to delete everything older then 2 years, then run the following command.

find . -type f -mtime +XXX -maxdepth 1 -exec rm {} \;

-maxdepth 1 – this means it will not go into sub folders of the working directory

The original definition did not specify the pathogens that were accepted as causes of reactive arthritis, and, in 1999, a panel of experts determined a specific list of gastrointestinal and urogenital pathogens that could be considered causative [2]. These included Chlamydia trachomatis, Yersinia, Salmonella, Shigella, and Campylobacter [2]. Escherichia coli, Clostridioides difficile, and Chlamydia pneumoniae have since been added to the list [3-7]. Other rare, infectious agents have been linked to reactive arthritis, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [8,9].

Reactive arthritis triggered by a sexually transmitted infection is also referred to as sexually acquired reactive arthritis (SARA) [ 10].

Two major clinical features that characterize reactive arthritis were identified [2]:

● An interval ranging from several days to weeks between the antecedent infection and arthritis

● A typically mono- or oligoarticular pattern of the arthritis, often involving the lower extremities, and sometimes associated with dactylitis and enthesitis

The term "reactive arthritis" has sometimes been used historically to refer to the clinical triad of postinfectious arthritis, urethritis, and conjunctivitis, which was formerly called Reiter syndrome [13,14]. However, these patients represent only a subset of patients with reactive arthritis [13,15].

A 2024 systematic review and meta-analysis found that the incidence of reactive arthritis following infection with Campylobacter, Escherichia, Salmonella, Shigella, and Yersinia was estimated as 3, 1, 4, 1 and 5 per 100 patients, respectively [18].

In a 2016 systematic literature review, the rate of chlamydia-induced arthritis has been estimated to be 3 to 8 percent, although most of the infections are asymptomatic [ 19].

The onset of reactive arthritis is usually acute. Patients typically present with an asymmetric oligoarthritis, usually one to four weeks following the inciting infection [2,6,11,12,25].The extent of the interval between infection and the onset of arthritis considered consistent with a reactive arthritis by expert consensus is a minimum of several days and a maximum of several weeks [2]. In particular, in Chlamydia-induced reactive arthritis, this may take up to four weeks [6].

In at least half of patients, all symptoms resolve in less than six months [ 26]; in most patients, symptoms resolve within one year.

The several types of clinical manifestations of reactive arthritis include:

● Symptoms of preceding enteric or genitourinary infection (see 'Preceding infection' below)

● Axial and/or peripheral musculoskeletal signs and symptoms (see 'Musculoskeletal signs and symptoms' below)

● Extraarticular signs and symptoms (see 'Extramusculoskeletal signs and symptoms' below)

Other than those symptoms due to the infection that has triggered the arthritis, the articular and extraarticular manifestations are similar regardless of the particular enteric or genitourinary organism or species of organism causing the disorder [27].

Although a large variety of pathogens, including streptococcus, have been described that may induce musculoskeletal symptoms, an arthritis is conventionally considered to be a reactive arthritis only if some of the typical musculoskeletal features occur (see 'Musculoskeletal signs and symptoms' below). Not infrequently, patients do not volunteer the history of infection until asked about this specifically, since most patients are not aware that the infections can be related to arthritis.

Peripheral arthritis – The typical picture of peripheral arthritis, seen in rheumatology clinics, is an acute-onset asymmetric oligoarthritis, often affecting the lower extremities, especially the knees [35] (picture 1). However, about 50 percent of patients have arthritis in the upper extremities, and some have polyarthritis in the small joints [33]. By convention, the minority of patients with arthritis that does not resolve within six months is defined as having chronic reactive arthritis.

Enthesitis – The enthesis is the site of insertion of ligaments, tendons, joint capsule, or fascia to bone; enthesitis (or enthesopathy), the term for inflammation around the enthesis, can occur in patients with reactive arthritis and other forms of spondyloarthritis (SpA). Swelling at the heels is among the most characteristic symptom of enthesitis. Common sites of heel involvement are at the insertions of the Achilles tendon and of the plantar fascia on the calcaneus. Pain, swelling, and local tenderness are suggestive clinical features. Estimates of the frequency of enthesitis in patients with reactive arthritis have ranged from 20 to 90 percent [33,36-39].

In one study in the US of patients with documented enteric infections and a symptom of reactive arthritis, enthesitis was more common than arthritis or inflammatory back pain, occurring in 89 percent of patients [33,36].

Dactylitis – Some patients also develop dactylitis, which typically presents as sausage digits (picture 2) [40]. The frequency of dactylitis in patients with chlamydia-induced reactive arthritis may be as high as 40 percent [34].

Axial signs and symptoms – Inflammatory low back pain is frequent as an accompanying symptom, but seldom as the only presenting symptom [34,36]. Inflammation in the spine or at the sacroiliac joints may be seen [41].

Inflammatory synovitis — The findings in synovial fluid are nonspecific and are characteristic of inflammatory arthritis, with elevated leukocyte counts, predominantly neutrophils. White blood cell (WBC) counts are typically between 2000 and 64,000 WBC per mm³ [11].

In hospital-based studies with more severely affected patients, frequencies as high as 60 to 80 percent have been reported [51]; however, estimates in population-based studies and analyses of disease outbreaks are generally much lower and occasionally have shown no increase in HLA-B27 prevalence compared with the general population [52]

Disseminated gonococcal infection (DGI) is estimated to occur in 0.5 to 3 percent of patients infected with N. gonorrhoeae [1-3].

Certain features may be more common among patients with DGI compared with uncomplicated gonococcal infection. As an example, in a case-control study, 119 patients with DGI were on average older (42 versus 29 years), less likely to be a male who has sex with only males (7 versus 31 percent), less likely to have been diagnosed with a bacterial sexually transmitted infection in the prior year (12 versus 38 percent), and more likely to report substance use (34 versus 5 percent) compared with 357 patients with uncomplicated gonococcal infection [4]. In this study, living with HIV infection was not associated with DGI.

A history of recent symptomatic genital infection is uncommon in individuals with disseminated gonococcal infection (DGI); asymptomatic mucosal infection is thought to increase the risk of dissemination due to delayed diagnosis, resulting in delays in antibiotic treatment [8,9]

The immunopathogenesis of DGI is uncertain. The hypothesis that inflammation rather than direct microbial invasion causes the clinical findings of DGI is supported by the frequent lack of N. gonorrhoeae growth from blood, skin, and synovial fluid cultures during disseminated infection (see 'Laboratory and microbiologic testing' below)

Fastidious growth requirements of N. gonorrhoeae could explain the sterile cultures, and more sensitive testing methods (such as immunofluorescence or molecular techniques) have identified organisms in synovial and skin samples that were culture negative [58-62].

Nevertheless, persistent synovitis in DGI can occur in culture and PCR-negative joints, and organisms can often be cultured from the genitourinary tract or other local sites in most cases of DGI, despite negative cultures elsewhere [ 63,64]. Thus, the sterile synovitis, tenosynovitis, and dermatitis associated with DGI may not always require viable N. gonorrhoeae, and other inflammatory mechanisms may be important.

Immune complex deposition may play a role; however, studies attempting to identify immune complexes among patients with DGI report conflicting results [65-67]. The observation that N. gonorrhoeae cell wall components can induce inflammation and arthritis in animal studies also supports an immune component to DGI [68]. Components of the cell wall and membrane stimulate the immune response and may remain as soluble factors that perpetuate inflammatory mediators with the potential to combat the infection and damage protective mucosa, perhaps facilitating bacterial invasion and dissemination [69].

Most patients with disseminated gonococcal infection (DGI) report feeling well up to the onset of the illness. Upon presentation, a range of clinical findings associated with DGI has been described (table 1) [8,70]. Those can be divided into two groups:

● A triad of tenosynovitis, dermatitis, and polyarthralgia without purulent arthritis (also called the "arthritis-dermatitis syndrome"). Those findings occur frequently in patients with DGI [9]. (See 'Tenosynovitis, dermatitis, polyarthralgia (also called arthritis-dermatitis syndrome)' below.)

● Purulent arthritis with or without associated findings. Fewer than 50 percent of patients with DGI present with actual arthritis [9]. (See 'Purulent arthritis' below.)

Those two classic forms may represent a spectrum of DGI [71]. Most patients who develop suppurative arthritis have not had preceding polyarthralgia or skin lesions, although patients with the polyarthralgia syndrome can develop purulent arthritis later in the disease course if not recognized and treated [14]

Tenosynovitis, dermatitis, polyarthralgia (also called arthritis-dermatitis syndrome) — This form of DGI generally occurs within two to three weeks of the primary infection and is characterized by the following features [8,82]:

● Fever, chills, and generalized malaise – These occur in the acute phase of infection. Fever may spontaneously disappear or diminish in magnitude as the disorder progresses, and so is not uniformly observed. As an example, in a study of 112 women with DGI, approximately 60 percent had a temperature >100.4°F (>38°C) on presentation [70].

● Polyarthralgia – This can involve small or large joints. Several joints can be affected, but symmetric joint involvement is uncommon. A distinguishing feature is the migratory nature of the arthralgias compared with other causes of septic arthritis [8,83].

● Tenosynovitis – This is a relatively common finding that is unique to DGI and is unusual in other forms of infectious arthritis [8,83]. It often involves multiple tendons simultaneously, particularly at the wrist, fingers, ankle, and toes [83]. (See "Infectious tenosynovitis", section on 'Clinical manifestations'.)

● Dermatitis – Skin findings are common and occur in approximately 75 percent of cases [14]. Typical lesions are painless, and patients may be unaware of them. Lesions are usually pustular or vesiculopustular (picture 1 and picture 2 and picture 3) [84], although hemorrhagic macules, papules, bullae, or nodules rarely occur. Rarely, patients with DGI can develop lesions that are urticarial or that resemble erythema nodosum or erythema multiforme [

...

Although Staphylococcus aureus is the most common cause of monomicrobial septic arthritis overall, among sexually active adults, N. gonorrhoeae is a particularly important consideration [90]. Nevertheless, the overall proportion of septic arthritis cases that are due to N. gonorrhoeae is low (0 to 3 percent) in various populations and geographic areas [91-95].

The possibility of disseminated gonococcal infection (DGI) should be considered in sexually active individuals (particularly those younger than 40 years, those with multiple partners, and all men who have sex with men) who present with arthralgias or joint pain concerning for septic arthritis. A low threshold for suspicion is important since not all patients will report sexual activity, and DGI has been reported in older adults [96], whom providers may assume not to be sexually active.

Accompanying skin lesions, particularly pustular or vesiculopustular lesions, and/or tenosynovitis (tenderness along the flexor sheath or pain with passive extension) should heighten suspicion for DGI.

A careful physical examination is often needed to detect the characteristic skin lesions of DGI (picture 1 and picture 2 and picture 3). Typical lesions may be mistakenly dismissed as unimportant furuncles or pimples by the patient or clinician.

Careful evaluation of the joints is also important. It is not unusual to see patients with only one or two joints that are involved. Small or large joints may be affected, and symmetric joint involvement is uncommon [85]. Tenosynovitis is often visible to the examining clinician, with redness and warmth along the tendon sheath. Its presence can usually be confirmed by eliciting pain along the tendon sheath with active or passive joint movement.

Blood cultures – At least two sets of blood cultures should be obtained. Cultures are diagnostic when positive and are also helpful in separating DGI from other conditions, such as septic arthritis due to Neisseria meningitidis or S. aureus, both of which may mimic the clinical features of DGI. The reported frequency of blood culture positivity in various case series ranges from 4 to 70 percent of cases [8,97-99]. Patients with the tenosynovitis, dermatitis, and polyarthralgia form of DGI may be more likely to have positive blood cultures, as such symptoms may reflect an earlier, bacteremic stage of disease [8,99].

Patients with the clinical features of DGI should have urogenital, rectal, and pharyngeal specimens submitted for microbiologic testing for N. gonorrhoeae. Often, patients with DGI have evidence of infection at urogenital, rectal, or pharyngeal sites despite lack of symptoms at these sites [14,97]. Nucleic acid amplification testing (NAAT) is the preferred diagnostic test [100].

For those with purulent arthritis, cultures for N. gonorrhoeae may only be positive in approximately 50 percent of cases or less [8,97,98].

and the laboratory should be alerted that gonococcal infection is a consideration so that the specimen can be processed and plated appropriately.

Cultures are even less likely to be positive for those who present with the tenosynovitis, dermatitis, and polyarthralgia, even if synovial fluid can be obtained.

The mean synovial fluid leukocyte count in septic arthritis is typically around 50,000 cells/microL [101,102]; in some cases of gonococcal arthritis, however, lower counts can be observed (approximately 20,000 cells/microL) (table 2).

Parenteral therapy with ceftriaxone 1 g intravenously every 24 hours is our preferred initial regimen for DGI.

Tenosynovitis, dermatitis, polyarthralgia — Patients with the triad of tenosynovitis, dermatitis, and arthralgia or synovitis, who have small or absent joint effusions, typically respond dramatically and quickly to treatment. We agree with the United States Centers for Disease Control and Prevention guidelines to continue antibiotic therapy for at least seven days as long as the clinical signs of infection are gone or nearly gone [109]. Once initial clinical improvement with ceftriaxone 1 g daily (or one of the alternative initial therapies discussed above) is noted for 24 to 48 hours, the treatment course can be completed with intramuscular ceftriaxone (500 mg for individuals <150 kg or 1 g for individuals ≥150 kg) every 24 hours.

Alternately, in cases in which an isolate of N. gonorrhoeae has been identified and susceptibility to fluoroquinolones, penicillin, and/or tetracycline has been demonstrated, oral therapy with ciprofloxacin (500 mg twice daily), amoxicillin (500 mg four times daily), or doxycycline (100 mg twice daily) can also be used.

Purulent arthritis — We generally treat patients with purulent arthritis with intravenous ceftriaxone (or one of the alternative initial therapies discussed above) until there is good evidence of response (eg, improvement in joint pain and effusion) (see 'Initial antimicrobial therapy' above). Clinical improvement and cure of purulent arthritis often require at least 7 to 14 days of parenteral therapy. The precise duration of treatment depends on the overall health status of the patient, including the presence of an immunocompromising condition and the rate of response to therapy. A duration longer than 14 days is appropriate for those with such comorbidities or slow rate of response.

Patients with purulent arthritis should generally also undergo joint drainage. That can be accomplished either with repeated needle aspirations or arthroscopically. Open surgical or arthroscopic drainage should be utilized for patients in whom needle aspirate is not successful or adequate (as assessed by continuing effusions, leukocytosis, fever, or severe joint pain).

Patients who have more than one episode of disseminated gonococcal infection should be screened for the presence of a deficiency in one of the terminal components of complement by obtaining an assay for total hemolytic complement activity [14].