text:
Q: Google API Geocode using JavaScript error when run I am attempting to print out an address on the console log. However, when I run the code I end up getting an error stating that
{
   "error_message" : "Invalid request. Missing the 'address', 'components', 'latlng' or 'place_id' parameter.",
   "results" : [],
   "status" : "INVALID_REQUEST"
}

I use an npm module called request and am trying to simply print out the address onto the log. I've tried other addresses and keep on running into the same issue. What exactly am I missing here ?
const request = require('request');

    request({
      url: 'https://maps.googleapis.com/maps/api/geocode/json?address%20=%201301%20lombard%20street%20philadelphia',
      //json = true
    }, (error, response, body) => {
      console.log(body);
    });

The formatting seems to be correct, based on the first example given in the link https://www.npmjs.com/package/request

A: Remove the %20 (space) after address in the link :)

A: I use other Google Maps API so going try to help you.
Please use your target address in 'address=1301%20lombard%20street%20philadelphia' format
https://maps.googleapis.com/maps/api/geocode/json?address=1301%20lombard%20street%20philadelphia&key=PASTE_YOUR_API_KEY
You will need API key. Head over to : https://developers.google.com/maps/documentation/javascript/get-api-key
your response will be :
{
   "results" : [
      {
         "address_components" : [
            {
               "long_name" : "1301",
               "short_name" : "1301",
               "types" : [ "street_number" ]
            },
            {
               "long_name" : "Lombard Street",
               "short_name" : "Lombard St",
               "types" : [ "route" ]
            },
            {
               "long_name" : "Washington Square West",
               "short_name" : "Washington Square West",
               "types" : [ "neighborhood", "political" ]
            },
            {
               "long_name" : "Philadelphia",
               "short_name" : "Philadelphia",
               "types" : [ "locality", "political" ]
            },
            {
               "long_name" : "Philadelphia County",
               "short_name" : "Philadelphia County",
               "types" : [ "administrative_area_level_2", "political" ]
            },
            {
               "long_name" : "Pennsylvania",
               "short_name" : "PA",
               "types" : [ "administrative_area_level_1", "political" ]
            },
            {
               "long_name" : "United States",
               "short_name" : "US",
               "types" : [ "country", "political" ]
            },
            {
               "long_name" : "19147",
               "short_name" : "19147",
               "types" : [ "postal_code" ]
            },
            {
               "long_name" : "1003",
               "short_name" : "1003",
               "types" : [ "postal_code_suffix" ]
            }
         ],
         "formatted_address" : "1301 Lombard St, Philadelphia, PA 19147, USA",
         "geometry" : {
            "location" : {
               "lat" : 39.9444071,
               "lng" : -75.16317189999999
            },
            "location_type" : "RANGE_INTERPOLATED",
            "viewport" : {
               "northeast" : {
                  "lat" : 39.9457560802915,
                  "lng" : -75.16182291970848
               },
               "southwest" : {
                  "lat" : 39.9430581197085,
                  "lng" : -75.16452088029151
               }
            }
         },
         "place_id" : "EiwxMzAxIExvbWJhcmQgU3QsIFBoaWxhZGVscGhpYSwgUEEgMTkxNDcsIFVTQSIbEhkKFAoSCU38VoEkxsaJEedji1ij51aUEJUK",
         "types" : [ "street_address" ]
      }
   ],
   "status" : "OK"
}

redpajama_set_name: RedPajamaStackExchange


text:
Precocious pubarche is associated with SGA, prematurity, weight gain, and obesity
Community child health, public health, and epidemiology
K A Neville,
J L Walker
Department of Endocrinology, Sydney Children's Hospital, Randwick, and School of Women's & Children's Health, University of New South Wales, Sydney, Australia
Dr K A Neville
Department of Endocrinology, Sydney Children's Hospital, High St, Randwick, NSW 2031, Australia; nevilleksesahs.nsw.gov.au
Background: Perinatal stress is thought to underlie the Barker sequelae of low birth weight, of which precocious pubarche may be a manifestation.
Aims: To explore whether prematurity as well as smallness for gestational age (SGA) predisposes to precocious pubarche, and the potential role of excess weight gain during childhood.
Methods: Retrospective chart review of 89 children (79 girls) with precocious pubarche.
Results: Sixty five per cent were overweight/obese at diagnosis, compared with 19–24% of Australian children. Thirty five per cent had a history of SGA and 24% of prematurity. Weight SDS increased from birth to diagnosis in 91% of children. The mean change in weight SDS from birth to diagnosis was greater in those who were SGA (2.8, 95% CI 2.2 to 3.4) versus AGA (1.7, 95% CI 1.3 to 2.2), with no difference in the incidence of overweight/obesity. The latter was lower among children born premature (40% versus 72% term) but was associated with a mean increase in weight of 1.3 SDS during childhood. Nine out of ten girls and boys with precocious pubarche had at least one of the three risk factors studied.
Conclusions: Both prematurity and SGA were associated with precocious pubarche, as was overweight/obesity, irrespective of size or gestation at birth. Excess weight gain in childhood may predispose to precocious pubarche in susceptible individuals.
AGA, appropriate for gestational age
BA, bone age
BMI, body mass index
BW, birth weight
GA, gestational age
PI, Ponderal Index
SDS, standard deviation score
SGA, small for gestational age
http://dx.doi.org/10.1136/adc.2004.053959
The development of precocious pubarche, the appearance of sexual hair in girls under the age of 8 years and boys under the age of 9 years,1 has been linked in girls with a past history of low birth weight.2,3 Moreover, a proportion of girls with precocious pubarche have been shown to develop polycystic ovarian disease4,5 (PCOS) and hyperinsulinism,6 a predictor of later cardiovascular disease.7 Precocious pubarche therefore may form part of the spectrum of pathology associated with low birth weight, as originally elaborated in the Barker hypothesis.8 Studies based on this hypothesis have suggested that poor growth in utero or during the first year of life may be associated with permanent changes in the hormonal milieu that promote the development of hyperinsulinism,9 type 2 diabetes mellitus,10 central obesity,11 and ischaemic heart disease12,13 later in life. The underlying mechanisms proposed include activation of a stress response resulting in chronically increased secretion of CRH, ACTH, and cortisol in utero.13,14 Similar chronic activation might be expected postnatally in premature infants who are at increased risk of respiratory distress, infection, and undernutrition.
Rapid weight gain in childhood has been shown to increase the risk of ischaemic heart disease conferred by small size at birth,15 and is postulated to be an important trigger for the development of subsequent metabolic abnormalities in those with a pre-existing susceptibility. Anecdotally, precocious pubarche has been thought to be more common in children who are overweight, and recent data in French children provide evidence for this.16 Rapid weight gain in childhood might also link small size at birth and the subsequent development of precocious pubarche.
To investigate the contribution of birth size, gestational age, and childhood weight gain to the development of precocious pubarche in Australian children, we conducted a retrospective study of children diagnosed with precocious pubarche in our clinic.
A retrospective chart review was performed of all patients presenting between December 1988 and May 2001 who were coded in the database of the Endocrine Department of Sydney Children's Hospital as having precocious pubarche. Precocious pubarche was defined as the onset of sexual hair at less than 8 years for girls and 9 years for boys,1 with sufficient duration of follow up and clinical and/or laboratory data to exclude other pathology, including the development of true precocious puberty.
Eighty nine children (79 girls) were identified as having a diagnosis of precocious pubarche and included in the study. Potential adrenal pathology was excluded biochemically in 85/89 children with an adrenal hormone profile and/or ACTH stimulation test, with the diagnosis resting on clinical grounds in the remaining four. The median age of onset of precocious pubarche in girls was 6.7 years (range 2.7–8.0) and boys 8.0 years (range 5.4–8.6). Of the seven girls aged <4 years, all had adrenal pathology excluded on biochemical grounds, a median bone age (BA) advance of 0.8 years (range 0–2.3 years) and a median follow up period of 4 years (range 3.3–6.0 years). Data obtained for analysis from the patients' files included height and weight at diagnosis, gestational age (available in 84/89), birth weight (81/84), birth length (58/81), and BA (84/89).
Birth weights were expressed as a standard deviation score (SDS) and percentile for GA using recent Australian standards.17 Where a birth length was also available, a Ponderal Index (PI; weight/length3) was calculated and was classified as either above or below the 10th centile for Australian neonates.18 Because the PI relates weight to height, it may be a better indicator of nutritional constraint in utero and intrauterine growth retardation than birth weight alone.19 Children were classified as small for gestational age (SGA) if the birth weight and/or Ponderal Index were less than the 10th centile for GA. Prematurity was defined as a GA less than 37 weeks.
Weight, height, and BMI (weight/height2) at diagnosis were expressed as SDS and centiles in accordance with published data.20,21 The difference between the chronological age (CA) and BA at diagnosis was calculated. Using the BMI at diagnosis, children were defined as overweight or obese according to the recently developed and published Cole standards.22 These standards relate a child's age and sex adjusted BMI SDS to a BMI of 25 kg/m2 (overweight) or 30 kg/m2 (obese) at age 18 years and therefore allow comparison across populations and over time. Gain in weight during childhood was assessed by comparing the difference between birth weight SDS and diagnosis weight SDS.
All statistical analyses were performed using the Statistical Package for Social Sciences (SPSS Inc., Chicago, IL, version 11.0 for Windows). Anthropometric measures were expressed as either mean (95% CI) or median [range] unless otherwise indicated. Means between groups were compared by independent t tests. Categorical data were analysed using cross tabulation and the χ2 test. Pearson's correlation coefficient was used to describe the correlation between two continuous variables. Statistically significance was defined as a p value less than 0.05.
At initial presentation for precocious pubarche the group was tall with a mean height SDS of 0.8 (0.6 to 1.1), consistent with the mean bone age advance over chronological age of 0.9 years (0.7 to 1.1). The mean weight SDS was 1.7 (1.3 to 2.0; table 1). Thirty of the 89 children were overweight (33.7%) and 28/89 obese (31.4%). Fifty eight (65.1%) children were therefore overweight or obese (table 1) compared with the recently published rate of overweight/obesity in Australian children of 19–24%, defined by the same standards.23
Auxological parameters in 89 children with precocious pubarche according to their weight status, gestation, and birth weight
In the 81 children in whom a birth weight (BW) and GA were available, the mean BW SDS was −0.4 (−0.7 to −0.2) and was less than the 10th centile for GA in 17/81 (21%; table 1). A Ponderal Index could be calculated for 58/81 and was less than the 10th centile in 16/58 (28%). Twenty eight of the 81 children (35%) had a BW and/or PI less than the 10th centile and were defined as SGA (table 1).
Of 84/89 children for whom GA was available, 20 (24%) were premature, significantly higher than the rate of prematurity in New South Wales of 6.7%24 (p<0.001, one way χ2). There was no difference in the rate of SGA among those who were premature (25%) compared with those born at term (38%; p = 0.3, table 1). The incidence of overweight/obesity was significantly lower in those who were premature (40%) versus those born at term (72%; p = 0.01, table 1), although still higher than the rate of overweight/obesity in the general Australian child population (p<0.001, one way χ2).
The mean gain in weight (ΔWt) SDS from birth to diagnosis was 2.0 (1.7 to 2.4), with 90% (80/89) experiencing an increase in weight SDS. When analysed according to size at birth, there was no difference in weight SDS, BMI SDS, or incidence of overweight/obesity comparing those who were originally SGA to those who were appropriate for gestational age (AGA) (table 1). However, as by definition the mean birth weight SDS of the SGA children was lower than that of the AGA children, their "gain in weight" during childhood was significantly greater, with a mean ΔWt SDS from birth to diagnosis of 2.8 (2.2 to 3.4) versus 1.7 (1.3 to 2.2) for the AGA group (p = 0.005, table 1). The mean gain in weight SDS from birth to diagnosis in the children who were premature was significantly less than for the term group (1.3 (0.7 to 1.9) versus 2.3 (1.9 to 2.7); p = 0.02, table 1).
Seventy eight of the 89 (88%) children studied were overweight/obese and/or had a history of SGA and/or prematurity. Of the 31/89 children who were of normal weight at diagnosis, GA was recorded in 30 and birth weight +/− length in 29/30. Forty per cent (12/30) were premature and 41% (12/29) were SGA, with 67% (20/30) premature and/or SGA. Their mean gain in weight SDS from birth to diagnosis was 0.8 (0.3 to 1.2).
What is already known on this topic
Low birth weight increases the risk of a number of adult diseases, as originally postulated by the Barker hypothesis
Precocious pubarche has been associated with low birth weight and hyperinsulinism, and therefore may form part of the spectrum of disease encompassed by the Barker hypothesis
Because of the small number of boys (consistent with published sex ratios1), statistical analysis was repeated after their exclusion with similar results (data not shown). When the 10 boys with precocious pubarche were analysed separately, the rate of overweight/obesity was 80% (8/10), 30% (3/10) had a past history of prematurity, and 33% (3/9) were SGA. Only 1/10 was not overweight/obese, premature, or SGA, as was the case when boys and girls were analysed together (table 1).
Compared with published Australian standards, the children in our study with precocious pubarche had an increased incidence of overweight/obesity and an increased likelihood of having been SGA or premature, with 9/10 girls and boys presenting with at least one of these factors. The novel observation that prematurity is associated with an increased risk of precocious pubarche is consistent with the precocious pubarche being one of the sequelae of low birth weight and perinatal stress. The increase in weight SDS documented from birth to diagnosis in all groups (table 1) suggests that excess weight gain in childhood may provide the trigger for the development of precocious pubarche as is thought to be the case for other manifestations of the Barker hypothesis.
The prominence of overweight/obesity in the children studied is consistent with the postulated role for weight gain in the modulation of adrenal androgen secretion.25 The mean gain in weight during childhood of 2 SDS (table 1) in our study greatly exceeded that of 0.3 SDS shown in the ALSPAC longitudinal study of children followed from birth to 5 years.26 Sixty five per cent of the children presenting with precocious pubarche were overweight or obese, three times the rate of overweight/obesity in the Australian child population.23 The frequency of obesity (31%) we observed was similar to that recently reported in French children presenting with precocious pubarche.16 In children, the greatest increase in urinary DHEAS secretion occurs in the same year as the greatest increase in BMI,25 and in adults, experimentally induced fluctuations in weight have been shown to correlate directly with urinary adrenal androgen secretion.27,28 Insulin has been implicated in the regulation of adrenal androgen secretion in in-vitro studies.29 The increased plasma insulin concentrations and decreased insulin sensitivity associated with increasing weight may underlie the link between adrenal androgen production and body mass.
A history of SGA and/or prematurity was also more frequent among the children presenting with precocious pubarche than expected in the general Australian population,17,18,24 with 34% born SGA and 24% premature. Moreover, two thirds of the 31 children who were of normal body weight at presentation had a history of SGA and/or prematurity. Previous studies have described an association between SGA and the later development of precocious pubarche,5,6,16 but have not explored the potential effect of prematurity alone. Hormonal studies of premature infants born small or appropriate for gestational age have yielded conflicting results;30–32 however it is possible that the prenatal and/or postnatal stresses to which premature infants are subjected induce similar permanent reprogramming of the endocrine and metabolic pathways as is proposed for growth restricted infants. Of note, large population studies8,15,33,34 examining the Barker hypothesis have linked low birth weight per se with later disease, without discriminating between children born prematurely or growth retarded.
Prematurity as well as smallness for gestational age is more frequent than expected in children with precocious pubarche
Overweight/obesity is more frequent in children with precocious pubarche than in the general population
The association of precocious pubarche with SGA, prematurity, and with excess weight gain in childhood suggests that precocious pubarche may be a marker for hyperinsulinism
Weight gain during childhood may be critical to the development of precocious pubarche in susceptible individuals. Epidemiological studies suggest that in children with low birth weight, relatively small increases in weight SDS and BMI during childhood magnify the risk of metabolic and endocrine sequelae.15 In twins discordant for birth size studied in late childhood, the lower birth weight twin had higher plasma concentrations of DHEAS than the higher birth weight twin if there had been catch-up in weight SDS of a degree similar to that observed in our study.35 Although our children with a past history of prematurity had a smaller increase in weight SDS during childhood (1.2 SDS) and a lower rate of overweight/obesity (40%) than children born at term (table 1), both were higher than predicted by population studies.23,26 Even among the 20 premature and/or SGA children of normal weight at diagnosis, the median increase in weight SDS of 0.8 SD was greater than that observed in the ALSPAC study.26 Our data do not allow us to determine the independent contributions of low birth weight and increase in weight SDS during childhood to the development of precocious pubarche; however the effects of low birth weight and increased weight gain during childhood might be expected to be additive if the common underlying mechanism is hyperinsulinism. Decreased insulin sensitivity has been documented in children with a history of low birth weight36 and in girls of normal body weight with precocious pubarche,6 especially if there is a history of low birth weight.2 Moreover, a recent study37 showed that treatment with an insulin sensitiser of normal weight girls with a history of precocious pubarche and low birth weight improved body composition, decreased lipid abnormalities, and prevented progression to polycystic ovarian disease, suggesting that hyperinsulinism contributes to the pathogenesis of precocious pubarche in children of low birth weight.
A caveat to our conclusion that overweight/obesity and perinatal stress predispose to the development of precocious pubarche is the known ascertainment bias of hospital based studies.38 Children who are overweight, or have a history of other problems (for example, prematurity or SGA) may be more likely than other children to present to a hospital outpatient clinic, simply because they suffer from another condition and may have more encounters with medical practitioners leading to their referral. The relevance of the diagnosis of precocious pubarche, however, lies with whether it is a marker for something else because it is not a condition for which treatment is either required or available. The associations we observed are consistent with data suggesting that precocious pubarche may be a clinical marker for decreased insulin sensitivity, and this has implications for the counselling and follow up of affected children.
Ibanez L, Dimartino-Nardi J, Potau N, et al. Premature adrenarche—normal variant or forerunner of adult disease. Endo Rev2000;21:671–96.
Ibanez L, Potau N, Francois I, et al. Precocious pubarche, hyperinsulinism and ovarian hyperandrogenism in girls: relation to reduced fetal growth. J Clin Endocrinol Metab1998;83:3558–62.
Dimartino-Nardi J . Premature adrenarche: findings in prepubertal African-American and Caribbean-Hispanic girls. Acta Pædiatr Suppl1999;433:72–7.
Ibanez I, Potau N, deZegher F. Anovulation after precocious pubarche: early markers and time course on adolescence. J Clin Endocrinol Metab1999;84:2691–5.
Ibanez L, Potau N, Virdis R, et al. Postpubertal outcomes in girls diagnosed of premature pubarche during childhood: increased frequency of functional ovarian hyperandrogenism. J Clin Endocrinol Metab1993;76:1599–603.
Ibanez L, Potau N, Zampolli M, et al. Hyperinsulinism and decreased insulin-like growth factor binding protein-1 are common features in prepubertal and postpubertal girls with a history of premature pubarche. J Clin Endocrinol Metab1997;82:2283–8.
Isomaa B, Almgren P, Tuomi T, et al. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care2001;24:683–9.
Barker DJP. Fetal origins of coronary heart disease. BMJ1995;311:171–4.
Phillips DIW, Barker DJP, Hales CN, et al. Thinness at birth and insulin resistance in adult life. Diabetologia1994;37:150–4.
McKeigue PM, Leon DA, Berglund L, et al. Relationship of birthweight and ponderal index to non-insulin dependent diabetes and insulin response to glucose challenge in men aged 50–60 years. Diabet Med1994;11 (suppl 17) :S17.
Law CM, Barker DJ, Osmond C, et al. Early growth and abdominal fatness in adult life. J Epidemiol Community Health1992;46:184–6.
Barker DJ, Winter PD, Osmond C, et al. Weight in infancy and death from ischaemic heart disease. Lancet1989;2:577–80.
Barker DJ, Gluckman PD, Godfrey KM, et al. Fetal nutrition and cardiovascular disease in adult life. Lancet1993;341:938–41.
Goland RS, Jozak S, Warren WB, et al. Elevated levels of umbilical cord plasma corticotropin-releasing hormone in growth-retarded fetuses. J Clin Endocrinol Metab1993;77:1174–9.
Erikkson JG, Forsén T, Tuomilehto J, et al. Early growth and coronary heart disease in later life: longitudinal study. BMJ2001;322:949–53.
Charkaluk ML, Trivin C, Brauner R. Premature pubarche as an indicator of how body weight influences the onset of adrenarche. Eur J Pediatr2004;163:89–93.
Beeby PJ, Bhutap T, Taylor LK. New South Wales population-based birthweight percentile charts. J Paediatr Child Health1996;32:512–18.
Guaran RL, Wein P, Sheedy M, et al. Update of growth percentile for infants born in an Australian population. Aust N Z Obstet Gynaecol1994;34:39–50.
Fay RA, Dey PL, Saadie CM, et al. Ponderal index: a better definition of the 'at risk' group with intrauterine growth problems than birth-weight for gestational age in term infants. Aust N Z J Obstet Gynaecol1991;31:17–19.
Hamill PV, Drizd TA, Johnson CL, et al. Physical growth: National Center for Health Statistics percentiles. Am J Clin Nutr1979;32:607–29.
Rolland-Cachera MF, Cole TJ, Sempe M, et al. Body mass index variations; centiles from birth to 87 years. Eur J Clin Nutr1991;45:13–21.
Cole TJ, Bellizzi MC, Flegal KM, et al. Establishing a standard definition for childhood overweight and obesity worldwide: international survey. BMJ2000;320:1240–3.
Booth ML, Wake M, Armstrong T, et al. The epidemiology of overweight and obesity among Australian children and adolescents, 1995–97. Aust N Z J Public Health2001;25:162–9.
NSW Department of Health. New South Wales Mothers and Babies 2000. NSW Public Health Bulletin Supplement 2001;12:S3.
Remer T, Manz F. Role of nutritional status in the regulation of adrenarche. J Clin Endocrinol Metab1999;84:3936–44.
Ong KKL, Ahmed ML, Emmett PM, et al. Association between postnatal catch-up growth and obesity in childhood: prospective cohort study. BMJ2000;320:967–71.
Forbes GB, Brown MR, Welle SL, et al. Hormonal response to overfeeding. Am J Clin Nutr1989;49:608–11.
Hendrikx A, Heyns W, de Moor P. Influence of a low-calorie diet and fasting on the metabolism of dehydroepiandrosterone sulfate in adult obese subjects. J Clin Endocrinol1968;28:1525–33.
Hines GA, Smith ER, Azziz R. Influence of insulin and testosterone in adrenocortical steroidogenesis in vitro; preliminary studies. Fertility and Sterility2001;76:730–5.
Turnipseed MR, Bentley K, Reynolds JW. Serum dehydroepiandrosterone sulfate in premature infants and infants with intrauterine growth retardation. J Clin Endocrinol Metab1976;43:1219–25.
Lee MM, Rajagopalan L, Berg GJ, et al. Serum adrenal steroid concentrations in premature infants. J Clin Endocrinol Metab1989;69:1133–6.
Kari MA, Raivio KO, Stenman UH, et al. Serum cortisol, dehydroepiandrosterone sulfate, and steroid-binding globulins in preterm neonates: effect of gestational age and dexamethasone therapy. Pediatr Res1996;40:319–24.
Stein CE, Fall CH, Kumaran K, et al. Fetal growth and coronary heart disease in south India. Lancet1996;348:1269–73.
Rich-Edwards JW, Stampfer MJ, Manson JE, et al. Birth weight and risk of cardiovascular disease in a cohort of women followed up since 1976. BMJ1997;315:396–400.
Francois I, deZegher F. Adrenarche and fetal growth. Pediatr Res1997;41:440–2.
Hofman PL, Cutfield WS, Robinson EM, et al. Insulin resistance in short children with intrauterine growth retardation. J Clin Endocrinol Metab1997;82:402–6.
Ibanez L, Ferrer A, Ong K, et al. Insulin sensitization early after menarche prevents progression from precocious pubarche to polycystic ovary syndrome. J Pediatr2004;144:23–9.
Berkson J . Limitations of the application of fourfold table analysis to hospital data. Biometrics Bull1946;2:47–53.
Competing interests: none declared
Copyright 2005 Archives of Disease in Childhood
Top cited articles
Copyright © 2020 BMJ Publishing Group Ltd & Royal College of Paediatrics and Child Health. All rights reserved.

redpajama_set_name: RedPajamaCommonCrawl


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Hi there! I have just successfully completed my final year of medical school and I love teaching students junior to me! Throughout my time at medical school, I have given revision lectures to younger years in preparation for exams, I have also privately tutored Maths, Biology and Chemistry to school children both online and in person. I believe that using one's own knowledge to help another succeed is one of the greatest feelings and this is why I love to teach so much. I like to base my lessons on the students' preferences and use lots of quizzes and questions to ensure that they are confident on each topic.


text:
Q: What is the risk of auto-appending mysql_close & session_write_close to all PHP scripts? What is the risk of using php's auto_append_file to automatically add:

session_write_close();
  mysql_close();

To all files?
In working with a customer's application, I found that sessions and database connections were hanging open for some reason.  As a quick fix, we added the code above via the auto_append_file.
This immediately resolved the issue of Apache threads staying in the Sending Reply state and reduced server loads considerably.
We are considering using this technique more often when the customer lacks sufficient resources or time to find the problematic code and fix it.
Edit
The question is not about best practices. I fully understand that this should not be required but I can reproducibly show the a reduction of hung Apache processes with this code added.  The question is about the risk or negative impact would such functions cause.

A: As mentioned in the comments the driver should close the connection and the session is written and closed at the end of the script's execution anyway.
Also, you should be using mysqli or PDO, not mysql! (MySQL extension is deprecated as of PHP 5.5.0)
Anyway, a better idea when you want to do that kind of thing (execute something right at the end of the script) would be to register a shutdown function to do it (DRY):
http://www.php.net//manual/en/function.register-shutdown-function.php
(And an even better one is to keep track of whatever resources you are using and release them right at the point where you know your program will not be needing them any more. It's more efficient, and leaves no doubt about what's happening with them.)

A: From the documentation for session_write_close():

Session data is usually stored after your script terminated without the need to call session_write_close(), but as session data is locked to prevent concurrent writes only one script may operate on a session at any time.

And from the documentation for mysql_close():

Using mysql_close() isn't usually necessary, as non-persistent open links are automatically closed at the end of the script's execution. See also freeing resources.

Also worth noting from mysql_close(), using no link identifier...

If the link identifier is not specified, the last link opened by mysql_connect() is assumed. If no connection is found or established, an E_WARNING level error is generated.

Keeping all of the above in mind:

*

*Calling the above functions shouldn't be necessary as they're automatically handled when a script terminates.

*Calling mysql_close() in a script will only a) close the most recently opened link or b) throw a warning because no links were ever opened.

*If you need scripts to give up resources as soon as they're done with them, using auto_append_file won't help you because of point #1.  You'll need to modify the scripts themselves.

*Database connections hanging open is a sign of a hung or long-running script.  If the script terminated, then the database link should have as well.  (Again, point #1)


text:
Trevor's Top 5 Games of 2020
By: Trevor Paul
Published: Jan 5, 2021
2020 was a rough year for all of us but it was a pretty great year for games. I played some of my favorite games in recent memory and so coming up with a top 5 was obviously quite difficult this time around. Anyway, here are my top 5 this year with some honorable mentions.
5. Spider-Man: Miles Morales
Insomniac's Spider-Man was a game I absolutely adored on the PlayStation 4 and once Miles Morales was announced, I was so happy that we would have the opportunity to play it at the launch of the new PlayStation 5 and it definitely didn't disappoint. The game was marketed as a sort of spin off to the previous Spider-Man title, similar to Uncharted: Lost Legacy, so my expectations were set a bit lower when I learned this but I ended up being blown away at everything this game had to offer. The presentation, story, characters, and new gameplay mechanics all hit home for me.
4. Persona 5 Royal
Persona is my favorite series hands down. I obsess over these games and Persona 5 was no different. Royal takes things to an all new level with new characters, extra story, a new dungeon, and a ton of quality of life improvements. I put hundreds of hours into Persona 5 and Royal combined and I don't regret a single second of it. This is a masterpiece and an absolute must play for fans of JRPGs.
3. The Last of Us Part 2
The Last of Us Part 2 is dark, painful, and incredibly bleak and maybe 2020 wasn't the best year for a game like this, but I'm super glad I got to play it. TLoU Part 2 does incredible things with storytelling and character development and while the mechanics didn't change much from the first go around, the story itself made it all worth it. Naughty Dog managed to add another hit to its resume and even though there was a lot of controversy surrounding this one, I still really enjoyed it.
2. Final Fantasy VII Remake
Final Fantasy VII Remake was a game I almost never expected to see. It had been so long since it was announced, I was at the point of thinking if we did see it, it might not be all that great. I was so wrong, this game is incredible. It's easily the best looking game I've seen on the PlayStation 4, and seeing these characters in a modern light made me fall in love with them all over again. Plus the new combat mechanics were complex enough to keep me engaged and challenged throughout. I'm disappointed it was split into separate games, but I can't wait to play the next one, whenever that rolls out.
1. Ghost of Tsushima
Ghost of Tsushima is my game of the year. It takes a lot of the classic open world mechanics and refines them to a point of near perfection. The combat is fun and the world is beautiful. I am a sucker for Samurai and this game is easily my favorite representation. It may not be a perfectly accurate depiction but it's incredibly fun and the story kept me engaged throughout. I loved Ghost of Tsushima and I really hope it gets a sequel or spin off of some sort. I would love to play more.
This one is a special one for me. The original Mafia on the PS2 still holds as one of my all time favorite games to this day. The ultra realistic mechanics and incredibly challenging gameplay were something I always remembered it for but the story was something I always thought was a love letter to fans of classic mob flicks. Mafia Definitive Edition may be one of the best remakes I've ever played. Everything from the original carries over with incredible presentation and I couldn't have been more impressed with the game this time around.
Demon's Souls Remake
The Demon's Souls Remake is incredible. I never played the original, at least not much anyway, but I was excited to dip my toes into this one. I recently started getting into Souls games this year and got hooked so this remake came at the perfect time. And from what I understand it stays true to the original. It's one I keep coming back to and may be one of my favorite Souls games period.
Animal Crossing is typically a game I get into very casually. New Horizons on the other hand was a bit different because I quickly became obsessed with it. It was all I played for a while and then my wife also became hooked, and then my daughter, and so it quickly became a family game for us. I spent a ton of time in Animal Crossing and I still really enjoy checking back in and seeing what's happening at different times of the year.
Tagged: animal crossing new horizons, Final Fantasy VII Remake, Ghost of Tsushima, GOTY 2020, Persona 5, Spiderman Miles Morales, The Last of Us Part II
Filed Under: Fanatical Five
Trevor Paul
Trevor is a passionate fan of games and technology. It all started when he picked up an NES controller at age 5. It was love at first sight. Trevor believes that Gameplay is key but he appreciates good storytelling in games as well. All games are fascinating and writing about them is something that he has always enjoyed doing.
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Is the Last of Us Part II Too Dark?


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Home / Books / Pathogenicity Islands and Other Mobile Virulence ... / Chapter
Chapter 8 : The Virulence Plasmid of Shigellae: an Archipelago of Pathogenicity Islands?
Authors: Claude Parsot1, Philippe J. Sansonetti1
Affiliations: 1: Unité de Pathogénie Microbienne Moléculaire, Unité INSERM U389, Institut Pasteur, 25 rue du Dr. Roux, 75724 Paris Cedex 15, France
Content Type: Monograph
Category: Microbial Genetics and Molecular Biology
Chapter DOI: 10.1128/9781555818173.ch8
References (111)
The Virulence Plasmid of Shigellae: an Archipelago of Pathogenicity Islands?, Page 1 of 2
Shigella strains are gram-negative, nonsporulating, nonencapsulated, facultative aerobic, nonmotile, straight rods that belong to the family Enterobacteriaceae and to the tribe Escherichiaeae. These observations suggest that virulence plasmids are made up of conserved building blocks and that some differences between various plasmids might be the result of shuffling of these building blocks. This chapter focuses on genes carried by the virulence plasmid that are or might be involved in the pathogenicity of Shigella. The virulence plasmid is an IncFII replicon, and functions involved in plasmid maintenance and stability have been recently described. Three genes carried by the virulence plasmid have been implicated in the ability of Shigella to move within the cytoplasm of infected cells: icsA (virG), sopA (icsP),and virK. The current model proposes that binding of H-NS to the virB promoter at low temperature prevents its activation by VirF. SepA homologs such as PssA from Shiga toxin-producing E. coli and EspP from enterohemorrhagic E. coli are also encoded by virulence plasmids and are flanked by sequences related to IS600,IS911,IS203, and IS7. Two different genes, designated apy and phoN-Sf, encoding periplasmic phosphatases about 25 kDa have been cloned from the virulence plasmid of two S. flexneri isolates of serotype 2a. So far, all the proteins identified as or proposed to be effectors of the specific interactions that occur between Shigella and host cells are encoded by the virulence plasmid.
Citation: Parsot C, Sansonetti P. 1999. The Virulence Plasmid of Shigellae: an Archipelago of Pathogenicity Islands?, p 151-165. In Kaper J, Hacker J (ed), Pathogenicity Islands and Other Mobile Virulence Elements. ASM Press, Washington, DC. doi: 10.1128/9781555818173.ch8
Mobile Genetic Elements
Outer Membrane Proteins
Virulence Plasmid
The Virulence Plasmid of Shigellae: an Archipelago of Pathogenicity Islands?
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/content/10.1128/9781555818173.chap8.fig8-1
Genetic organization of the entry region. The 31-kb entry region of the Shigella virulence plasmid is shown in a discontinuous manner, and the gene order reads from top to bottom and from left to right. Shigella genes are shown by open arrows (not to scale), and their names are indicated in bold type. Numbers indicate the size (in base pairs) of intergenic regions. Homologous genes present in the SPI-1 region at centisome 68 of the Salmonella chromosome (see references 33 and 56 for reviews) are indicated in standard characters below the Shigella genes; gene clusters are indicated by thin arrows.
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Schematic genetic map of pWR100, the virulence plasmid of S. flexneri M90T. The virulence plasmid is shown in a circular form, on which the position of genes is indicated by thick lines and their direction of transcription is indicated by arrows. The positions of virF, ipaH1.4, ipaH2.5, phoN,and senA have not been determined. Numbers refer to the coordinates on the plasmid, in kilobases.
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MEM INST OSWALDO CRUZ, RIO DE JANEIRO, 109(4) June 2014
PAGES: 452-458 DOI: 10.1590/0074-0276130408 Full paper
Triatominae species of Suriname (Heteroptera: Reduviidae) and their role as vectors of Chagas disease
Hélène Hiwat+
Department of Entomology, Bureau of Public Health, Paramaribo, Suriname
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Nine species of Triatominae, representing three tribes and five genera, are currently known in Suriname. An annotated list of the species based on the collections of the Bureau of Public Health (Suriname), the National Zoological Collection Suriname and the National History Museum Leiden (the Netherlands) is provided. Additionally, the results of several years of opportunistic collection in two domestic environments are presented. The most common species are Rhodnius pictipes Stål, 1972, Rhodnius robustus Larrouse, 1972 and Panstrongylus geniculatus (Latreille, 1811). The significance of the species as vectors of Chagas disease in Suriname is discussed.
Triatominae
Reduviidae
The surveillance and control of Chagas disease (American trypanosomiasis) is given high priority by most Latin American countries. However, the disease is not well known in the Guianas (Guyana, Suriname and French Guiana) and research efforts are limited. Furthermore, active surveillance and control are in initial phases or have yet to be developed (Luquetti & Schofield 2004, PAHO 2009, Salamanca-Dejour et al. 2012). Relatively few cases have been reported in these countries. In Suriname, three acute cases of Chagas disease were reported: one in 2001 (Oostburg et al. 2003) and the other two in 2012 and 2013 (S Vreden, unpublished observations). Based on the patients' lack of international travel history, these cases were considered autochthonous cases; one of them was a male infant who had not been out of the capital, Paramaribo. Two chronic cases had been detected serologically some 20 years before (Rawlings et al. 2001) and recent serological surveillance of the blood bank revealed five new chronic cases (S Vreden, unpublished observations). These cases were all considered autochthonous cases.
Haematophagous Triatominae, vectors of Chagas disease, are also relatively unknown in the Guianas and investigations into their diversity and distribution in the three countries are scarce (Lent & Wygodzinsky 1979, Bérenger et al. 2009). Lent and Wygodzinsky (1979) mentioned the occurrence of Triatoma maculata (Erichson, 1848), Eratyrus mucronatus Stål, 1859, Pans-trongylus geniculatus (Latreille, 1811), Panstrongylus lignarius (Walker, 1873), Rhodnius pictipes Stål, 1872, Rhodnius prolixus Stål, 1859 and Microtriatoma trinidadensis (Lent, 1951) in Suriname. This was partially based on an investigation by Lent (1943); although in Lent's study the presence of Triatoma rubrofasciata (De Geer, 1773) was recognised as well. Abad-Franch and Monteiro (2007) considered the Triatominae of the wider "humid Guyana" (which includes Guyana, Suriname and French Guiana) and for this region added Rhodnius robustus Larrousse, 1927 (genotype IV), Rhodnius amazonicus Almeida, Santos & Sposina, 1973, Rhodnius paraensis Sherlock, Guitton & Miles, 1977 and Panstrongylus rufotuberculatus (Champion, 1899) to the list, while speculating about the presence of R. prolixus Stål, 1859, Triatoma dimidiata (Latreille, 1811), Triatoma nigromaculata (Stål, 1859) and Cavernicola pilosa Barber, 1937. T. rubrofasciata, as in Lent and Wygodzinsky (1979), is not included in their species list for this region.
Over the last decade, an increased interest in Chagas disease and its vectors has developed in Suriname, leading to serological surveys and collections of Triatominae. The results of these Triatominae collections are reported here. This information, combined with an assessment of the available historical data on the subject, results in a comprehensive Triatominae species list for Suriname. The vector importance of the species is also discussed.
An overview of the Triatominae species of Suriname was generated based on the specimens and collection data available at the collections of the Bureau of Public Health in Suriname (BOG) and the National Zoological Collection of Suriname (NZCS), Anton de Kom University, on the information provided by the Natural History Museum of Leiden (NHML) (the Netherlands) and on a literature review. Suriname obtained independence from the Netherlands in 1975. As flora and fauna specimens collected during the colonial years were often transported to the Netherlands and stored at the NHML, the information on the Triatominae collection of this museum was included in this study.
The Republic of Suriname is situated on the Caribbean coast between Guyana and French Guiana, north of Brazil. The country is divided into 10 districts (Fig. 1) that cover three major ecological landscapes: the northern coastal area, the southern forested highlands and the savannah belt in between. The coastal area is mainly lowland with swamps and mangroves, but also has shell ridges; it is the most populated part of the country and almost all national agriculture is performed that region. The highlands in the interior are almost completely covered with tropical rainforest; however, deforestation, especially due to gold mining, is increasing significantly. This area has some inselbergs or tepuis and small savannah areas along the south-southeastern border. The savannah belt stretches from east to west and separates the coastal lowlands from the interior highlands (Fig. 2).
Approximately 90% of the country is uninhabited. Of the approximately 500,000 inhabitants, 70% are concentrated in and around Paramaribo. Another 25% live in small towns along the roads and rivers of the coastal area. The remaining 5% of the population live in small villages in the savannah belt and interior, mostly along the Marowijne, Suriname and Saramacca rivers. In addition, there is a growing population of Brazilian mineral prospectors (garimpeiros; estimated to be at least 15,000 people) involved in the rapidly growing, small-scale gold mining activities in the interior.
Suriname's tropical rainforest climate, with an average temperature of 27ºC and an average humidity of approximately 80%, is advantageous for a number of Triatominae species.
Active collection of Triatominae was performed by the author as part of an NZCS project in 2002. Field surveys were conducted in Kwamalasamutu (south Suriname, on the border with Brazil) and in Djoemoe and Nieuw-Aurora (central Suriname, along Suriname River) using live-bait traps [according to Abad-Franch et al. (2000)] and by the dissection of palm trees. Following this project and as a result of mutual interest, the author and two colleagues started opportunistic collection of the Triatominae encountered in and around their residences.
The current combined amount of Triatominae specimens in the three collections (NHML, NZCS and BOG) is 429 and represents seven species (Table I): 62.5% R. pictipes, 20.3% P. geniculatus and 9.6% R. robustus. The specimens of the NHML were collected between 1887-1965. The NZCS holds specimens collected from 1998 and the BOG collections started in 2005. A vast majority of the NZCS and BOG specimens conserved since 2002 originate from the opportunistic collection by the author and colleagues from two of the three residences. Table II provides an overview of these Triatominae, which were found at a residence in rural surroundings in the district of Wanica between 2002-2005 and at a residence, also in rural surroundings, in the district of Saramacca between 2002-2012. At the Wanica residence, a total amount of 58 Triatominae specimens were collected within the four years (R. pictipes, P. geniculatus, P. rufotuberculatus, P. lignarius), mostly attracted to a light on the balcony. The Saramacca residence yielded 133 Triatominae in 11 years (R. pictipes, R. robustus, P. geniculatus). Most of these specimens were collected indoors. All these specimens were included in either the NZCS or the BOG insect collections (Table I).
The active collection of Triatominae in 2002 yielded very little. Collection with live-bait traps was unsuccessful. The dissection of palm trees resulted in one adult R. pictipes from Kwamalasamutu and one R. robustus nymph from Nieuw Aurora, both from maripa palm (Attalea maripa). The R. pictipes adult was found near an opossum (Didelphidae) nest, where it most likely found its blood meals. The R. robustus nymph was reared to adulthood before incorporation into the collection. These specimens were included in the NZCS collection (Table I).
Confirmed species - Six of the seven species of Triatominae from Suriname currently represented in the historical collection of the NHML were also found since 1998, which confirms their presence in the country. T. maculata, collected in colonial times, was not found recently. According to Lent and Wygodzinsky (1979), a specimen of M. trinidadensis, collected in Paramaribo, used to be present at the NHML. However, this is no longer the case and the species was not found in the country during the recent collections. The Triatominae species known to be present in Suriname are E. mucronatus, P. geniculatus, Panstrongylus mitarakaensis, P. rufotuberculatus, P. lignarius, R. pictipes and R. robustus.
The presence of R. robustus, P. rufotuberculatus and P. mitarakaensis in the country was not reported previously. P. mitarakaensis (Bérenger & Blanchet 2007) is a recently discovered species. It was obtained from a locality at the Mitaraka mountain range, situated between the Litani River and Marowijne River, which is part of the southern border range between Suriname and French Guiana.
Species in need of confirmation - The presence of four species requires confirmation. M. trinidadensis was not collected recently. Nonetheless, its presence in Suriname is entirely possible because a specimen was recently found in French Guiana, less than 200 km from Suriname (Bérenger et al. 2009). T. maculata was collected in colonial times, but has not been seen found since. A similar situation occurred in French Guiana (Bérenger et al. 2009), where records of its presence (Carcavallo et al. 1999) could not be confirmed. The species shows an inclination for occurrences in peridomestic or domestic environments (Lent & Wygodzinsky 1979, Luitgards-Moura et al. 2005, Reyes-Lugo et al. 2011). The fact that the species has not been found since its first recordings allows for speculation that it may no longer exist in the country or that previous identifications may have been incorrect. The presence of T. rubrofasciata in Suriname was mentioned by Lent (1943) based on a study by Stoll in 1788. The distribution range of T. rubrofasciata extends from Florida and Caribbean islands to the northern and eastern Atlantic coasts of South America (Carcavallo et al. 1999) and the species is reported from port cities throughout its range (Lent & Wygodzinsky 1979, Braga et al. 1998). T. rubrofasciata is known for its transmission of Trypanosoma conorhini among rats (Braga et al. 1998). Its presence in Suriname would be consistent with its known distribution and is possible, though the species is unlikely to be abundant. Some specimens are known from Cayenne (French Guiana), collected in 1975, but the species has not been collected since (Bérenger et al. 2009).
The previous inclusion of Suriname in the distribution area of R. prolixus (Lent & Wygodzinsky 1979) is suspected due to misidentified R. robustus specimens. R. robustus is rather common and the two species are notoriously difficult to separate morphologically (Miles et al. 1981, Harry 1993a, b, Monteiro et al. 2003). The distribution range of R. prolixus may in fact exclude the Guiana Shield (Monteiro et al. 2003, Pavan & Monteiro 2007), which will make its presence in the country even more unlikely.
Species likely to be present - Some triatomine species known from bordering regions or due to their currently known distribution range are likely to be present in Suriname as well. C. pilosa, R. amazonicus and R. paraensis were collected from northern Brazil (state of Pará) and French Guiana (Carcavallo et al. 1999, Bérenger et al. 2009) and are likely to be present in the country.
Of the seven confirmed Triatominae species from Suriname, only three can be considered relatively abundant: P. geniculatus, R. pictipes and R. robustus (Table I). All three species are likely to contribute directly or indirectly [via contamination of food sources (Nóbrega et al. 2009)] to the transmission of Trypanosoma cruzi to the human population (Lent & Wydgonzinsky 1979, Barrett 1991, Oostburg et al. 2003, Gurgel-Gonçalves et al. 2012). The collection data from the NZCS and BOG reveal that, although there is no domestic colonisation, it is common for the adults of these three species to enter residences, which is as likely in the forest as it is in rural areas and in the capital (R. robustus excluded because it was not collected in the capital). It is thought that, depending on the peridomestic vegetation characteristics, these species, especially R. robustus and R. pictipes, may even establish large colonies near houses, surviving by opportunistic feeding on mammals (Abad-Franch et al. 2005).
R. pictipes is the most common species in all three insect collections and was most often encountered during the opportunistic collections in and around the residences in Wanica and Saramacca (Table II) (71.7% of the total). P. geniculatus was the second most frequently encountered species in the NHML and NZCS collections, but is absent from the BOG collection. Its potential as a Chagas disease vector is thought to be significant due to its broad ecological range and its frequent occurrence in peridomestic habitats and domiciliary invasion by adults (Gurgel-Gonçalves et al. 2012). P. geniculatus was the second most common species collected from the Wanica residence, but was encountered only once at the Saramacca residence. In contrast, the Saramacca residence had many R. robustus specimens, whereas no specimens of this species were encountered in or around the Wanica residence (Table II). Considering that both residences had an abundance of nearby vegetation (including palm trees) and a number of dogs and other domestic animals, which provide a blood source around the house, it is difficult to explain these differences. Environmental issues, such as vegetation diversity and characteristics (Abad-Franch et al. 2005, 2010), the (resulting) diversity in the availability of wild blood sources and the availability of light sources as attractants (Castro et al. 2010) may have played a role.
In the forests of the interior, the Maroon, Amerindian and garimpeiro populations often live in thatch-roofed or zinc-roofed huts or houses with wooden walls. The relatively poor housing conditions, combined with the increased use of electric lights as an attractant for the vectors (Castro et al. 2010), provide opportunity for the accidental entry of Triatominae into houses. Factors that may further promote the entry of Triatominae into houses include land use changes (e.g., deforestation for gold mining) (Barrett 1991, Abad-Franch et al. 2005) and the custom of keeping hunting dogs and chickens near sleeping quarters.
Taking into account that the common Triatominae species found in Suriname are palm-inhabiting species, Chagas disease can be considered an occupational risk for thatch and palm fruit harvesters. In addition, palm fruit consumers can be considered at risk for oral transmission (Roque et al. 2008, Nóbrega et al. 2009). Beverages made from the fruit of Euterpe luminosa (açai) are commercially available throughout the country.
T. cruzi transmission among wild mammals includes opossum and armadillo (Roque et al. 2008). Opossums (Didelphis spp) are common in all eco-habitats in Suriname and bring the sylvatic cycle to domestic environments, thus adding to the transmission risk. Armadillo (Dasypodinae) and a number of rodents (especially Dasyproctidae), also considered part of the T. cruzi wild reservoir (Solís-Franco et al. 1997, Roque et al. 2008), are regularly included in the diet of people living in the interior of the country, which results in the risk of oral transmission.
The number of Triatominae specimens collected from the two rural residences each year is surprisingly high [up to 31 specimens in one year (2009) to the Saramacca residence] (Table II). Both residences are near high vegetation that includes palm trees and have some domestic animals (especially dogs) living outside the house. This is a common situation in the coastal rural areas. The risk of triatomine-to-person contact appears to be considerable in such environments and needs to be studied further.
The residences in Paramaribo are mostly well-built, one or two-story brick homes with small trees and palms in the surrounding yards and sometimes air-conditioning. Entry into houses by Triatominae appears to be a bit less common than in rural areas, though it is certainly not rare and may have been the source of the first case of acute chagasic cardiopathy in Suriname (Oostburg et al. 2003). The patient, living in a suburban residential area of Paramaribo, had adult P. geniculatus in his yard.
The actual risk of T. cruzi transmission, of course, depends largely on the infection rate of the vectors. Unfortunately, this information is not yet available for Suriname for any of the species found in the country. In comparison, a study in the Brazilian Amazon revealed an infection rate for R. pictipes of 65% (Valente et al. 2009). Determining the infection rate for the three most common species in the country will be one of the priorities of future studies and the determination of the seroprevalence of T. cruzi infection among the population of Suriname is a priority as well. Studies in Guyana and French Guiana indicate an overall T. cruzi seroprevalence of 0.5% for these countries (Aznar et al. 2004, PAHO 2009). In contrast, information on the seroprevalence of T. cruzi in the animal reservoir of Suriname does not exist. Studies on this subject will need to be developed and executed. The annotated list of Surinamese Triatominae is given below.
Bolboderini Usinger, 1944, M. trinidadensis (Lent, 1951) - The inclusion of Suriname in the distribution range of M. trinidadensis was based on a specimen collected in Paramaribo and conserved at the NHML (Lent & Wygodzinsky 1979). No other reports of M. trinidadensis collection in Suriname are known. Unfortunately, the one specimen at the NHML no longer exists. The species is known from bromeliads and was collected under tree bark (Lent & Wygodzinsky 1979), but has also been discovered (in all developmental stages) in peridomestic environments (De la Riva et al. 2001). Distribution: district of Paramaribo.
Rhodniini Pinto, 1926, R. pictipes Stål, 1872 - R. pictipes is a widespread silvatic species that is frequently attracted to light and is known to enter houses on occasion (Lent & Wygodzinsky 1979, Torres & Cabrera 2010). It is the most common species collected in Suriname and was often collected in domestic habitats. Distribution: districts of Paramaribo, Commewijne, Wanica, Para (Mapane), Brokopondo (Sara Creek), Saramacca, Coronie, Marowijne (Galibi) and Sipaliwini (Benzdorp, Nieuw Aurora, Apoera, Coeroeni-island, Kaboeri Creek, Bakhuys, Kwamalasamutu).
R. robustus Larrousse, 1927 - Some of the R. robustus specimens from Suriname were initially thought to be R. prolixus, but mt-DNA sequence analysis of the Suriname specimens confirms them as "type 4" R. robustus [following the designation of Monteiro et al. (2003), which conforms to the estimated distribution of genotypes in Abad-Franch and Monteiro (2007)]. R. prolixus itself has not been found in Suriname. Distribution: districts of Saramacca, Brokopondo (Klaaskreek), Para (Republiek), Marowijne (Galibi) and Sipaliwini (Nieuw Aurora).
Triatomini Jeannel, 1919, E. mucronatus Stål, 1859 - E. mucronatus is a sylvatic species with little epidemiological significance (Lent & Wygodzinsky 1979). It can be found in a variety of habitats, including dry and wet tropical forests (Cuba et al. 2002). The one specimen found by the NZCS was collected in a recreational room at Brownsberg Nature Park, an ecotourist site situated at 500 m above sea level in a humid tropical forest. Its role as a vector of Chagas disease is considered insignificant (Barrett 1991), but evidence of domestic capture exists (Torres & Cabrera 2010). Distribution: districts of Paramaribo, Brokopondo (Brownsberg) and Para (Zanderij).
P. geniculatus (Latreille, 1811) - P. geniculatus is a frequently encountered species in Suriname and is believed to have been the vector responsible for the first acute case of Chagas disease recorded in the country (Oostburg et al. 2003). Adults of this species are commonly attracted to light and encountered in peridomestic environments (Lent & Wygodzinsky 1979, Torres & Cabrera 2010). The species is thought to have the potential for domestication and was found breeding in pigsties near human dwellings in Brazil (Valente 1999). Most specimens from Suriname were collected in (peri)domestic surroundings. Distribution: districts of Paramaribo, Commewijne, Wanica, Para (Mapane), Saramacca and Sipaliwini (Nieuw Aurora, Sipaliwini savannah).
P. lignarius (Walker, 1873) - The one specimen of P. lignarius found by the NZCS came from a peridomestic situation, again most likely attracted by an electric light. This species was originally described by Walker, in 1873, but was then redescribed by Lent (1943) based on a Surinamese specimen provided by DC Geijskes, a Dutch entomologist. Distribution: districts of Wanica and Sipaliwini (Bakhuys).
P. mitarakaensis Bérenger and Blanchet, 2007 - P. mitarakaensis was described as a new species by Bérenger and Blanchet (2007) based on a specimen collected from a locality in the southeast of the Mitaraka Mountains (TumakHumak Mountain Range at the border with Brazil), which is part of the southern border of Suriname with French Guiana. Distribution: district of Sipaliwini [TumacHukac (Mitaraka Mountains)].
P. rufotuberculatus (Champion, 1899) - P. rufotuberculatus is also frequently attracted to electric light (Lent & Wygodnzinsky 1979, Salomón et al. 1999). It is known mainly from low, dry areas, but may also be found in zones of humid premontane forests (Abad-Franch et al. 2001). The species has been found in domestic environments elsewhere (Torres & Cabrera 2010). As originally described by Champion (1899), P. rufotuberculatus shows considerable morphological variation. The specimens encountered in Suriname have a reddish connexivum with a rectangular dark spot in each segment, slightly biconcave and a thin black band close to the intersegmental suture. The reddish carinae, limiting the central depression of the scutellum, appear to be similar to those found in specimens from Panama and Colombia [as described by Salomón et al. (1999)] and distinct from specimens from Costa Rica, Venezuela, Peru, Bolivia and Brazil, which generally present the scutellum entirely black. All post-colonial specimens originate from one residence in the district of Wanica. Distribution: districts of Paramaribo and Wanica.
T. maculata (Erichson, 1848) - One specimen of T. maculata was reportedly captured in Paramaribo. This was in 1963, when the capital had greater abundance of vegetation, including palm trees. No specimens have since been collected. T. maculata is a species with sylvatic and (peri) domestic occurrences (Luitgards et al. 2005, Reyes-Lugo et al. 2011). Considering that the species is not commonly found in a humid coastal habitat, the record needs confirmation . Distribution: district of Paramaribo.
To the NHML and the NZCS, for sharing of information, to my colleagues and friends A van Sauers-Muller and A Gangadin, for collecting Triatominae in their free time, to Dr F Monteiro, who carried out DNA sequencing of R. robustus specimens from Suriname, to Drs L Resida and Dr CJ Schofield, for reviewing an earlier version of the paper, and to the two anonymous reviewers who's remarks helped to improve the paper.
Abad-Franch F, Ferraz G, Palomeque FS, Grijalva MJ, Aquilar HM, Miles MA 2010. Modeling disease vector occurrence when detection is imperfect: infestation of Amazonian palm trees by triatomine bugs at three spatial scales. PLoS Negl Trop Dis 4: 1-11.
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Received 20 August 2013
Accepted 2 May 2014


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