Most SIDS cases occur at ages one to four months. This probably reflects a specific, temporary physiological vulnerability during this time. At birth, infants have an immune system that is biased toward a Th2 response, which would make them more susceptible to certain infections and manifestations of those infections. At the ages of greatest risk of sudden infant death, maternal antibody levels have decreased while the infant's own immune system is still immature. Only 2 or 3 percent of SIDS deaths occur after the age of one year.
The socioeconomic associations with SIDS are nearly identical with those of chorioamnionitis, which is the cause of perinatal illnesses blamed on smoking. Smoking, black race, lower socioeconomic status, etc., are all associated with both, and these are just markers for markers for earlier and more frequent exposure to a larger number of pathogens postnatally as well as prenatally.
In The Netherlands, the prone sleeping position was rarely
infants before 1972. After 1971, publicity from the Dutch medical and
popular media promoting this position increased its use from about 10%
to 55-65% of infants. From 1969 to 1983-4, the death rates from SIDS
rose from 0.44 per 1000 in 1969 to between 1.08 and 1.31 per 1000 in
1977-87. Also during this period, the percentage of women smokers aged
20-34 years declined from 58% to around 35%. SIDS death rates in The
Netherlands dropped sharply, to 0.44 per 1000 in 1991, after
publicity advocating placing
infants on their backs to sleep instead (AC Engelberts, GA de Jonge, PJ
analysis of trends in the incidence of sudden infant death in The
Netherlands 1969-89. Paediatr Child Health 1991 Dec;27(6):329-333;
Sleeping position for infants and cot death in The Netherlands 1985-91.
GA de Jonge, RJ Burgmeijer, AC Engelberts, J Hoogenboezem, PJ Kostense,
AJ Sprij. Arch Dis Child 1993 Dec;69(6):660-663).
The contribution of changes in the prevalence of prone
sleeping position to the decline in Sudden Infant Death Syndrome in
Tasmania. T Dwyer, AL Ponsonby, L Blizzard, NM Newman, JA Cochrane.
JAMA 1995 Mar 8;273(10):783-789. "The Tasmanian SIDS rate decreased (P
< .01) from 3.8 (95% confidence interval [CI], 3.5 to 4.2)
per 1000 live births from 1975 through 1990 to a rate of 1.5 (95% CI,
0.9 to 2.2) deaths per 1000 live births in 1991 through 1992."
News. Cot deaths. BMJ 1995
Jan 7;310(6971):7-10; Trends in rates and seasonal
distribution of sudden infant deaths in England and Wales, 1988-92. EA
Gilman, KK Cheng, HR Winter, R Scragg. BMJ
1995 Mar 11;310(6980):631-632. "[S]udden infant death rates rose more
or less continuously from 1971 to a peak of 2.30 deaths per 1000 live
births in 1988. Rates then fell steadily to 1.44 in 1991 and abruptly
to 0.70 in 1992."
The epidemic of SIDS in Norway 1967-93: changing effects of
factors. AK Daltveit, N Řyen, R Skjćrven, LM Irgensa. Arch
Dis Child 1997 Jul;77:23-27. "The SIDS rate was 1.25 in 1967, reached a
peak of 2.69 in 1988 and declined to 0.59 in 1993."
Case-control study of current validity of previously described
factors for SIDS in The Netherlands. MP l'Hoir, AC Engelberts, GT van
Well, P Westers, GJ Mellenbergh, WH Wolters, J Huber. Arch Dis Child
1998 Nov;79(5):386-393. In 1995, the death rates had declined to 0.26
per 1000 livebirths.
Changes in the epidemiology of sudden infant death syndrome in
Sweden 1973-1996. B Alma, S G Norveniusa, G Wennergrena, R
Skjćrvenb, N Řyenb, J Mileradc, M Wennborgc, J Kjaerbecka,
K Helweg-Larsend, L M Irgensb, on behalf of the Nordic Epidemiological
SIDS Study. Arch Dis Child 2001;84:24-30. In Sweden, between 1973 and
1992, there was a dramatic rise in the rates of sudden, unexplained
infant deaths, from about 0.3 to 1.1 per thousand. In 1992, after
publicity advocating face-up instead of face-down sleeping for infants,
there was an even more dramatic fall in the incidence, with the rates
returning to 1973 levels over a period of six years (Fig. 1). [These
changes in the incidence of SIDS do not correlate at all with the
small, steady declines in smoking during the same 26-year period.
as in the United States, the rates of both low birth weight and preterm
births were higher in the 1990s than in the 1970s - cast].
Needless to say, rather than abandon their false hypothesis
smoking, the anti-smoking ideologues deliberately deceive the public by
claiming that odds ratios for SIDS increased for smoking and
prematurity. In fact, the phony smoking risk is based upon using
defective studies that do not include pathological examinations for
chorioamnionitis, which is the real cause of both preterm births and
most other poor perinatal outcomes. In the absence of pathological
exams, 90% of these cases are missed. (See "Chorioamnionitis
Causes Perinatal Illnesses Blamed on Smoking.")
Changes in the Classification of Sudden Unexpected Infant
United States, 1992–2001. MH Malloy, M MacDorman. Pediatrics 2005
May;115:1247-1253. MacDorman is with the US National Center for Health
Statistics, Hyattsville, Maryland. "The all-cause postneonatal
mortality rate declined 27% and the postneonatal SIDS rate declined 55%
between 1992 and 2001. However, for the period from 1999 to 2001 there
was no significant change in the overall postneonatal mortality rate,
whereas the postneonatal SIDS rate declined by 17.4%. Concurrent
increases in postneonatal mortality rates for unknown and unspecified
causes and suffocation account for 90% of the decrease in the SIDS rate
between 1999 and 2001." Their work is designed more to obfuscate than
to clarify, because that brief 2-year span receives the most attention!
Overall, however, the death rates from the 2 ICD chapters "Symptoms,
Signs, and Ill-Defined Conditions" and "External Causes of Injury"
which contain all of the sudden unexpected infant deaths rose after
1970 and remained high until approximately 1990, when they declined;
while residual deaths fell.
Prevention of sudden infant death syndrome (SIDS) due to an active health monitoring system 20 years prior to the public "Back to Sleep" campaigns. M Vennemann, D Fischer, G Jorch, T Bajanowski. Arch Dis Child 2006 Apr;91(4):324-326. Rates of death from SIDS were lower in East Germany than in West Germany. One reason for this is that guidelines from the Ministry of Health in 1972 forbade day-care centers to place babies to sleep in a prone position, while the "Back to Sleep" Campaign in West Germany didn't begin until 1992.Vennemann - Arch Dis Child 2006 full article / PubMed Central
Overall Postneonatal Mortality and Rates of SIDS. RD Goldstein, FL Trachtenberg, MA Sens, BJ Harty, HC Kinney. Pediatrics 2015 Dec;137(1):e20152298. From US Mortality Multiple Causes Records for 1983 to 2012. "SIDS and non-SIDS postneonatal mortality rates were concordant over time. Important variance was seen 1994 to 1996, coinciding with Back-to-Sleep initiation. Other variance, eliminated in the cumulative composite, appeared related to differences in diagnostic practices. Changes in SIDS rates resembled changes in mortality from congenital malformations, respiratory distress of the newborn, and diseases of the circulatory system. SIDS rates for low birth weight infants followed broader postneonatal trends."Goldstein / Pediatrics 2015 full article
The α3 and α4 nicotinic acetylcholine receptor (nAChR) subunits in the brainstem medulla of sudden infant death syndrome (SIDS). A Aishah, T Hinton, KA Waters, R Machaalani. Neurobiol Dis 2019 Jan 18;125:23-30 [Epub ahead of print]. 7 infants who died with a known cause of death, 8 SIDS I, and 27 SIDS II. "Results showed that only α4 changes (increase) were evident in SIDS, occurring in the hypoglossal and cuneate nuclei of SIDS II infants and the nucleus of the spinal trigeminal tract of SIDS I infants," while "cigarette smoke exposure was only associated with decreased α4 in cribriform fibre tracts." "Combined, these findings suggest that abnormalities in endogenous acetylcholine synthesis and regulation may underlie the altered α3 and α4 nAChR subunit expressions in the SIDS brainstem medulla since the changes were not related to cigarette smoke exposure."Aishah - Neurobiol Dis 2019 abstract / PubMed
reason that sleeping position is
important is not known. But, after the change in infants' sleeping
position from prone to supine, most SIDS cases apparently result from
other underlying causes, most likely of an infectious nature.
Infant respiratory death rates mirror sudden infant deaths (Letter re Gilman). DL Crombie, KW Cross, DM Fleming. BMJ 1995 Jun 17;310(6994):1603. "The authors put forward as one possible explanation of these falls the interaction between the prone sleeping position and the underlying pathogenic mechanisms that it affects. In this regard, we would draw attention to the fact that the secular and seasonal trends in the monthly numbers of sudden infant deaths over recent years have been mirrored by those for infant deaths attributable to respiratory disease. The figure shows the two series for the years 1986-92. The concordance between these two series is evident in the summer troughs as well as the winter peaks. This phenomenon suggests that whatever has led to the seasonal variation and decreasing trend in sudden infant deaths, including the pronounced decrease during 1992, has produced a similar pattem for infant deaths attributable to respiratory disease. Furthermore, we have shown that during 1986-90 there was a close association between the monthly incidence of respiratory infectious diseases in the age group 0-4 years."
An infectious aetiology of sudden infant death syndrome. AR Highet. J Appl Microbiol 2008 Sep;105(3):625-635. Review. "Consistent pathological findings are seen which display similarities to the pathogenesis of toxaemic shock and/or sepsis. The major risk factors for SIDS parallel those for increased colonization and serious bacterial infections and the natural variation in the incidence of SIDS cases is typical of an infectious disease. The roles played by viral infection, immunoregulatory genes and suspected bacterial species are discussed herein."Highet - J Appl Microbiol 2008 abstract / PubMed
Histological findings in unclassified sudden infant death, including sudden infant death syndrome. G Liebrechts-Akkerman, JV Bovée, LC Wijnaendts, A Maes, PG Nikkels, RR de Krijger. Pediatr Dev Pathol 2013 May-Jun;16(3):168-176. 200 Dutch cases. "An explanation for the cause of death in 19 patients (10.2%) was found. Twelve patients had bronchopneumonia, 3 showed extensive aspiration, 2 had signs of a metabolic disorder, 1 had sepsis, and 1 had meningitis. Frequent nonspecific findings were congestion (66%), edema (47%), small hemorrhages (18%), and lymphoid aggregates (51%) in the lungs; congestion of the liver (23%); and asphyctic bleeding in the kidney (44%), adrenal gland (23%), and thymus (17%). Statistical associations were found for infection with starry sky macrophages in the thymus (P = 0.004), with calcification (P = 0.023), or with debris in the Hassal's corpuscles (P = 0.034). In this study, in 10.2% of cases the histological findings were incompatible with SIDS or USID. Furthermore, several frequent nonspecific histological findings in the thymus that point toward an infection were found."Liebrechts-Akkerman - Pediatr Dev Pathol 2013 abstract / PubMed
An Acute Respiratory Infection of a Physiologically Anemic Infant is a More Likely Cause of SIDS than Neurological Prematurity. DT Mage, ML Latorre, AG Jenik, EM Donner. Front Neurol 2016 Aug 23;7:129. "From extensive SIDS vital statistics data and published epidemiologic studies, we developed probability models to explain the mathematical behavior of SIDS meeting the four constraints mentioned above. We, then, compare these SIDS properties to infant death from acute respiratory infection (ARI), and infant death from encephalopathy, unspecified (EU). Comparisons show that SIDS are congruent with ARI and are not consistent with EU and that these probability models not only fit the SIDS data but they also predict and fit the male fraction of all infant and child mortality from birth through the first 5 years of their life."Mage - Front Neurol 2016 full article / PubMed Central
The sudden infant death syndrome and epidemic viral disease. KE Nelson, MA Greenberg, MA Mufson, VK Moses. Am J Epidemiol 1975 May;101(5):423-430. 778 sudden infant deaths and 3244 hospital admissions of children under 18 months for respiratory disease. "Four outbreaks of respiratory syncytial (RS) virus infections, three outbreaks of influenza A virus infections, and several small clusters of parainfluenza virus infections occurred during the course of this study. Influenza A was the only virus infection found to have a statistically significant association with SIDS. Although environmental temperature was also significantly correlated with SIDS, the association with influenza A virus infection was independent of this temperature effect and neither association was strong."Nelson - Am J Epidemiol 1975 abstract / PubMed
PCR-based diagnosis of enterovirus and parvovirus B19 in
paraffin-embedded heart tissue of children with suspected sudden infant
death syndrome. A Baasner, R Dettmeyer, M Graebe, J Rissland, B Madea.
Lab Invest 2003 Oct;83(10):1451-1455. 60 SIDS cases and 36 controls
with well-known causes of sudden death. Enteroviruses were found in 14
SIDS cases versus 0 controls; parvovirus B19 was found in 7 SIDS cases
vs 3 controls.
Virological analysis in the diagnosis of sudden children
medico-legal approach. A Fernández-Rodríguez, S
Ballesteros, F de Ory,
JE Echevarría, R Alvarez-Lafuente, G Vallejo, J Gómez.
Forensic Sci Int
2006 Aug 10;161(1):8-14. 64 cases. "According to pathological findings,
death could only be attributed to an adenovirus infection in one
amygdalitis with upper airways stenosis and asphyxia. Human herpes
virus 6 (HHV-6) was detected by PCR in one case with pathological
findings characteristic of SIDS. Recent infection by respiratory
syncytial virus (RSV), Epstein-Barr virus (EBV) and cytomegalovirus
(CMV) were also detected. Meanwhile, 85.9% of the cases yielded
negative viral results. Twenty-eight infants were finally categorised
as SIDS. Pathological findings of infection were detected in 12
patients despite the negativity of viral analyses."
Detection of human herpesvirus-6, Epstein-Barr virus and cytomegalovirus in formalin-fixed tissues from sudden infant death: a study with quantitative real-time PCR. R Alvarez-Lafuente, B Aguilera, MA Suárez-Mier, B Morentin, G Vallejo, J Gómez, A Fernández-Rodríguez. Forensic Sci Int 2008 Jul 4;178(2-3):106-111. 11 SIDS cases and 9 controls, by PCR. "The comparison of the whole viral DNA prevalence in cases and tissue sections between SIDS and controls showed a statistical significance (72.7% vs. 22.2%, p=0.025; 41.1% vs. 10.3%, p=0.001, respectively); in particular, we found a statistical significant difference for the EBV DNA prevalence among cases (p=0.042) and tissues (p=0.048), and a statistical significant difference for the HHV-6 DNA prevalence among cases (p=0.017)."Alvarez-Lafuente - Forensic Sci Int 2008 abstract / PubMed
The role of post-mortem investigations in determining the
sudden unexpected death in infancy. MA Weber, MT Ashworth, RA Risdon,
JC Hartley, M Malone, NJ Sebire. Arch Dis Child 2008
Dec;93(12):1048-1053. "Retrospective analysis of >1500
post-mortem examinations carried out by specialist paediatric
pathologists at a single centre during a 10-year period according to a
common autopsy protocol that included the use of detailed ancillary
investigations... Of 1516 paediatric post-mortem examinations, 546
presented as SUDI. In 202 infants (37%), death was explained by the
autopsy findings. The other 344 cases (63%) remained unexplained. Of
the explained deaths, over half (58%) were infective, most commonly due
to pneumonia (22%). The component of the post-mortem examination that
primarily determined the final cause of death was histological
examination in 92 infants (46%), macroscopic examination in 61 (30%),
microbiological investigations in 38 (19%) and clinical history in 10
Pandemic (H1N1) 2009-associated deaths detected by unexplained death and medical examiner surveillance. CH Lees, C Avery, R Asherin, J Rainbow, R Danila, C Smelser, A Schmitz, S Ladd-Wilson, KB Nolte, K Nagle, R Lynfield. Emerg Infect Dis 2011 Aug;17(8):1479-1483. "During the pandemic (H1N1) 2009 outbreak, Minnesota, New Mexico, and Oregon used several surveillance methods to detect associated deaths. Surveillance using unexplained death and medical examiner data allowed for detection of 34 (18%) pandemic (H1N1) 2009-associated deaths that were not detected by hospital-based surveillance."Lees - Emerg Infect Dis 2011 full article / PubMed Central
Detection and toxin production of Staphylococcus aureus in
infant death cases in Hungary. Z Csukás, K Töró, I
Jankovics, F Rozgonyi, P Sótonyi. Acta Microbiol Immunol Hung
2001;48(2):129-141. 13 SIDS cases, 9 non-SIDS, 100 healthy infants. "S.
aureus was isolated from 54% of SIDS cases and 37% from healthy infants
/OR = 1.986 (95% Confidence interval = 0.55-7.33), p = 0243/. The
enterotoxin and TSST-1 toxin producing activity of S. aureus showed the
characteristic difference. The toxigenic S. aureus was detected in 46%
of SIDS cases and 16% of healthy infants /OR = 4.5 (95% CI =
1.15-17.72), p = 0.010/. The distribution of toxigenic and nontoxigenic
isolates was 86% in SIDS cases and 43% in healthy infants /OR = 7.875
(CI = 0.78-191.89), p = 0.041/."
Infection and sudden unexpected death in infancy: a systematic
retrospective case review. MA Weber, NJ Klein, JC Hartley, PE Lock, M
Malone, NJ Sebire. Lancet 2008 May 31;371(9627):1848-1853.
"Significantly more isolates from infants whose deaths were explained
by bacterial infection (78/322, 24%) and from those whose death was
unexplained (440/2306, 19%) contained group 2 pathogens than did those
from infants whose death was explained by a non-infective cause
(27/243, 11%; difference 13.1%, 95% CI 6.9-19.2, p<0.0001 vs
bacterial infection; and 8.0%, 3.2-11.8, p=0.001 vs unexplained).
Significantly more cultures from infants whose deaths were unexplained
contained Staphylococcus aureus (262/1628, 16%) or Escherichia coli
(93/1628; 6%) than did those from infants whose deaths were of
non-infective cause (S aureus: 19/211, 9%; difference 7.1%, 95% CI
2.2-10.8, p=0.005; E coli: 3/211, 1%, difference 4.3%, 1.5-5.9,
Dynamics and determinants of Staphylococcus aureus carriage in
infancy: the Generation R Study. A Lebon, JA Labout, HA Verbrugh, VW
Jaddoe, A Hofman, W van Wamel, HA Moll, A van Belkum. J Clin Microbiol
2008 Oct;46(10):3517-3521. 443 infants sampled at 1.5, 6, and 14
months. "The main difference between our findings and the studies on
determinants of carriage by Bogaert et al. and Peacock et al. is our
failure to identify family size, passive smoking, or breast-feeding as
significant determinants of carriage (2, 16). However, our data on
breast-feeding seems to be more precise than those of the earlier
studies, with very little missing data; furthermore, our data cover a
larger cohort of children in the same age group (first year of life)
than do the two previously mentioned studies."
Sterile site infection at autopsy in sudden unexpected deaths
infancy. PN Goldwater. Arch Dis Child 2009 Apr;94(4):303-307. Autopsy
report review of 130 sudden infant death syndrome (SIDS) cases (2004
definition), 32 cases of sudden unexpected death in infancy (SUDI) due
to infection and 33 cases of non-infectious sudden deaths. "10.76% of
SIDS had S aureus present in a sterile site, compared with 18.75% of
cases of infection-related deaths. S aureus was not found in sudden
accidental deaths. The incidence of coliform bacteria in NSS in SIDS
was not significantly different from that seen in deaths from other
Staphylococcal toxins in sudden unexpected death in infancy: experience from a single specialist centre. MA Weber, JC Hartley, NJ Klein, RA Risdon, M Malone, NJ Sebire. Forensic Sci Med Pathol 2011 Jun;7(2):141-147. 470 autopsies with bacteriological investigations. "There were significantly more cases with S aureus isolated in unexplained SUDI (40%) compared to non-infective SUDI (21%; difference 19.0%, 95% CI 5.4% to 29.3%, P = 0.006)... There is a significantly higher prevalence of S aureus in unexplained SUDI compared to non-infective SUDI, but no significant difference in the proportion with toxigenic S aureus strains isolated between the groups."Weber - Forensic Sci Med Pathol 2011 abstract / PubMed
SIDS, infection could be linked. Researchers study E. coli byproduct. By Emma Ross, The Associated Press 2002 Apr 26. "'Mainstream researchers have concentrated on respiratory obstruction as a possible mechanism, without any evidence that would support such a mode of death,' said Dr. Paul Goldwater, who presented his study at the European Congress of Clinical Microbiology and Infectious Diseases in Milan. 'Those researchers ignored autopsy findings that consistently show wet, heavy lungs in SIDS babies. This is never seen' in cases of suffocation, said Goldwater, a researcher at the Women's and Children's Hospital in North Adelaide, Australia. Such a lung condition is often seen in cases of infection. Autopsies also consistently show small hemorrhages on the heart and lungs -- which is rare in suffocation -- and the blood of SIDS babies is unclotted, which is something never seen in suffocation cases, he added. Furthermore, he said, SIDS deaths captured on medical monitors have shown that these babies died of a shock-like process, Goldwater said. 'The serum from babies who have died of SIDS is toxic to chick embryos and mice -- indicating the presence of a toxin,' he said." The bacteria was found in all SIDS babies and 80% of normal babies, but all SIDS babies versus no healthy babies had the E coli curlin protein in their bloodstreams.Goldwater / Pittsburgh Post-Gazette 2002
Sudden infant death
syndrome: a critical review of approaches to research. PN Goldwater.
Arch Dis Child 2003 Dec;88(12):1095-1100. Review.
Supporting evidence is that "Enteric infections alter bowel permeability which allows absorption of otherwise excluded food components [and presumably also bacteria and bacterial products -cast]. Several studies of both human and porcine models indicate that significant quantities of unwanted proteins can be absorbed by damaged gut tissue and that maximum expression of diarrhea corresponds with peak protein uptake." (JA Lindsay. Chronic sequelae of foodborne illnes. Emerging Infectious Diseases 1997 Oct-Dec;3(4):.) E coli (along with other pathogens) could be responsible for damaging the gut.Lindsay / EID 1997 full article
Expression of and cytokine activation by Escherichia coli curli fibers in human sepsis. Z Bian, A Brauner, Y Li, S Normark. J Infect Dis 2000 Feb;181(2):602-612. "These data, therefore, provide direct evidence that curli are expressed in vivo in human sepsis and suggest a possible role for curli and CsgA" in human E coli sepsis.Bian - J Infect Dis 2000 abstract / PubMed
Activation of inducible nitric oxide synthase/nitric oxide by curli fibers leads to a fall in blood pressure during systemic Escherichia coli infection in mice. Z Bian, ZQ Yan, GK Hansson, P Thoren, S Normark. J Infect Dis 2001 Feb 15;183(4):612-619.Bian - J Infect Dis 2001 abstract / PubMed
Role of Escherichia coli curli operons in directing amyloid fiber formation. MR Chapman, LS Robinson, JS Pinkner, R Roth, J Heuser, M Hammar, S Normark, SJ Hultgren. Science 2002 Feb 1;295(5556):851-855. "Amyloid is associated with debilitating human ailments including Alzheimer's and prion diseases. Biochemical, biophysical, and imaging analysis revealed that fibers produced by Escherichia coli called curli were amyloid."Chapman - Science 2002 abstract / PubMed
The frequency of molecular detection of virulence genes
cytolysin A, high-pathogenicity island and cytolethal distending toxin
of Escherichia coli in cases of sudden infant death syndrome does not
differ from that in other infant deaths and healthy infants. AR Highet,
AM Berry, KA Bettelheim, PN Goldwater. J Med Microbiol 2009 Mar;58(Pt
3):285-289. In 145 SIDS and 101 dead control and healthy infants, there
was no correlation of SIDS with clyA (cytolysin A), irp2
[high-pathogenicity island (HPI)-specific gene] and cdt (cytolethal
The protozoan Pneumocystis carinii has been known chiefly as an opportunistic infection that causes pneumonia in AIDS patients and others with immune deficiencies. It is generally considered harmless in normal infants and adults. Howwever, studies by Vargas et al in three different countries have shown that infants classified as SIDS deaths are more likely to have clusters of P carinii in their lungs than those who died of other causes. P carinii was found in a relatively high proportion of cases, from 15 top 35 percent. Reduced levels of lung surfactant have been hypthesized to trigger sudden death in a number of SIDS cases, and decreased surfactant has been found in the lungs of animals in the early stages of P carinii infection.
Association of primary Pneumocystis carinii infection and sudden infant death syndrome. SL Vargas, CA Ponce, WT Hughes, AE Wakefield, JC Weitz, S Donoso, AV Alloa, P Madrid, S Gould, JJ Latorre, R Avila, S Benveniste, M Gallo, J Belletti, R Lopez. Clin Infect Dis 1999 Dec;29(6):1489-1493; Pneumocystis carinii infection linked to sudden infant death syndrome. Medscape - Reuters Health 2000 Jan 11.Vargas - Clin Infect Dis 1999 abstract / PubMed
The impact of CMV on the respiratory burst of macrophages in
response to Pneumocystis carinii. AL Laursen, SC Mogensen, HM Andersen,
PL Andersen, S Ellermann-Eriksen. Clin Exp Immunol 2001
Feb;123(2):239-246. "Infection of human monocyte-derived macrophages
with CMV decreased the respiratory burst when cells were stimulated
with opsonized zymosan or Pneumocystis carinii (P. carinii)... The
effect was most pronounced in cells obtained from CMV antibody-negative
Identification of Pneumocystis carinii in the lungs of infants dying of sudden infant death syndrome. DJ Morgan, SL Vargas, M Reyes-Mugica, JN Walterspiel, W Carver, F Gigliotti. Pediatr Infect Dis J 2001 Mar;20(3):306-309. P carinii found in 14% of 79 SIDS deaths in Rochester, NY.Morgan - Pediatr Infect Dis J 2001 abstract / PubMed