The Incubation Period of Poliomyelitis

Sartwell, Philip E.

doi:10.2105/ajph.42.11.1403

Cited by 34 publications

(20 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The epidemiologist Philip E. Sartwell (1908Sartwell ( -1999, who previously acted as chairman of the Department of Epidemiology, Johns Hopkins School of Hygiene and Public Health, contributed most to the foundation of incubation period distribution modeling [50]. Dr. Sartwell initially found that the incubation period of acute infectious diseases tends to follow lognormal distribution [12], and applied the distribution to various diseases [51,52].…”

Section: Lognormal Distribution Proposed By Philip Sartwellmentioning

confidence: 99%

Early efforts in modeling the incubation period of infectious diseases with an acute course of illness

Nishiura

2007

Emerg Themes Epidemiol

View full text Add to dashboard Cite

The incubation period of infectious diseases, the time from infection with a microorganism to onset of disease, is directly relevant to prevention and control. Since explicit models of the incubation period enhance our understanding of the spread of disease, previous classic studies were revisited, focusing on the modeling methods employed and paying particular attention to relatively unknown historical efforts. The earliest study on the incubation period of pandemic influenza was published in 1919, providing estimates of the incubation period of Spanish flu using the daily incidence on ships departing from several ports in Australia. Although the study explicitly dealt with an unknown time of exposure, the assumed periods of exposure, which had an equal probability of infection, were too long, and thus, likely resulted in slight underestimates of the incubation period.After the suggestion that the incubation period follows lognormal distribution, Japanese epidemiologists extended this assumption to estimates of the time of exposure during a point source outbreak. Although the reason why the incubation period of acute infectious diseases tends to reveal a right-skewed distribution has been explored several times, the validity of the lognormal assumption is yet to be fully clarified. At present, various different distributions are assumed, and the lack of validity in assuming lognormal distribution is particularly apparent in the case of slowly progressing diseases. The present paper indicates that (1) analysis using well-defined short periods of exposure with appropriate statistical methods is critical when the exact time of exposure is unknown, and (2) when assuming a specific distribution for the incubation period, comparisons using different distributions are needed in addition to estimations using different datasets, analyses of the determinants of incubation period, and an understanding of the underlying disease mechanisms.

show abstract

Section: Lognormal Distribution Proposed By Philip Sartwellmentioning

confidence: 99%

Early efforts in modeling the incubation period of infectious diseases with an acute course of illness

Nishiura

2007

Emerg Themes Epidemiol

View full text Add to dashboard Cite

show abstract

“…Severe infection of brainstem nuclei, most often the vagus nucleus, has been observed in fatal cases of bulbar poliomyelitis in humans (39) and in chimpanzees and monkeys fed poliovirus. Lastly, the temporal events of reovirus infection correspond well to analyses of natural poliovirus infection (40,41), allowing for increased transport time within the longer axons of humans. Although both poliovirus and reovirus mount a viremia that can be terminated by antiviral antibody, evidence from reovirus that antibody can prevent neuronal infection (20) and that T3C9 spreads to the CNS through nerves from the intestinal tract supports the concept of neural spread ofpoliovirus to the CNS after extraneural replication (5)(6)(7).…”

Section: Resultsmentioning

confidence: 60%

Direct spread of reovirus from the intestinal lumen to the central nervous system through vagal autonomic nerve fibers.

Morrison

Sidman

Fields

1991

Proc. Natl. Acad. Sci. U.S.A.

101

View full text Add to dashboard Cite

A crucial event in the pathogenesis of sys- A fundamental unresolved issue in systemic infections with viruses entering a host through the gastrointestinal tract is the route by which virus penetrates the central nervous system (CNS) to cause encephalitis (1-4). Virus could potentially enter the nervous system by direct spread from infected plexuses of nerve fibers in the wall of the alimentary tract (5) or from nerve endings in secondarily infected muscle and visceral organs (6, 7). Alternatively, virus could gain entry to the bloodstream and then penetrate the nervous system through the meninges or through blood vessel endothelium in sites where the blood-brain barrier may be more permeable (8-10): the choroid plexus, hypothalamus, and area postrema. For poliovirus, the most well-studied neurotropic enteric virus of humans, the preponderance of opinion currently favors blood-borne spread to the CNS once viremia has commenced (2, 3, 11, 12), but spread by direct peripheral nerve penetration has not been disproven.The mammalian reoviruses are a group of enteric viruses that have been useful in deciphering the genetic basis of viral pathogenesis (13). Reoviruses enter a host from the intestinal lumen through M cells overlying ilea! Peyer's patches (14) and undergo primary replication in the intestine (15,16 The small intestine is innervated primarily by sympathetic and parasympathetic fibers of the autonomic nervous system and by sensory nerve fibers. Neuronal cell bodies of each of these fiber types have an anatomically distinct location that can be observed in histologic sections: parasympathetic in the dorsal motor nucleus of the vagus nerve (DMNV), sympathetic in the intermediolateral cell column of the thoracic and lumbar spinal cord (T4-L2), and sensory in the dorsal root ganglia of the thoracic spinal cord and the nodose ganglia of the vagus nerve (21). We have examined serial sections of brain, spinal cord, and small intestine from newborn mice inoculated perorally with T3C9 to determine the location of initial virus infection in the nervous system. Neurons of the myenteric plexus of the small intestine immediately adjacent to Peyer's patches were initially infected. Subsequently, viral antigen appeared in the CNS in neurons of the DMNV, indicating that serotype 3 reovirus spreads from the intestinal tract directly to regional nerves and then through parasympathetic fibers to the CNS. MATERIALS AND METHODSVirus. Reovirus serotype 3, field isolate strain clone 9 (T3C9; refs. 20 and 22), was derived from laboratory stocks by double plaque purification. Lysates of second-passage stocks grown on L929 mouse fibroblast monolayers were used for virus purification (23).Titer Determination. Virus titer was determined by standard plaque assay (24). Blood samples were frozen and thawed twice, disrupted by sonication, and assayed in duplicate after serial 1:10 dilutions.Inoculations. Purified virions were diluted in endotoxinfree saline (for subcutaneous injections) or distilled water (for peroral inoculation...

show abstract

“…For more than 100 years, there have been intriguing empirical observations of "right-skewed" distributions in a remarkably wide range of phenomena related to disease [55][56][57][58][59]. Examples include withinpatient incubation periods for infectious diseases like typhoid fever [55,56], polio [58], measles [60] and acute respiratory viruses [61]; exposure-based outbreaks like anthrax [62] (see [61,63] for more recent reviews); rates of cancer incidence after exposure to carcinogens [64]; and times from diagnosis to death for patients with various cancers [65] or leukemias [66].…”

Section: B Applications To Medicine: Epidemic and Disease Incubationmentioning

confidence: 99%

“…It is this 3-parameter lognormal distribution that has been frequently noted in empirical studies of disease incubation times. Originally proposed and elaborated by Sartwell [57][58][59] as a curve-fitting model, its seeming generality has led to it being called "Sartwell's Law." But it has always lacked a theoretical underpinning.…”

Section: Times To Partial Takeover: Truncationmentioning

confidence: 99%

Takeover times for a simple model of network infection

2017

View full text Add to dashboard Cite

We study a stochastic model of infection spreading on a network. At each time step a node is chosen at random, along with one of its neighbors. If the node is infected and the neighbor is susceptible, the neighbor becomes infected. How many time steps T does it take to completely infect a network of N nodes, starting from a single infected node? An analogy to the classic "coupon collector" problem of probability theory reveals that the takeover time T is dominated by extremal behavior, either when there are only a few infected nodes near the start of the process or a few susceptible nodes near the end. We show that for N 1, the takeover time T is distributed as a Gumbel distribution for the star graph, as the convolution of two Gumbel distributions for a complete graph and an Erdős-Rényi random graph, as a normal for a one-dimensional ring and a two-dimensional lattice, and as a family of intermediate skewed distributions for d-dimensional lattices with d 3 (these distributions approach the convolution of two Gumbel distributions as d approaches infinity). Connections to evolutionary dynamics, cancer, incubation periods of infectious diseases, first-passage percolation, and other spreading phenomena in biology and physics are discussed.

show abstract

The Incubation Period of Poliomyelitis

Cited by 34 publications

References 11 publications

Early efforts in modeling the incubation period of infectious diseases with an acute course of illness

Early efforts in modeling the incubation period of infectious diseases with an acute course of illness

Direct spread of reovirus from the intestinal lumen to the central nervous system through vagal autonomic nerve fibers.

Takeover times for a simple model of network infection

Contact Info

Product

Resources

About