Infectious disease natural history, complications and prognosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [3]
Natural History, Complications and Prognosis
One of the ways to prevent or slow down the transmission of infectious diseases is to recognize the different characteristics of various diseases.[1] Some critical disease characteristics that should be evaluated include virulence, distance traveled by victims, and level of contagiousness. The human strains of Ebola virus, for example, incapacitate its victims extremely quickly and kills them soon after. As a result, the victims of this disease do not have the opportunity to travel very far from the initial infection zone.[2] Also, this virus must spread through skin lesions or permeable membranes such as the eye. Thus, the initial stage of Ebola is not very contagious since its victims experience only internal hemorrhaging. As a result of the above features, the spread of Ebola is very rapid and usually stays within a relatively confined geographical area. In contrast, the Human Immunodeficiency Virus (HIV) kills its victims very slowly by attacking their immune system.[3] As a result, many of its victims transmit the virus to other individuals before even realizing that they are carrying the disease. Also, the relatively low virulence allows its victims to travel long distances, increasing the likelihood of an epidemic.
Another effective way to decrease the transmission rate of infectious diseases is to recognize the effects of small-world networks.[1] In epidemics, there are often extensive interactions within hubs or groups of infected individuals and other interactions within discrete hubs of susceptible individuals. Despite the low interaction between discrete hubs, the disease can jump to and spread in a susceptible hub via a single or few interactions with an infected hub. Thus, infection rates in small-world networks can be reduced somewhat if interactions between individuals within infected hubs are eliminated (Figure 1). However, infection rates can be drastically reduced if the main focus is on the prevention of transmission jumps between hubs. The use of needle exchange programs in areas with a high density of drug users with HIV is an example of the successful implementation of this treatment method. [6] Another example is the use of ring culling or vaccination of potentially susceptible livestock in adjacent farms to prevent the spread of the foot-and-mouth virus in 2001.[4]
General methods to prevent transmission of pathogens may include disinfection and pest control.
Immunity
Infection with most pathogens does not result in death of the host and the offending organism is ultimately cleared after the symptoms of the disease have waned.[5] This process requires immune mechanisms to kill or inactivate the inoculum of the pathogen. Specific acquired immunity against infectious diseases may be mediated by antibodies and/or T lymphocytes. Immunity mediated by these two factors may be manifested by:
- a direct effect upon a pathogen, such as antibody-initiated complement-dependent bacteriolysis, opsonoization, phagocytosis and killing, as occurs for some bacteria,
- neutralization of viruses so that these organisms cannot enter cells,
- or by T lymphocytes which will kill a cell parasitized by a microorganism.
The immune system response to a microorganism often causes symptoms such as a high fever and inflammation, and has the potential to be more devastating than direct damage caused by a microbe.[3]
Resistance to infection (immunity) may be acquired following a disease, by asymptomatic carriage of the pathogen, by harboring an organism with a similar structure (crossreacting), or by vaccination. Knowledge of the protective antigens and specific acquired host immune factors is more complete for primary pathogens than for opportunistic pathogens.
Immune resistance to an infectious disease requires a critical level of either antigen-specific antibodies and/or T cells when the host encounters the pathogen. Some individuals develop natural serum antibodies to the surface polysaccharides of some agents although they have had little or no contact with the agent, these natural antibodies confer specific protection to adults and are passively transmitted to newborns.
Host genetic factors
The clearance of the pathogens, either treatment-induced or spontaneous, it can be influenced by the genetic variants carried by the individual patients. For instance, for genotype 1 hepatitis C treated with Pegylated interferon-alpha-2a or Pegylated interferon-alpha-2b (brand names Pegasys or PEG-Intron) combined with ribavirin, it has been shown that genetic polymorphisms near the human IL28B gene, encoding interferon lambda 3, are associated with significant differences in the treatment-induced clearance of the virus. This finding, originally reported in Nature,[6] showed that genotype 1 hepatitis C patients carrying certain genetic variant alleles near the IL28B gene are more possibly to achieve sustained virological response after the treatment than others. Later report from Nature[7] demonstrated that the same genetic variants are also associated with the natural clearance of the genotype 1 hepatitis C virus.
References
- ↑ 1.0 1.1 Watts, Duncan (2003). Six degrees: the science of a connected age. London: William Heinemann. ISBN 0-393-04142-5.
- ↑ Preston, Richard (1995). The hot zone. Garden City, N.Y.: Anchor Books. ISBN 0-385-49522-6.
- ↑ 3.0 3.1
- ↑ Ferguson NM, Donnelly CA, Anderson RM (2001). "The foot-and-mouth epidemic in Great Britain: pattern of spread and impact of interventions". Science. 292 (5519): 1155–60. doi:10.1126/science.1061020. PMID 11303090. Unknown parameter
|month=ignored (help) - ↑
- ↑ Ge D; Fellay J; Thompson AJ; et al. (2009). "Genetic variation in IL28B predicts hepatitis C treatment-induced viral clearance". Nature. 461 (7262): 399–401. doi:10.1038/nature08309. PMID 19684573. Unknown parameter
|author-separator=ignored (help) - ↑ Thomas DL; Thio CL; Martin MP; et al. (2009). "Genetic variation in IL28B and spontaneous clearance of hepatitis C virus". Nature. 461 (7265): 798–801. doi:10.1038/nature08463. PMC 3172006. PMID 19759533. Unknown parameter
|author-separator=ignored (help)