Listeriosis natural history, complications and prognosis

Jump to navigation Jump to search

Listeriosis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Listeriosis from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Screening

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

MRI

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Listeriosis natural history, complications and prognosis On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Listeriosis natural history, complications and prognosis

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Listeriosis natural history, complications and prognosis

CDC on Listeriosis natural history, complications and prognosis

Listeriosis natural history, complications and prognosis in the news

Blogs on Listeriosis natural history, complications and prognosis

Directions to Hospitals Treating Listeriosis

Risk calculators and risk factors for Listeriosis natural history, complications and prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Overview

Natural History

The majority of cases of listeriosis are sporadic. ALthough the source is usually unknown, contaminated food is the most common vehicle of transmission. Some patients may be transitory carriers of the bacteria, without having the disease. Once the bacteria penetrate the gastrointestinal lining, it will travel through the blood to otherwise aseptic sites, such as the CNS, the uterus, and sometimes the heart, being responsible for diseases such as:

  • Febrile gastroenteritis
  • Infection in pregnancy
  • Sepsis of unknown origin
  • Bacteremia
  • CNS Infection
  • Endocarditis
  • Focal infections

The mean incubation period for febrile gastroenteritis following listeriosis is 24h, however, these may range from 6h up to 10 days. In the case of the remaining invasive diseases, the mean incubation period is 35 days, ranging from 1 up to 91 days.[1][2][3]

Febrile Gastroenteritis

Febrilegastroenteritis accounts for less than 1% of reported bacterial food-born infections occurring usually after ingestion of a large inoculum of bacteria from contaminated foods. Illness typically occurs 24 hours after ingestion of contaminated food, presenting with symptoms such as fever, nausea, vomiting and watery diarrhea.

It generally lasts for 2 days and the patient experiences complete recovery from the symptoms. Some patients may be asymptomatic for the disease, while others, immunocompromised, pregnant women and elder patients, in rare cases, present with invasive infection. L. monocytogenes infection should be considered when outbreaks of foodborne gastroenteritis surge and stool cultures fail to identify the pathogen[4].

Infection in Pregnancy

Pregnant women have greater risk of contracting listeriosis since during pregnancy there is a slight impairment of cell-mediated immunity. Lysteria is also able to proliferate in the placenta, in hard-to-reach areas for the immune system. Infection occurs more frequently during the third trimester of gestation, with an estimated 17 fold increase[5], presenting most commonly with flu-like symptoms, such as fever and chills.

The infection may be mild and the diagnosis missed when blood cultures are not obtained. Since bacteremia with no CNS involvement is common rule in pregnant women with listeriosis, blood cultures should always be obtained in pregnant women who present with fever, with no other possible cause, such as UTI or pharyngitis. Because cell-to-cell transmission facilitates maternal-fetal transmission[6], listeriosis in pregnant women, can result in fetal death, premature birth, or infected newborns.

Among pregnant women with listeriosis, 2/3 of the surviving infants develop clinical neonatal listeriosis.[7]. The newborn also has great risk of developing granulomatosis infantiseptica, a severe in utero infection resulting from transplacental transmission, in which infants may present with:

L. monocytogenes is one of the three major causes of neonatal meningitis, worldwide. The early diagnosis and treatment of pregnant women infected with Listeria may lead to the birth of a normal healthy child.[8]

Sepsis of Unknown Origin

Occurs in patients of all ages. Neonates usually tend to acquire the infection during or after birth. When this occurs during the first week of life, it usually manifests as sepsis, while after this first week, it tends to have more variable manifestations, such as meningitis.

Early onset of sepsis is associated with higher neonatal mortality. In this case, L. monocitogenes can be isolated from conjunctivae, amniotic fluid, meconium, placental blood, with higher concentrations of bacteria being found in the neonatal lung and gut, which suggests that infection is acquired in uterus, by inhalation of infected amniotic fluid.[9]

Bacteremia

After the neonatal period, the most common manifestation of listeriosis is bacteremia without and evident focus of infection. The clinical manifestations may include fever, myalgias and nausea.

Often times, healthy individuals who experience these manifestations do not have blood cultures, they have higher probability of transient bacteremias going undetected.[10]

CNS Infection

Endocarditis

Focal Infections

Most focal infections do not have specific characteristics. These infections occur more often in immunocompromised patients, and include:

Complications

Invasive disease might complicate into:[11][12]

  • Reinfection (rare)

Prognosis

The prognosis of Listeriosis depends on the health status of the host:[17]

  • Healthy older children and adults have a lower death rate.
  • Listeriosis in a fetus or infant results in a poor outcome with a high death rate.
  • Even with prompt treatment, some listeriosis cases result in death. This is particularly likely in older adults and in persons with other medical conditions.

References

  1. Ooi ST, Lorber B (2005). "Gastroenteritis due to Listeria monocytogenes". Clin Infect Dis. 40 (9): 1327–32. doi:10.1086/429324. PMID 15825036.
  2. Dalton CB, Austin CC, Sobel J, Hayes PS, Bibb WF, Graves LM; et al. (1997). "An outbreak of gastroenteritis and fever due to Listeria monocytogenes in milk". N Engl J Med. 336 (2): 100–5. doi:10.1056/NEJM199701093360204. PMID 8988887.
  3. Linnan MJ, Mascola L, Lou XD, Goulet V, May S, Salminen C; et al. (1988). "Epidemic listeriosis associated with Mexican-style cheese". N Engl J Med. 319 (13): 823–8. doi:10.1056/NEJM198809293191303. PMID 3137471.
  4. Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0-443-06839-9.
  5. Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0-443-06839-9.
  6. Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0-443-06839-9.
  7. Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0-443-06839-9.
  8. Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0-443-06839-9.
  9. Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0-443-06839-9.
  10. Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0-443-06839-9.
  11. Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0-443-06839-9.
  12. "Listeriosis".
  13. 13.0 13.1 Gray, M. L., and A. H. Killinger. 1966. Listeria monocytogenes and listeric infection. Bacteriol. Rev. 30:309-382.
  14. Armstrong, R. W., and P. C. Fung. 1993. Brainstem encephalitis (Rhombencephalitis) due to Listeria monocytogenes: case report and review. Clin. Infect. Dis. 16:689-702.
  15. Holland, S., E. Alfonso, H. Gelender, D. Heidemann, A. Mendelsohn, S. Ullman, and D. Miller. 1987. Corneal ulcer due to Listeria monocytogenes. Cornea 6:144-146.
  16. Whitelock-Jones, L., J. Carswell, and K. C. Rassmussen. 1989. Listeria pneumonia. A case report. South African Medical Journal 75:188-189.
  17. "Listeria".

Template:WH Template:WS