Listeriosis natural history, complications and prognosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
Listeriosis is commonly transmitted through contaminated food. The clinical presentation of the disease is related to the previous health status of the patient. Although asymptomatic carriers may be found, the disease is commonly manifested as a febrile gastroenteritis. Other more invasive manifestations of the disease include: sepsis of unknown origin, bacteremia, CNS infection, endocarditis and focal infections. Possible complications of listeriosis include: ARDS, rhabdomyolysis, acute renal failure and pneumonia.
Natural History
The majority of cases of listeriosis are sporadic. Although the source is often unknown, contaminated food is the most common vehicle of transmission. Some patients may be transitory carriers of the bacteria without showing signs of the disease. Once the bacteria penetrate the gastrointestinal lining, it will travel through the bloodstream 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, this 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:
- disseminated abscesses
- granulomas in multiple internal organs (brain, lungs, liver, spleen and kidneys)
- papular or ulcerative skin lesions.
- most infants with this disease are stillborn or die soon after birth.
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]
- Listerial meningoencephalitis is more common in neonates after 3 days of age, as well as in immunocompromised and elderly adults.
- Adults presenting Listerial sepsis, are most commonly immunocompromised or elderly, and typically present with fever and chills. Septic shock can occur with brain and/or meningeal involvement, leading to meningoencephalitis or cerebritis.
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
Because L. monocytogenes has tropism for the brain stem and meninges, unlike other causes of bacterial meningitis, Listeria tends to cause parenchymal brain infections. Therefore, most patients will experience altered consciousness, seizures and/or movement disorders, and will truly have meningoencephalitis.
Central Nervous System infection is commonly manifested by meningoencephalitis, while cerebritis is a less common manifestation. "In a study from the Massachusetts General Hospita, with CNS listeriosis outside neonatal period and pregnancy, the most common predisposing factor for developing listerial meningitis was malignancy, the second most common factor being transplantation, followed by alcoholism and liver disease, immunosuppression and steroid treatment, diabetes mellitus and HIV".[11]
Meningoencephalitis
Occurs more frequently in neonates after 3 days of age, in immunocompromised, and elderly patients. The clinical presentation can range from mild fever and mental status changes, to a more aggressive course with coma. There may also be an encephalic component, which will present with focal neurological signs, such as cranial nerve abnormalities, ataxia, and hemiplegia.
Cerebritis/ Encephalitis
Results from direct hematogenous invasion of cerebral parenchyma, with or without meningeal involvement, probably sign of an early localised infection of the parenchyma, which may eventually progress into brain abscess. Cerebritis may occur alongside meningitis in the same patient. In these cases, the clinical picture is dominated by altered consciousness or cognitive disfunction, but may also manifest as[12] fever and hemiplegia.
Rhombencephalitis
Rare manifestation of CNS infection, which more commonly affects healthy individuals through the ingestion of food contaminated with Listeria, often in outbreaks. Rhombencephalitis often follows a biphasic course, beginning with headache, fever, Nausea and vomiting, for the first 4 days. Afterwards, this phase is followed by a period characterized by abut onset of asymmetric cranial nerve palsies, ataxia, decreased consciousness, seizures, sensory deficits and respiratory failure.
In this type of the disease, mortality is high and the survivors tend to experience serious sequelae.
Brain abscess
Most cases occur in high risk patients. The subcortical abscesses tend to be located in the thalamus, pons and/or medulla, sites which are rarely affected by other bacteria.[13].
Spinal cord infection
Rare cases of spinal cord involvement have been reported. However, when spinal cord is affected in the setting of acute bacterial meningitis of uncertain etiology, L. monocytogenes should be considered"[14].
Focal Infections
Most focal infections do not have specific characteristics. These infections occur more often in immunocompromised patients, and include:
- Skin or eye infections
- Oculoglandular syndrome, pneumonia, empyema, myocarditis, lymphadenitis, septic arthritis, osteomyelitis and necrotizing fasciitis.
- Brain abscess and spinal abscesses, as well as cholecystitis, resulting from hematogenous dissemination.
- Acute hepatitis, simulating viral hepatitis, seen in patients with disseminated infections.
- Peritonitis, seen in cirrhosis and continuous ambulatory peritoneal dialysis patients.
Endocarditis
Listerial endocarditis usually leads to native and prosthetic valve disease, having an elevated rate of septic complications. Listerial endocarditis alone, may be an indicator of a GI tract abnormality, such as cancer[15].
Complications
Invasive disease might complicate into:[16][17]
- Disseminated intravascular coagulation
- ARDS
- Rhabdomyolysis
- Acute Renal Failure
- Septicemia[18], meningitis (or meningoencephalitis)[18]
- Encephalitis[19]
- Corneal ulcer[20]
- Pneumonia[21]
- Intrauterine or cervical infection in pregnant women, may result in:
- Spontaneous abortion (2nd/3rd trimester)
- Stillbirth
- Surviving neonates of Fetomaternal Listeriosis may suffer from:
- Granulomatosis infantiseptica - pyogenic granulomas distributed over the whole body, and may suffer from physical retardation
- Influenza-like symptoms, including persistent fever usually precede the onset of the aforementioned disorders.
- Reinfection (rare)
Prognosis
The prognosis of Listeriosis depends on the health status of the host:[22]
- 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
- ↑ Ooi ST, Lorber B (2005). "Gastroenteritis due to Listeria monocytogenes". Clin Infect Dis. 40 (9): 1327–32. doi:10.1086/429324. PMID 15825036.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ "Listeriosis".
- ↑ 18.0 18.1 Gray, M. L., and A. H. Killinger. 1966. Listeria monocytogenes and listeric infection. Bacteriol. Rev. 30:309-382.
- ↑ 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.
- ↑ 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.
- ↑ Whitelock-Jones, L., J. Carswell, and K. C. Rassmussen. 1989. Listeria pneumonia. A case report. South African Medical Journal 75:188-189.
- ↑ "Listeria".