Fièvre typhoïde / Typhoid fever

Fièvre typhoïde

Fièvre typhoïde
Classification et ressources externes
CIM-10A01.0
CIM-9002
Taches rose sur la poitrine d'un patient atteint de la typhoide

La fièvre typhoïde (du grec tuphos, torpeur) ou typhus abdominal est une maladie infectieuse décrite en 1818 par Pierre Bretonneau, causée par une bactérie de la famille Entérobactérie, du genre des salmonelles, et dont les espèces responsables sont: Salmonella enterica - typhi ou paratyphi A, B, C - . Salmonella enterica typhi est encore appelée bacille d'Eberth.

Sommaire

Épidémiologie

zones d'endémie en 2000 (rouge : forme endémie, marron : moyenne endémie

D'après l'Organisation mondiale de la santé, le nombre de patients atteints dans le monde serait compris entre 16 et 33 millions de personnes, avec plus de 200 000 décès annuellement1.

La contamination se fait par l'ingestion de boissons ou aliments souillés par les selles d'un homme infecté, malade, ou porteur sain. La typhoïde a rapidement régressé en France et en Europe suite à la javellisation de l'eau de boisson généralisée- du moins en ville- à partir de 1910 2.

La maladie est quasiment absente des pays développés, mais reste fréquente dans les autres. Sa prévalence est importante en Asie du Sud-Est, en Asie centrale et en Afrique du Sud. Le germe le plus souvent responsable reste Salmonella typhi, près de dix fois plus fréquemment retrouvé que les Salmonella paratyphi.

Aspects cliniques

Quarante-huit heures après la contamination, survient un épisode de diarrhée transitoire. Cet épisode dure une dizaine de jours (8 à 15), et correspond à la période d'incubation, pendant laquelle il y a multiplication des salmonelles dans les ganglions mésentériques; il précède la phase de dissémination du germe dans le sang (septicémie).

Au début de la phase septicémique, on observe des troubles mineurs:

  • de possibles saignements de nez (épistaxis), une langue blanchâtre (dite saburrale);
  • douleurs abdominales, diarrhée ou constipation, abdomen augmenté de volume et tendu météorisme.
  • insomnie, fatigabilité (asthénie);
  • maux de tête (sans raideur de la nuque,);
  • une rate grossie (splénomégalie);
  • une fièvre atteignant un plateau à 40 °C, sans accélération du pouls : on parle d'une dissociation pouls-température;

Le malade est prostré, la prostration pouvant aller jusqu'à la torpeur, le délire, et à des signes digestifs intenses (diarrhées). C’est la destruction des salmonelles, qui, libérant une substance toxique, l'endotoxine, provoque des ulcérations responsables d'hémorragies et de perforations digestives. Cette phase est responsable des complications, qui peuvent entraîner le décès dans 30 % des cas en l'absence de traitement.

Le diagnostic

  • Le germe n'est retrouvé dans le sang (hémoculture) que dans 60 % des cas. Il peut être retrouvé de manière inconstante dans les selles et dans les urines.
  • Le bilan sanguin standard ne montre que des anomalies non spécifiques : nombre habituellement normal des globules blancs, qui sont parfois diminués (leucopénie), parfois diminution du nombre de plaquettes sanguines, signalant des formes graves.
  • La recherche d'anticorps dirigés contre les antigènes O et H des salmonelles (test de Widal) ne permet pas de distinguer une infection actuelle d'une atteinte ancienne et guérie. Il existe depuis d'autres tests plus spécifiques, mais de réalisation difficile dans un pays du tiers monde.

Traitement et prévention

Le germe était initialement sensible au chloramphénicol, mais de nombreuses résistances apparurent dans les années 1970, et ce traitement, aux nombreux effets secondaires, a été progressivement abandonné. De même, des résistances à d'autres antibiotiques (co-trimoxazole et amoxicilline) sont apparues dans les années 1980.

Après avoir hospitalisé et isolé le malade, le traitement fait appel actuellement aux fluoroquinolones de deuxième génération ou à la ceftriaxone. La réhydratation, souvent par voie intraveineuse, est impérative pour compenser les pertes liquidiennes secondaires à la diarrhée. Un traitement contre la fièvre (antipyrétique) peut parfois être nécessaire.

Traitement préventif

La prévention passe par l'amélioration des conditions d'hygiène dans les pays d'endémie et par la vaccination. Les visiteurs doivent se méfier de l'eau locale et de la nourriture crue.

En 1888, André Chantemesse (créant le sérum de Chantemesse) et Widal démontrent la possibilité d'un vaccin contre la typhoïde3, qui sera développé par Sir Almroth Wright en 1896 (Pfeiffer lui en disputera l'antériorité 4). Le vaccin contre la typhoïde a servi dans le passé5, et encore récemment6, comme agent de la pyretothérapie / pyrothérapie.

Déclaration obligatoire

En France, en Belgique, au Liban et au Maroc cette maladie est sur la liste des maladies infectieuses à déclaration obligatoire.

Voir aussi

Article connexe

  • Mary Mallon, première porteuse saine reconnue du bacille de la typhoïde
http://fr.wikipedia.org/wiki/Fièvre_typhoïde

Typhoid fever

Typhoid Fever
Classification and external resources

Rose spots on the chest of a patient with typhoid fever due to the bacterium Salmonella Typhi
ICD-10A01.0
ICD-9002
DiseasesDB27829
eMedicineoph/686med/2331
MeSHD014435

Typhoid fever, also known as Salmonella Typhi or commonly just typhoid,[1] is a common worldwide illness, transmitted by the ingestion of food or water contaminated with the feces of an infected person.[2] The bacteria then perforate through the intestinal wall and are phagocytosed by macrophages. The organism is a Gram-negative short bacillus that is motile due to its peritrichousflagella. The bacterium grows best at 37 °C/99 °F – human body temperature.

This fever received various names, such as gastric feverthe bendsabdominal typhusinfantile remittent feverslow fevernervous feverpythogenic fever, etc. The name of " typhoid " was given by Louis in 1829, as a derivative from typhus.

The impact of this disease falls sharply with the application of modern sanitation techniques.

Contents

Symptoms

Incidence of typhoid fever
 Strongly endemic
 Endemic
 Sporadic cases

Typhoid fever is characterized by a slowly progressive fever as high as 40 °C (104 °F), profuse sweating, gastroenteritis, and nonbloody diarrhea. Less commonly, a rash of flat, rose-colored spots may appear.[3]

Classically, the course of untreated typhoid fever is divided into four individual stages, each lasting approximately one week. In the first week, there is a slowly rising temperature with relative bradycardiamalaise, headache and cough. A bloody nose (epistaxis) is seen in a quarter of cases and abdominal pain is also possible. There is leukopenia, a decrease in the number of circulating white blood cells, with eosinopenia and relative lymphocytosis, a positive diazo reaction and blood cultures are positive for Salmonella typhi or paratyphi. The classic Widal test is negative in the first week.

In the second week of the infection, the patient lies prostrate with high fever in plateau around 40 °C (104 °F) and bradycardia (sphygmothermic dissociation), classically with a dicrotic pulse wave. Delirium is frequent, frequently calm, but sometimes agitated. This delirium gives to typhoid the nickname of "nervous fever". Rose spots appear on the lower chest and abdomen in around a third of patients. There are rhonchi in lung bases. The abdomen is distended and painful in the right lower quadrant where borborygmi can be heard. Diarrhea can occur in this stage : six to eight stools in a day, green with a characteristic smell, comparable to pea soup. However, constipation is also frequent. The spleen and liver are enlarged (hepatosplenomegaly) and tender, and there is elevation of liver transaminases. The Widal reaction is strongly positive with antiO and antiH antibodies. Blood cultures are sometimes still positive at this stage. (The major symptom of this fever is the fever usually rises in the afternoon up to the first and second week.)

In the third week of typhoid fever, a number of complications can occur :

The fever is still very high and oscillates very little over 24 hours. Dehydration ensues and the patient is delirious (typhoid state). By the end of third week the fever has started reducing (defervescence). This carries on into the fourth and final week.

Diagnosis

Diagnosis is made by any bloodbone marrow or stool cultures and with the Widal test (demonstration of salmonella antibodies against antigens O-somatic and H-flagellar). In epidemics and less wealthy countries, after excluding malariadysentery or pneumonia, a therapeutic trial time with chloramphenicol is generally undertaken while awaiting the results of Widal test and cultures of the blood and stool.[4]

The term "enteric fever" is a collective term that refers to typhoid and paratyphoid.[5]

Treatment

The rediscovery of oral rehydration therapy in the 1960s, and proven in the Bangladesh Liberation War, provided a simple way to prevent many of the deaths of diarrheal diseases in general.

Where resistance is uncommon, the treatment of choice is a fluoroquinolone such as ciprofloxacin[5][6] otherwise, a third-generation cephalosporin such as ceftriaxone or cefotaxime is the first choice.[7][8][9] Cefixime is a suitable oral alternative.[10][11]

Typhoid fever in most cases is not fatal. Antibiotics, such as ampicillinchloramphenicoltrimethoprim-sulfamethoxazoleAmoxicillin and ciprofloxacin, have been commonly used to treat typhoid fever in developed countries. Prompt treatment of the disease with antibiotics reduces the case-fatality rate to approximately 1%.

When untreated, typhoid fever persists for three weeks to a month. Death occurs in between 10% and 30 % of untreated cases[citation needed]. In some communities, however, case-fatality rates may reach as high as 47 %.[citation needed]

Resistance

Resistance to ampicillin, chloramphenicol, trimethoprim-sulfamethoxazole and streptomycin is now common, and these agents have not been used as first line treatment now for almost 20 years.[citation needed] Typhoid that is resistant to these agents is known as multidrug-resistant typhoid (MDR typhoid).

Ciprofloxacin resistance is an increasing problem, especially in the Indian subcontinent and Southeast Asia. Many centres are therefore moving away from using ciprofloxacin as first line for treating suspected typhoid originating in South America, India, Pakistan, Bangladesh, Thailand or Vietnam. For these patients, the recommended first line treatment is ceftriaxone. It has also been suggested Azithromycin is better at treating typhoid in resistant populations than both fluoroquinolone drugs and ceftriaxone.[12] Azithromycin significantly reduces relapse rates compared with ceftriaxone.

There is a separate problem with laboratory testing for reduced susceptibility to ciprofloxacin: current recommendations are that isolates should be tested simultaneously against ciprofloxacin (CIP) and against nalidixic acid (NAL), and that isolates that are sensitive to both CIP and NAL should be reported as "sensitive to ciprofloxacin", but that isolates testing sensitive to CIP but not to NAL should be reported as "reduced sensitivity to ciprofloxacin". However, an analysis of 271 isolates showed that around 18% of isolates with a reduced susceptibility to ciprofloxacin (MIC 0.125–1.0 mg/l) would not be picked up by this method.[13] It is not certain how this problem can be solved, because most laboratories around the world (including the West) are dependent on disc testing and cannot test for MICs.

Prevention

Doctor administering a typhoidvaccination at a school in San Augustine County, Texas

Sanitation and hygiene are the critical measures that can be taken to prevent typhoid. Typhoid does not affect animals and therefore transmission is only from human to human. Typhoid can only spread in environments where human feces or urine are able to come into contact with food or drinking water. Careful food preparation and washing of hands are crucial to preventing typhoid.

A vaccine against typhoid fever was developed during World War II by Ralph Walter Graystone Wyckoff[14]. There are two vaccines currently recommended by the World Health Organization for the prevention of typhoid:[15]these are the live, oral Ty21a vaccine (sold as Vivotif Berna) and the injectable Typhoid polysaccharide vaccine (sold as Typhim Vi by Sanofi Pasteur and Typherix by GlaxoSmithKline). Both are between 50% to 80% protective and are recommended for travelers to areas where typhoid is endemic. Boosters are recommended every 5 years for the oral vaccine and every 2 years for the injectable form. There exists an older killed whole-cell vaccine that is still used in countries where the newer preparations are not available, but this vaccine is no longer recommended for use, because it has a higher rate of side effects (mainly pain and inflammation at the site of the injection).[15]

1939 conceptual illustration showing various ways that typhoid bacteria can contaminate a water well (center)

Transmission

Flying insects feeding on feces may occasionally transfer the bacteria through poor hygiene habits and public sanitation conditions. Public education campaigns encouraging people to wash their hands after defecating and before handling food are an important component in controlling spread of the disease. According to statistics from the United States Center for Disease Control, the chlorination of drinking water has led to dramatic decreases in the transmission of typhoid fever in the U.S.

A person may become an asymptomatic carrier of typhoid fever, suffering no symptoms, but capable of infecting others. According to the Centers for Disease Control approximately 5% of people who contract typhoid continue to carry the disease after they recover. The most famous asymptomatic carrier was Mary Mallon (commonly known as "Typhoid Mary"), a young cook who was responsible for infecting at least 53 people with typhoid, three of whom died from the disease. Mallon was the first apparently perfectly healthy person known to be responsible for an "epidemic".

Death rates for typhoid fever in the U.S. 1906–1960

Many carriers of typhoid were locked into an isolation ward never to be released in order to prevent further typhoid cases. These people often deteriorated mentally, driven mad by the conditions they lived in.[16]

Epidemiology

With an estimated 16–33 million cases of annually resulting in 216,000 deaths in endemic areas, the World Health Organization identifies typhoid as a serious public health problem. Its incidence is highest in children and young adults between 5 and 19 years old.[17]

Heterozygous advantage

It is thought that cystic fibrosis may have risen to its present levels (1 in 1600 in UK) due to the heterozygous advantage that it confers against typhoid fever.[18] The CFTR protein is present in both the lungs and the intestinal epithelium, and the mutant cystic fibrosis form of the CFTR protein prevents entry of the typhoid bacterium into the body through the intestinal epithelium.

History

Around 430–424 B.C.E., a devastating plague, which some believe to have been typhoid fever, killed one third of the population of Athens, including their leader Pericles. The balance of power shifted from Athens toSparta, ending the Golden Age of Pericles that had marked Athenian dominance in the ancient world. Ancient historian Thucydides also contracted the disease, but he survived to write about the plague. His writings are the primary source on this outbreak. The cause of the plague has long been disputed, with modern academics and medical scientists considering epidemic typhus the most likely cause. However, a 2006 study detectedDNA sequences similar to those of the bacterium responsible for typhoid fever.[19] Other scientists have disputed the findings, citing serious methodologic flaws in the dental pulp-derived DNA study.[20] The disease is most commonly transmitted through poor hygiene habits and public sanitation conditions; during the period in question, the whole population of Attica was besieged within the Long Walls and lived in tents.

Mary Mallon ("Typhoid Mary") in a hospital bed (foreground). She was forcibly quarantined as a carrier of typhoid fever in 1907 for three years and then again from 1915 until her death in 1938.

In the late 19th century, typhoid fever mortality rate in Chicago averaged 65 per 100,000 people a year. The worst year was 1891, when the typhoid death rate was 174 per 100,000 people.[21] The most notorious carrier of typhoid fever—but by no means the most destructive—was Mary Mallon, also known as Typhoid Mary. In 1907, she became the first American carrier to be identified and traced. She was a cook in New York. She is closely associated with fifty-three cases and three deaths.[22] Public health authorities told Mary to give up working as a cook or have her gall bladder removed. Mary quit her job but returned later under a false name. She was detained and quarantined after another typhoid outbreak. She died of pneumonia after 26 years in quarantine.

In 1897, Almroth Edward Wright developed an effective vaccine. In 1909, Frederick F. Russell, a U.S. Army physician, developed an American typhoid vaccine and two years later his vaccination program became the first in which an entire army was immunized. It eliminated typhoid as a significant cause of morbidity and mortality in the U.S. military.

Most developed countries saw declining rates of typhoid fever throughout the first half of the 20th century due to vaccinations and advances in public sanitation and hygiene. Antibiotics were introduced in clinical practice in 1942, greatly reducing mortality. Today, incidence of typhoid fever in developed countries is around 5 cases per 1,000,000 people per year.

An outbreak in the Democratic Republic of Congo in 2004–05 recorded more than 42,000 cases and 214 deaths.[17]

Typhoid fever was also known as suette milliaire in nineteenth-century France.

Famous victims

Famous people who have had the disease include:

Died in 9 of January , 1934 by Typhoid fever.

In fiction

  • Gilbert Blythe (of the Anne of Green Gables series) almost dies of typhoid fever in Anne of the Island by L.M. Montgomery.
  • Walter Blythe (son of Anne and Gilbert Blythe in the latter Anne of Green Gables books) was in recovery from typhoid in "Rilla of Ingleside" and this is seen as the reason why he does not enlist at the onset of WWI
  • Johann "Hanno" Buddenbrook, in Thomas Mann's novel, Buddenbrooks, dies of typhoid fever, and the book includes a long medical description of the disease and its effects.
  • John H. Watson (Sherlock Holmes' famed companion) nearly died of typhoid contracted in India, and returned to England for convalescence – where he first met the detective.
  • Scarlet O'Hara's mother and sisters in Gone With the Wind
  • Suttree in the Cormac McCarthy novel of the same name nearly dies of typhoid fever in the final scenes of the novel.
  • In the 1950 western Stars in My Crown, the town is devastated by typhoid spread by a school's well.

See also

Further reading

External links

http://en.wikipedia.org/wiki/Typhoid_fever

Kauffman-White classification

The Kauffman and White classification scheme is a classification system that permits serological varieties of the genus Salmonella to be differentiated from each other. This scheme differentiates isolates by determining which surface antigens are produced by the bacterium. First, the "O" antigen type is determined. "O" antigens are the polysaccharides associated with the lipopolysaccharide of the bacterial outer membrane. Having found the "O" antigen group, the "H" antigen is determined. The "H" antigens are proteins associated with the bacterial flagella (singular; flagellum). Salmonellas exist in two phases; a motile phase and a non-motile phase. These are also referred to as the specific and non-specific phases. Different "H" antigens are produced depending on the phase in which the salmonella is found. Non-motile isolates may be "switched" to the motile phase using a Cragie tube - bacteria are inoculated down the center of a hollow tube in a semi-solid nutrient agar. Those bacteria that become motile can then swim out of the bottom of the tube and are recovered from the agar outside of the tube. Pathogenic strains of Salmonella typhi carry an additional antigen, "Vi", so-called because of the enhanced virulence of strains that produce this antigen, which is associated with a bacterial capsule.

"O"-groupSerovar"O" antigensPhase 1 (motile) "H" antigensPhase 2 (non-motile) "H" antigens
AS.paratyphi A1,2,12ano phase 2 antigen
 S. paratyphi A var. durazzo2,12ano phase 2 antigen
BS. paratyphi B1,4,5,12b1,2
 S. paratyphi B var. odense1,4,12b1,2
 S. java1,4,5,12b(1,2)
 S. limete1,4,12,27b1,5
 S. typhimurium1,4,5,12i1,2
 S. typhimurium var. copenhagen1,4,12i1,2
 S. agama4,12i1,6
 S. abortus-equi4,12no phase 1 antigene,n,x
 S. abortus-ovis4,12c1,6
 S. agona4,12f,g,sno phase 2 antigen
 S. brandenburg4,12l,ve,n,z15
 S. bredeney1,4,12,27l,v1,7
 S. derby1,4,5,12f,gno phase 2 antigen
 S. heidelberg1,4,5,12r1,2
 S. saint-paul1,4,5,12e,h1,2
 S. salinatis4,12d,e,hd,e,n,z15
 S. stanley4,5,12d1,2
C1S. paratyphi C6,7,c1,5
 S. cholerae-suis6,7c1,5
 S. cholerae-suis var. kuunzendorf6,7(c)1,5
 S. decatur6,7c1,5
 S. typhi-suis6,7c1,5
 S. bareilly6,7y1,5
 S. infantis6,7r1,5
 S. menston6,7g,s,tno phase 2 antigen
 S. montevideo6,7g,m,sno phase 2 antigen
 S. oranienburg6,7m,tno phase 2 antigen
 S. thompson6,7k1,5
C2S. bovis-morbificans6,8r1,5
 S. newport6,8e,h1,2
DS. typhi9,12,Vidno phase 2 antigen
 S. ndolo9,12d1,5
 S. dublin1,9,12g,pno phase 2 antigen
 S. enteritidis1,9,12g,mno phase 2 antigen
 S. gallinarum1,9,12no phase 1 antigenno phase 2 antigen
 S. pullorum(1),9,12no phase 1 antigenno phase 2 antigen
 S. Panama1,9,12l,v1,5
 S. miami1,9,12a1,5
 S. sendai1,9,12a1,5
E1S. anatum3,10e,h1,6
 S. give3,10l,v1,7
 S. london3,10l,v1,6
 S. meleagridis3,10e,hl,w
E2S. cambridge3,15e,hl,w
 S. newington3,15e,h1,6
E3S. minneapolis(3),(15),34e,h1,6
E4S. senftenberg1,3,19g,s,tno phase 2 antigen
 S. simsbury1,3,19no phase 1 antigenz27
FS. aberdeen11i1,2
GS. cubana1,13,23z29no phase 2 antigen
 S. poona13,22z1,6
HS. heves6,14,24d1,5
 S. onderstepoort1,6,14,25e,h1,5
IS. Brazil16a1,5
 S. hvittingfoss16be,n,x
OthersS. kirkee17b1,2
 S. adelaide35f,gno phase 2 antigen
 S. locarno57z29z42
  • Antigens in brackets are those that are rarely expressed in that serovar.

The cost of maintaining a full set of antisera precludes all but reference laboratories from performing a complete serological identification of salmonella isolates. Most laboratories stock only a limited range of antisera, and the choice of stock sera is largely determined by the nature of the specimens to be processed.

A common set of working antisera is shown below:

O-antiseraH-antisera
polyvalent-O, groups A-Gpolyvalent-H, specific and non-specific
2-O, group Apolyvalent-H, non-specific factors 1,2,5,6,7
4-O, group Ba-H (S. paratyphi A)
6, 7-O, group C1b-H (S. paratyphi B)
8-O, group C2c-H (S. paratyphi C)
9-O, group Dd-H (S. typhi)
3, 10, 15, 19-O group Ee,h-H (S. newport)
11-O, group Ff,g-H (S. derby)
13, 22-O, group Gg,m-H (S. enteritidis)
 i-H (S. typhimurium)
 k-H (S. thompson)
 l,v-H (S. london)
 m,t-H (S. oranienburg)
 r-H (S. bovis morbificans)

Laboratories that are likely to investigate typhoid also carry antiserum raised against the Vi antigen.

A set of "Rapid Diagnostic Sera" is also held and is used for determination of common specific H-antigens except i-H. After obtaining a positive agglutination with the polyvalent-H specific and non-specific antiserum, the three RDS antisera are used to identify the H antigen present. Depending on the pattern of positive and negative reactions with the RDS antisera, the specific H antigen may be identified:

antigenRDS1RDS2RDS3
bagglutinationagglutinationno agglutination
dagglutinationno agglutinationagglutination
Eagglutinationagglutinationagglutination
Gno agglutinationno agglutinationagglutination
kno agglutinationagglutinationagglutination
Lno agglutinationagglutinationno agglutination
ragglutinationno agglutinationno agglutination

E = polyvalent for eh, enx, etc.
G = polyvalent for gm, gp, 
etc.
L = polyvalent for lv, lw, 
etc.


Comments