Typhoid and Cholera Flashcards
(29 cards)
Two organisms prevalent in disasters
- Both begin as intestinal disease
- One causes fever, other bloodless massive water loss
- one invasion-based. other toxin
Typhoid or Enteric Fever
- Caused by specific serotype of a subspecies of Salmonella enterica.
- There are many types of subspecies and serotypes
- Salmonella enterica subspecies enterica serotype typhi causes typhoid fever.
- Salmonella enterica serotype enteritidis causes gastro enteritis.
- Salmonella enterica serotypes paratyphi A, B and C cause paratyphoid fever ( weaker version of fever).
Typhoid Fever
- Rare in developed countries that are now termed as High Income Countries
- More prevalent in low/ middle income countries
Salmonella species
- Gram-negative bacilli (rod shaped)
- oxidase negative
- highly motile by peritrichous flagella ( flagella that cover the whole cell)
- Differentiate by serotyping
Typhoid fever: Identification
Blood culture, stool (xylose lysine deoxycholate, XLD media). Serology using antibodies to detect for antigens in patient blood: Widal test-50% effective: Serotype typhi Kaufmann-White agglutination. O or somatic antigen- IgM appears early. Vi antigen - surface polysaccharide and important Virulence factor. H or flagella antigen - IgG appear later. A,B,C Para typhi have O and H antigens. ELISA: uses antigens specific to each serotype to detect antibodies for differentiation.
Typhoid Disease transmission
- Through ingestion of food or drink contaminated by faeces/ urine of infected people
- Healthy carriers excluded from handling food to avoid continued contamination as symptoms usually develop 1-3 weeks after exposure and can be mild or severe with a healthy carrier state following acute illness.
Typhoid Disease symptoms
- Develop 1-3 weeks after exposure, may be mild or severe.
- High fever, malaise, headache, constipation or diarrhoea, rose-coloured spots on the chest, enlarged spleen and liver.
Typhoid disease treatment
- Antibiotics
- widespread resistance to common antimicrobials
Typhoid Route of transmission
- Typhi and paratyphi
strains are primarily pathogens of humans. - Rarely if ever isolated from other animals
- Ingestion of organisms from an individual or contaminated source (human faeces)
- Healthy carriers excluded from handling food to avoid continued contamination as symptoms usually develop 1-3 weeks after exposure and can be mild or severe with a healthy carrier state following acute illness.
Infective dose though to be about 10^6 and 10^9 (some <103 for typhi). Variation in virulence- low acidity of host stomach, immunosuppression
Typhoid Colonisation, spread and clinical disease
Enter via M cells (non typhoid). Bind to host via fimbriae to CFTM ( Cystic fibrosis transmembrane conductance receptor). Type III secretion system induces bacterial mediated endocytosis (BME). Up-regulate CFTM, so more entry. First bacteraemia/stage: causes initial symptoms. Replicate inside macrophages released to mesenteric lymph nodes and then to cells of phagocyte system (liver, gall bladder, spleen, kidney and bone marrow). 7-10 days incubation period. Second: after further multiplication organism pass into the blood- spread to other organs.
Typhoid Clinical Disease
- Coincides with symptoms; fever
Further invasion of intestine from gall bladder can lead to perforation due to intense immune response. Incubation period can be 5 to 50 days although its usually 2 weeks
Typhoid Symptoms
Often vague – dry cough, nose bleeds with anorexia, dull continuous headache, abdominal tenderness and discomfort. Diarrhoea uncommon – many may complain of constipation. Anaemia, leukopenia and if untreated temperature will rise step wise for 1st week, Remain high for 7-10 days ,Fall during 3rd and 4th week. Brachycardia, Hepatomegaly and splenatomegaly. Jaundice if reaches liver. Rash of rose spots. Intestinal haemorrhage and perforation are serious complications. Relapse in 5-10% cases – less severe. Mild, asymptomatic or 20% mortality if untreated
Cases and Vaccines - Typhoid
-WHO: 21 million typhoid cases and 216,000-600,000 typhoid-related deaths annually worldwide. Typhoid vaccines available internationally, both considered safe and effective: Injectable polysaccharide vaccine based on the purified Vi antigen (aka Vi-PS vaccine) for children < two years of age. Live attenuated oral Ty21a vaccine available in capsules for > five years of age.
Vi and other virulence factors
Vi Antigen : Immunosuppressive, so prevents diarrheal disease. Anti phagocytic, allows survival in macrophages. Reduces complement killing. Resistance to oxidative burst
Antibiotics
Fever, so systemic, so you do use them
Resistance to Chloramphenicol , co-trimoxazole, ampicillin, ciprofloxacin (also in non-typhoid strains due to farm use of antibiotics). If bacteria is sensitive use ciprofloxacin. If resistant: ceftriaxone ( cephalosporin) and azithromycin (long half-life macrolide): risk of utli-drug resistance.
Vaccinations WHO Recommendations
WHO recommends use of the Vi-PS and Ty21a vaccines to control endemic disease and for outbreak control and typhoid fever vaccination programmes implemented to control the disease including: health education, water quality and sanitation improvements, and training of health professionals in diagnosis and treatment.
Cholera bacteriae: Vibrio cholerae
Vibrio cholerae. Gram negative bacilli “comma shaped”. Oxidase positive. Motile – single polar flagellum. Tolerant to alkali – growth range pH 6.8 to 10.2. More than 130 serotypes. Vibrio cholerae O1 is the main cause of epidemic cholera.
Cholera- Serogroups
- Two serogroups of V.cholera - O1 and O139
- New variant strains detected in several parts of Asia and Africa. Non-O1 and non-0138: cause mild diarrhoea but not epidemics: dont have the cholera toxin.
Cholera reservoirs
- Main reservoirs of V. cholerae are people and aquatic sources such as brackish water and estuaries, often associated with algal blooms.
- Recent studies indicate global warming creates favourable environment for bacteria
Cholera - Pathology
- Cholera: acute intestinal infection caused by ingestion of food or water contaminated with bacterium V. Cholerae
- Short incubation period, produces an enterotoxin that causes a copious painless watery diarrhoea. Vomiting also occurs in most patients.
- Most persons infected with V. cholerae dont become ill, although bacterium is present in their faeces for 7-14 days.
- 80-90% of illness= mild or moderate severity and are difficult to distinguish clinically from other types of acute diarrhoea.
- Less than 20% of ill persons develop typical cholera with signs of moderates or severe dehydration.
Cholera- Incomplete data
- Global threat and remains a challenge in countries without safe drinking water and adequate sanitiation
- Disease no longer poses a threat to countries with minimum standards of hygiene
- Limitations in surveillance systems and fear of trade and travel sanctions mean cases are unaccounted for. True burden of disease is estimated to be 4 million cases and 140,000 deaths annually.
Cholera - biotypes
- Serotype: Antibody will bind
- Biotype: more on the phenotype and what it will do
- Two biotypes of V.Cholera O1 serotypes
- Classical and El Tor
- Both biotypes produce major virulence factors toxin-coregulated pilus (TCP) and cholera toxin (CT)
- El Tor produces haemolysin and is resistant to Polymixin B
- Vibrio cholerae serogroup O139 emerged in 1992 in Madras
Cholera transmission
Waterborne
Water contaminated with human faeces
Organism commonly found as resident of aquatic environment in non-endemic areas
Cholera - Clinical Disease
Vibrio cholerae ingested – small dose. Multiplies in alkaline small intestine. Organisms migrate and adhere to epithelial cells (toxin co-regulated pilus). Adherent bacteria produce cholera toxin – powerful enterotoxin. Toxin activates the adenylate cyclase enzyme. Leads to overproduction of cAMP – cyclic adenosine monophosphate. Inhibits Na and Cl uptake and consequently water. Serious loss of water and electrolytes
