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Stevany 405080070
TYPHOID
Definition
Typhoid fever is a systemic disease characterized by fever and abdominal pain and caused by dissemination of S. Typhi or S. Paratyphi
Typhoid fever
Human are the only host for S. Typhi and S. Paratyphi Additional non spesific symptoms :
chills, headache, sweating, cold, malaise, and athralgias
GI symptoms:
Anorexia, nausea, vomiting, and diarrhea or less often constipation. Abdominal pain occurs in 30-40% of patients
Complication:
Intestinal perforation and/or GI hemorrhagi due to ulceration and necrosis of infiltrated Peyers Patches Long term salmonella carried in urine or stool develops in 1-4% patients, usually in association with disease in the bladder or the biliary and GIT
ETIOLOGY.
Typhoid fever is caused by Salmonella enterica serovar Typhi (S. Typhi), a gram-negative bacterium. A very similar but often less severe disease is caused by S. Paratyphi A and rarely by S. Paratyphi B (Schotmulleri) and S. Paratyphi C (Hirschfeldii). The ratio of disease caused by S. Typhi to that caused by S. Paratyphi is about 10 to 1, although the proportion of S. Paratyphi infections is increasing in some parts of the world. Although S. Typhi shares many genes with Escherichia coli and at least 95% with S. Typhimurium, there are several unique gene clusters known as pathogenicity islands and others that have been acquired during evolution. The inactivation of single genes, as well as the acquisition or loss of single genes or large islands of DNA, may have contributed to host adaptation and restriction of S. Typhi. One of the most specific genes is for the polysaccharide capsule Vi. This is present in about 90% of all freshly isolated S. Typhi and has a protective effect against the bactericidal action of the serum of infected patients
Lie motionless and exhausted with your eyes halfclosed in what's known as the typhoid state Life-threatening complications often develop at this time.
Fourth week of illness Improvement may come slowly during the fourth week. Your fever is likely to decrease gradually until your temperature returns to normal in another week to 10 days. But signs and symptoms can return up to two weeks after your fever has subsided.
Week 1 Constipation
Diarrhea
Week 2 Common
Common (pea soup)
Week 3
Very common
Rare
Bloating with tympany Very common (84%) Diffuse mild abdominal pain intestinal perforation Hepatosplenomegaly Coated tongue Common Very common Very common
Rare
Transmition
Fecal-oral route S. typhi is passed in the feces and sometimes in the urine of infected people. You can contract the infection if you eat food handled by someone with typhoid fever who hasn't washed carefully after using the bathroom. You can also become infected by drinking water contaminated with the bacteria. Typhoid carriers Even after treatment with antibiotics, a small number of people who recover from typhoid fever continue to harbor the bacteria in their intestinal tract or gallbladder, often for years. These people, called chronic carriers, shed the bacteria in their feces and are capable of infecting others, although they no longer have signs or symptoms of the disease themselves.
EPIDEMIOLOGY.
It is currently estimated that over 21.7 million typhoid cases occur annually, with the vast majority of cases in Asia, with over 200,000 deaths. Additionally, an estimated 5.4 million cases occur due to paratyphoid. the age-specific incidence of typhoid may be highest in children <5 yr of age, with comparatively higher rates of complications and hospitalization.
Pathogenesis
Salmonella cause infection when 103-106 organisms are ingested. Conditions that reduce gastric acidity or decrease intestinal integrity increase susceptibility to infection. Organism penetrate the small intestine mucosa and traverse the intestinal layer through cells within peyers patches S.typhi and S.paratyphi survive within macrophages, then disseminate throughout the body via lymphatics, and ultimately colonize reticuloendothelial tissue. Nontyphoidal salmonella most commonly cause gastoenteritis, invading the large and small intestinal mucosa and resulting in massive polymorphonuclear leukocyte infiltration.
Risk factors
Work in or travel to areas where typhoid fever is endemic Work as a clinical microbiologist handling Salmonella typhi bacteria Have close contact with someone who is infected or has recently been infected with typhoid fever Have an immune system weakened by medications such as corticosteroids or diseases such as HIV/AIDS Drink water contaminated by sewage that contains S. typhi
Non-Typhoidal Salmonellosis
Most disease is caused by Salmonella Typhimurium or Salmonella enteritidis Gastroenteritis :
Nausea, vomiting, diarrhea, abdominal cramping and fever occurs 6-48 hours after exposure Diarrhea is usually loose, non bloody and moderate in volume. But stools are sometimes bloody Diarrhea is usually self limited, abating within 3-7 days and fever resolved within 72 hours in most cases Stool culture main remain positive >4-5 weeks
Extraintestinal infection
Up to 5% of patients are bacterimic, and 5-10% may develop localized infection, particularly in vascular sites (eg; aortic aneurysm)
Complications
Intestinal bleeding or perforation Intestinal bleeding is often marked by a sudden drop in blood pressure and shock, followed by the appearance of blood in your stool. Inflammation of the heart muscle (myocarditis) Pneumonia Inflammation of the pancreas (pancreatitis) Kidney or bladder infections Infections of the spine (osteomyelitis) Infection and inflammation of the membranes and fluid surrounding your brain and spinal cord (meningitis) Psychiatric problems such as delirium, hallucinations and paranoid psychosis
GASTROENTERITIS
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Definition
Inflammation of the mucous membrane of both stomach and intestine. (Source: Stedman's Medical Spellchecker, 2006 Lippincott Williams & Wilkins. )
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Risk Factors
Overcrowding Poverty Poor sanitation International travel For Children : Young age Immune deficiency Measles Malnutrition Lack of exclusive breast feeding
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VIRAL GASTROENTERITIS
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ETIOLOGY
ROTAVIRUS
vomiting, watery diarrhea, low grade fever, temporary lactose intolerance may occur infants & children, elderly, & immunocomprimised are especially vulnerable Nausea, vomiting, abdominal cramping, diarrhea, fever, myalgia, & some headache.
12-48 hr
12-60 hr
10-70 hr
2-9 hr
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LABORATORIUM TESTING
TREATMENT
ROTAVIRUS
Supportive care, severe diarrhea may require fluid and electrolyte replacement
Routine RT PCR & EM on fresh unpreserved stool samples. Clinical diagnosis, negative bacterial cultures, stools is negative for WBCs
Identification of the virus in early acute stool samples, serology, commercial ELISA
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BACTERIAL GASTROENTERITIS
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ETIOLOGY
INCUBATI ON PERIOD
1-3 days
DURATION OF ILLNESS
SALMONELLA SPP.
Diarrhea, fever, abdominal cramp, 4-7 hr vomiting, S.typhi & S.paratyphi produce typhoid with insidious onset characterized by fever, headache, constipation, malaise, chills, myalgia Abdominal cramp, fever, and diarrhea. Stools may contain blood and mucus 4-7 hr
SHIGELLA SPP.
24-48 hr
YERSINIA ENTEROCOLYTICA
24-48 hr
Appendicitis like symptom (diarrhea & vomiting, fever, abdominal pain) occur primarily in older children & young adult. May have a scarlitiform rash/ erythema nodosum Sudden onset af severe nausea & vomiting, abdominal cramp, diarrhea, & fever may be present
STAPHYLOCOCCUS AUREUS
1-6 hr
24-48 hr
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ETIOLOGY
INCUBATION PERIOD
DURATION OF ILLNESS
VIBRIO CHOLERAE
24-72 hr
Profuse watery diarrhea & vomiting, which can lead severe dehydration & death
CAMPYLOBACTER JEJUNI
2-5 days
2-10 days
E. COLI
1-8 days
Severe diarrhea that is often 4-10 days bloody, abdominal pain & vomiting. Usually little or fever is present. More common in children <4 yr old
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TREATMENT
Supportive care. Other than S.typhi & S.paratyphi , antibiotik arent indicate unless there is extraintestinal spread of the infection, condiser ampicillin, gentamicin, TMP-SMX or quinolones of indicate A.vaccin exist for S. typhi Supportive care, TMP-SMX recommeded in US, if organism is susceptible, nalidixicacid or quinolones may be indicated if organism is resistant Supportive care, if septicemia or other invasive disease occurs, antibiotic therapy with gentamicin or cefotaxime (doxycyclin & ciprofloxacin) Supportive care
SHIGELLA SPP.
YERSINIA ENTEROCOLYTICA
Stool, vomitus, or blood culture, yersinia requires special media to grow. Serology is available in research & referance laboratoies Normally a clinical diagnosis. Stool, vomitus & food can be tasted for toxin & culture if indicated
STAPHYLOCOCCUS AUREUS
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LABORATORIUM TESTING
TREATMENT
VIBRIO CHOLERAE Stool culture, V.chlerae requires special Supportive care with
media to grow, if V.chlerae is suspected, aggressive oral & IV must request specific testing rehydration. In cases of comfirmed chlorea, tetracyclin or doxycyclin is recommended for adult, TMPSMX for children
CAMPYLOBACTER JEJUNI
Routine Stool culture, compylobacter requires special media & incubation at 42 C to grow
Supportive care, for severe cases, antibiotics(erythromycin & quinolons) may be indicated early in the diarrhe
E. COLI
Stool culture: E.Coli 0157: H7 require special media to grow, if suspected, specific testing must be request
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SHIGELLA
Dysentery (i.e., small volume, frequent, bloody stools with tenemus and urgency) is the predominant symptom of colitis.
PATHOLOGY
The pathologic changes of shigellosis take place primarily in the colon, the target organ for shigellae. The changes are most intense in the distal colon, although pancolitis may occur. Grossly, localized or diffuse mucosal edema, ulcerations, friable mucosa, bleeding, and exudate may be seen. Microscopically, ulcerations, pseudomembranes, epithelial cell death, infiltration extending from the mucosa to the muscularis mucosae by polymorphonuclear and mononuclear cells, and submucosal edema occur.
CLINICAL MANIFESTATION
severe abdominal pain, high fever, emesis, anorexia, generalized toxicity, urgency, painful defecation occur.
PHYSICAL EXAMINATION
abdominal distention and tenderness, hyperactive bowel sounds, a tender rectum on digital examination.
The diarrhea may be watery and of large volume initially, evolving into frequent small-volume, bloody mucoid stools; however, some children never progress to the stage of bloody diarrhea, whereas in others the first stools are bloody. Significant dehydration related to the fluid and electrolyte losses in both feces and emesis can occur.
DIAGNOSIS
Presumptive data supporting a diagnosis of bacillary dysentery include the finding of fecal leukocytes (confirming the presence of colitis) Demonstration in peripheral blood of leukocytosis with a dramatic left shift (often with more bands than segmented neutrophils). Culture of both stool and rectal swab specimens optimizes the chance of diagnosing Shigella infection
DIAGNOSIS
Presumptive data supporting a diagnosis of bacillary dysentery include the finding of fecal leukocytes (confirming the presence of colitis) Demonstration in peripheral blood of leukocytosis with a dramatic left shift (often with more bands than segmented neutrophils). Culture of both stool and rectal swab specimens optimizes the chance of diagnosing Shigella infection
Vibrio Cholerae
Morphology
Comma shaped, curved aerobic rod 2-4um long. It is actively motile by means of a polar flagellum Produces convex, smooth, round colonies that are opaque and granular in transmitted light Grow at very high pH (8.5-9.5) & rapidly killed by acid. NaCl often stimulates their growth
Antigen Structure
A single heat labille flagellar H antigen O LPS (O group 1 & 139 classic cholera), non O1 / non O 139 cholera like disease
Vibrio Cholerae
Pathogenesis
Under natural conditions, V cholerae is pathogenic only for humans Ppl w/ normal gastric acidity may have to ingest as many as 10^10 or more to become infected (vehicle: water). When vehicle is food, 10^2-10^4 infected Predisposition factor: person w/ medication or condition that decreases stomach acidity V cholerae: not an invasive infection = do not reach blood stream but remain within GI tract. (attach to microvilli of the brush border of epithelial cells, multiply & liberate cholera toxin)
A1 component
A2 component
Ganglionside GM1 (ganglion receptor on enterocytes surface) mucosal receptor for subunit B
Promotes entry of subunit A into the cell
Activation increased intracellular CAMP Prolonged hypersecretion of water & electrolytes (increased sodium dependent chloride secretion) & absorption of sodium & chloride is inhibited)
Vibrio Cholerae
Clinical Finding
60% infection: asymptomatic Incubation period: 1-4 d Sudden onset of nausea & vomiting, profuse diarrhea with abd cramps; stools (rice water) contain mucus, epithelial cells, and large numbers of vibrios Rapid loss of fluid & electrolytes profound dehydration, circulatory collapse & anuria
Enterobacteriaceae
Morphology
Short gram negative rods E coli & most of the other form cicular, convex, smooth colonies with distinct edges. Salmonellae & shigellae produce colonies similar to e coli but do not ferment lactose. Some strains of e coli hemolysis on blood agar
Entecobacteriaceae:
Eschericia, klebsiella-enterobacter-serratia group, proteus-morganella-providencia group, c itrobacter, shigella, salmonella, other entecobacteriaceae (yersinia, edwardsiella, ewingella hafnia, cedecca, & kluyverra)
Enterobacteriaceae
Antigenic Structure
Complex: 150 different heat stable somatic O (LPS) antigens, > 100 heat labile K (capsular) antigens, >50 H (flagellar) antigen O antigen:
resistant to heat & alcohol, usually detected by bacterial agglutination. Ab reaction: mostly by IgM. Single organism may carry several O antigens. Spesific O types of e coli are found in diarrhea & URI
K antigens: may be associated with virulence, eg: e coli strains producing K1 Ag neonatal meningitis. K Ag of E coli attachment to epithelial cells prior to GI or URI H antigens: on flagella, removed by heat or alcohol. 2 forms: phase 1, phase 2 organisms tend to do phase variation
DENGUE FEVER
Definition
Dengue fever is a disease ranging from mild to severe caused by four related viruses spread by a particular species of mosquito. Mild dengue fever causes high fever, rash, and muscle and joint pain. More-severe forms of the disease dengue hemorrhagic fever and dengue shock syndrome can additionally cause severe bleeding, a sudden drop in blood pressure (shock) and death.
Symptoms
High fever, up to 105 F (40.6 C) A rash over most of your body, which may subside after a couple of days and then reappear Severe headache, backache or both Pain behind your eyes Severe joint and muscle pain Nausea and vomiting
Cause
Dengue fever is caused by any one of four dengue viruses spread by the Aedes aegypti mosquito.
Risk factors
Living or traveling in tropical areas Being in tropical and subtropical areas around the world Prior infection with a dengue fever virus Previous infection with a dengue fever virus increases your risk of a more severe form of the disease.
Complications
dengue hemorrhagic fever dengue shock syndrome heavy bleeding, shock death
MALARIA
Definition
Malaria produces recurrent attacks of chills and fever. Caused by a parasite that's transmitted by mosquitoes.
Symptoms
Moderate to severe shaking chills High fever Profuse sweating as body temperature falls Headache Nausea Vomiting Diarrhea
Risk factors
Young children and infants Travelers coming from areas with no malaria Pregnant women and their unborn children
Complications
Cerebral malaria Breathing problems Organ failure Severe anemia Low blood sugar
HEPATITIS A
Definition
Hepatitis A is a highly contagious liver infection caused by the hepatitis A virus. Hepatitis A is one of several types of hepatitis viruses that cause inflammation that affects your liver's ability to function. You're most likely to contract hepatitis A from contaminated food or water or from close contact with someone who's already infected. Mild cases of hepatitis A don't require treatment, and most people who are infected recover completely with no permanent liver damage.
Symptoms
Fatigue Nausea and vomiting Abdominal pain or discomfort, especially in the area of your liver on your right side beneath your lower ribs Loss of appetite Low-grade fever Dark urine Muscle pain Itching Yellowing of the skin and eyes (jaundice)
Hepatitis A is caused by infection with the hepatitis A virus. The hepatitis virus is usually spread when a person ingests tiny amounts of contaminated fecal matter. The hepatitis A virus infects the liver cells and causes inflammation. The inflammation can impair liver function and cause other signs and symptoms of hepatitis A.
Risk factors
Travel or work in regions with high rates of hepatitis A Are a man who has sexual contact with other men Use injected or noninjected illicit drugs Live with another person who has hepatitis A Work in a research setting where you may be exposed to the virus Receive clotting-factor concentrates for hemophilia or another medical condition
Prevention
Consider the hepatitis A vaccine Follow safety precautions when traveling Practice good hygiene
HEPATITIS B
Definition
Hepatitis B is a serious liver infection caused by the hepatitis B virus (HBV). For some people, hepatitis B infection becomes chronic, leading to liver failure, liver cancer, or cirrhosis a condition that causes permanent scarring of the liver.
Symptoms
Abdominal pain Dark urine Joint pain Loss of appetite Nausea and vomiting Weakness and fatigue Yellowing of your skin and the whites of your eyes (jaundice)
Causes
Sexual contact Sharing needles Accidental needle sticks From mother to child
Risk factors
Have unprotected sex with more than one partner Have unprotected sex with someone who's infected with HBV Have a sexually transmitted disease such as gonorrhea or chlamydia Are a man who has sexual contact with other men Share needles during intravenous (IV) drug use Share a household with someone who has a chronic HBV infection Have a job that exposes you to human blood Receive hemodialysis for end-stage kidney (renal) disease Travel to regions with high infection rates of HBV, such as Africa, Central and Southeast Asia, and Eastern Europe
Complications
Scarring of the liver (cirrhosis) Liver cancer Liver failure Hepatitis D infection Kidney problems Blood vessel inflammation (vasculitis)
HEPATITIS C
Definition
Hepatitis C is an infection caused by a virus that attacks the liver and leads to inflammation. Most people infected with the hepatitis C virus (HCV) have no symptoms.
Symptoms
Fatigue Fever Nausea or poor appetite Muscle and joint pains Tenderness in the area of your liver
Causes
Hepatitis C infection is caused by the hepatitis C virus (HCV). HCV is spread when you come in contact with contaminated blood. Examples of how HCV can be spread include:
Blood transfusions and organ transplants Shared needles Childbirth Sexual contact
Risk factors
Are a health care worker who has been exposed to infected blood Have ever injected illicit drugs Are HIV-positive Received a piercing or tattoo in an unclean environment using unsterile equipment Received a blood transfusion or organ transplant before 1992 Received clotting factor concentrates before 1987 Received hemodialysis treatments for a long period of time Were born to a woman with a hepatitis C infection
Complications
Scarring of the liver tissue (cirrhosis Liver cancer Liver failure
Prevention
Stop using illicit drugs Be cautious about body piercing and tattooing Practice safer sex if you choose to have sex