BRUCELLOSIS -
Brucellosis is a zoonosis transmitted to humans from infected animals
ETIOLOGY 4 species affecting humans: Brucella melitensis (most common and most virulent) acquired primarily from goats/sheep/camels; B. abortus from cattle; B. suis from hogs; and B. canis from dogs. Aerobic/gram-negative bacilli/uncapsulated/intracellular. Killed by boiling or pasteurization of milk and milk products. Remains viable for up to 40 days in dried soil contaminated with infected-animal urine, stool, vaginal discharge, and products of conception and for longer periods in damp soil.
Transmission: ingestion of untreated milk/milk products/raw meat/via inhalation during contact with animals.
PATHOGENESIS AND IMMUNITY complements opsonizes Brucella-- ingestion by PMN’s and activated macrophages --- it resist intracellular phagocytic killing (by as the suppression of the MPO- peroxide-halide system and the production of superoxide dismutase) --- multiply -- localizing in the liver, spleen, bones, kidneys, lymph nodes, heart valves, nervous system, and testes -- noncaseating granulomas typically develop (caseating granulomas and abscesses also described).
CLINICAL MANIFESTATIONS AND COMPLICATIONS
It is a systemic disease with protean manifestations. I Pd from 1 to 3 weeks to several months,The onset may be either abrupt or gradual . Symptoms are fever, chills, diaphoresis, headaches, myalgia, fatigue, anorexia, joint and low-back pain, weight loss, constipation, sore throat, and dry cough. Signs: no abnormalities/pallor/lymphadenopathy/hepatosplenomegaly/arthritis/spinal tenderness, /epididymoorchitis/rash/ meningitis/ cardiac murmurs/pneumonia.
Bones and Joints Although monarticular septic arthritis/ reactive asymmetric polyarthritis /osteomyelitis of the lumbar vertebrae. In Brucella septic arthritis and osteomyelitis, the peripheral white cell count is typically normal, while the erythrocyte sedimentation rate may be either normal or elevated.
Heart include endocarditis, myocarditis, pericarditis, aortic root abscess, mycotic aneurysms, thrombophlebitis with pulmonary aneurysm, and pulmonary embolism.
Respiratory Tract A flulike illness with sore throat, tonsillitis, and dry cough is common and usually mild. Hilar and paratracheal lymphadenopathy, pneumonia, solitary or multiple pulmonary nodules, lung abscess, and empyema have been reported.
Gastrointestinal Tract and Hepatobiliary System mild and may include nausea, vomiting, constipation, acute abdominal pain, and/or diarrhea. Non caseating granuloma in liver.
Genitourinary Tract unilateral or bilateral epididymoorchitis,prostatitis, tuboovarian abscess, salpingitis.
Central Nervous System Uncommon but serious and includes meningitis, meningoencephalitis, multiple cerebral or cerebellar abscesses.
Other The bone marrow of Brucella-infected patients frequently contains noncaseating granulomas. Among the hematologic complications of brucellosis are anemia, leukopenia, and thrombocytopenia.
DIAGNOSIS
The combination of potential exposure, consistent clinical features, and significantly raised levels of Brucella agglutinin (with or without positive cultures of blood, body fluid, or tissues) confirms the diagnosis of active brucellosis. In endemic areas a Brucella antibody titer of 1:320 or 1:640 is significant, while in nonendemic areas an antibody titer of 1:160 is considered significant.
TREATMENT
Single-agent therapy/short course for brucellosis has now been abandoned because of the high rates of failure and relapse. The combination of doxycycline and an aminoglycoside (gentamicin, streptomycin, or netilmicin) for 4 weeks followed by the combination of doxycycline and rifampin for 4 to 8 weeks is the most effective regimen. An alternative regimen consists of the doxycycline/rifampin combination given for 8 to 12 weeks. The doxycycline/aminoglycoside combination is more effective than the doxycycline/rifampin combination in that rifampin reduces levels of doxycycline in plasma.
In pregnancy, trimethoprim-sulfamethoxazole (TMP-SMZ) can be given in combination with rifampin for 8 to 12 weeks.
PROGNOSIS
Deaths attributable to brucellosis should be avoidable. Even before the discovery of antibiotics, the mortality rate was 2% and endocarditis was most frequently the cause of death. Morbidity due to brucellosis remains significant; its severity depends on the infecting Brucella species and is greatest with B. melitensis. Spinal damage, paraplegia, and other neurologic deficits may occur. Nerve deafness due to meningitis or secondary to treatment with streptomycin has been documented.
Tuesday, April 14, 2009
Infectious Diseases: Shigellosis
SHIGELLOSIS ---- By Dr Sandeep Tak
DEFINITION
- An acute infectious inflammatory colitis by Shigella grp also c/a bacillary dysentery
ETIOLOGIC AGENT
- Gm -ive, nonmotile bacilli, family Enterobacteriaceae
- 4 Shigella species (S. dysenteriae, S. flexneri, S. boydii, and S. sonnei)
- Characterized by its ability to invade intestinal epithelial cells and to cause infection and illness in humans, small inoculum is enough (a few hundred to few thousand organisms)
EPIDEMIOLOGY
- Poor sanitation help in spread / Pathogen only of humans and a few other primates
- Transmission fecal-oral route, generally via direct contact but sometimes through contaminated vectors such as food, water, flies, and fomites. high rate of secondary household transmission (20-40%)
PATHOGENESIS
- Orally ingested → low pH in stomach tolerated → invasion of colonic epithelial cells and cell-to-cell spread of infection → rapid multiplication → cell damage → mucosal ulceration → bloody diarrhea
- Once a single Shigella organism has invaded a single host cell, the entire process of bacterial escape from the phagocytic vesicle into the host cell's cytoplasm, multiplication, and cell-to-cell spread can take place without exposure of the bacterium to the extracellular milieu and to the host's defenses.
- S. dysenteriae type1-produce Shiga toxin → inhibiting protein synthesis
- Immunity develops and is serotype-specific
CLINICAL MANIFESTATIONS
- 25% asymptomatic, 25% develop transient fever, 25% have fever & self-limited watery diarrhea, and the remaining 25% had fever and bloody diarrhea/dysentery
- Dysentery is characterized by frequent passage (usually 10 to 30 times per day) of small-volume stools consisting of blood, mucus, and pus
- abdominal cramps and tenesmus, rectal prolapse, especially in young children.
- Severe dysentery is most likely in infection due to S. dysenteriae type 1, occurs less commonly with S. flexneri, and is least likely in S. sonnei infection.
- Severe shigellosis: toxic dilatation and colonic perforation, may be fatal.
- Endoscopy: hemorrhagic, with mucous discharge and focal ulcerations. The majority of lesions are in the distal colon and progressively diminish in the more proximal segments of large bowel.
Extraintestinal complications
- HUS may occur with S. dysenteriae type 1 infection. HUS usually develops toward the end of the first week of shigellosis, when dysentery is already resolving. Oliguria / anuria with renal failure and to severe anemia with congestive heart failure. 5 to 10% of patients with HUS die of the acute illness. Leukemoid reactions,thrombocytopenia is common.
- Less common: seizures, and reactive arthritis
D/DIAGNOSIS
- Shigellosis is the principal bacterial cause of bloody diarrhea
- The differential diagnosis includes inflammatory colitis due to other microbial agents: EHEC, EIEC, Campylobacter jejuni, Salmonella enteritidis, Yersinia enterocolitica, Clostridium difficile, and the protozoan Entamoeba histolytica. Ulcerative colitis and Crohn's colitis are among the "noninfectious" conditions.
TREATMENT
- The mild to moderate dehydration : oral rehydration
- Ampicillin (50 to 100 mg/kg per day in children or 2 g/d in adults, in divided doses) or
- Cotrimoxazole(8/40 mg/kg per day or DS tab twice a day in adults, given for 5 days)
- Ciproflox 500 BD x 3 days
- Ceftriaxone 1gm single dose
DEFINITION
- An acute infectious inflammatory colitis by Shigella grp also c/a bacillary dysentery
ETIOLOGIC AGENT
- Gm -ive, nonmotile bacilli, family Enterobacteriaceae
- 4 Shigella species (S. dysenteriae, S. flexneri, S. boydii, and S. sonnei)
- Characterized by its ability to invade intestinal epithelial cells and to cause infection and illness in humans, small inoculum is enough (a few hundred to few thousand organisms)
EPIDEMIOLOGY
- Poor sanitation help in spread / Pathogen only of humans and a few other primates
- Transmission fecal-oral route, generally via direct contact but sometimes through contaminated vectors such as food, water, flies, and fomites. high rate of secondary household transmission (20-40%)
PATHOGENESIS
- Orally ingested → low pH in stomach tolerated → invasion of colonic epithelial cells and cell-to-cell spread of infection → rapid multiplication → cell damage → mucosal ulceration → bloody diarrhea
- Once a single Shigella organism has invaded a single host cell, the entire process of bacterial escape from the phagocytic vesicle into the host cell's cytoplasm, multiplication, and cell-to-cell spread can take place without exposure of the bacterium to the extracellular milieu and to the host's defenses.
- S. dysenteriae type1-produce Shiga toxin → inhibiting protein synthesis
- Immunity develops and is serotype-specific
CLINICAL MANIFESTATIONS
- 25% asymptomatic, 25% develop transient fever, 25% have fever & self-limited watery diarrhea, and the remaining 25% had fever and bloody diarrhea/dysentery
- Dysentery is characterized by frequent passage (usually 10 to 30 times per day) of small-volume stools consisting of blood, mucus, and pus
- abdominal cramps and tenesmus, rectal prolapse, especially in young children.
- Severe dysentery is most likely in infection due to S. dysenteriae type 1, occurs less commonly with S. flexneri, and is least likely in S. sonnei infection.
- Severe shigellosis: toxic dilatation and colonic perforation, may be fatal.
- Endoscopy: hemorrhagic, with mucous discharge and focal ulcerations. The majority of lesions are in the distal colon and progressively diminish in the more proximal segments of large bowel.
Extraintestinal complications
- HUS may occur with S. dysenteriae type 1 infection. HUS usually develops toward the end of the first week of shigellosis, when dysentery is already resolving. Oliguria / anuria with renal failure and to severe anemia with congestive heart failure. 5 to 10% of patients with HUS die of the acute illness. Leukemoid reactions,thrombocytopenia is common.
- Less common: seizures, and reactive arthritis
D/DIAGNOSIS
- Shigellosis is the principal bacterial cause of bloody diarrhea
- The differential diagnosis includes inflammatory colitis due to other microbial agents: EHEC, EIEC, Campylobacter jejuni, Salmonella enteritidis, Yersinia enterocolitica, Clostridium difficile, and the protozoan Entamoeba histolytica. Ulcerative colitis and Crohn's colitis are among the "noninfectious" conditions.
TREATMENT
- The mild to moderate dehydration : oral rehydration
- Ampicillin (50 to 100 mg/kg per day in children or 2 g/d in adults, in divided doses) or
- Cotrimoxazole(8/40 mg/kg per day or DS tab twice a day in adults, given for 5 days)
- Ciproflox 500 BD x 3 days
- Ceftriaxone 1gm single dose
Infecious Diseases: Cholera
CHOLERA
Cholera is an acute diarrheal disease that can, in a matter of hours, result in profound, rapidly progressive dehydration and death.
ETIOLOGY AND EPIDEMIOLOGY - V. cholerae -155 serogroups. Divided into those that agglutinate in antisera to the O1 group antigen (V. cholerae O1) and those that do not (non-O1 V. cholerae). Serogroup O1 was, until the emergence of serogroup O139, the exclusive cause of epidemic cholera. v. cholerae O139 (also called V. cholerae Bengal)
V. cholerae O1 exists in two biotypes, classical and El Tor,. Each biotype is further subdivided into two serotypes, termed Inaba and Ogawa.
Ingestion of water/food contaminated by human No known animal reservoir. ID50 is reduced in hypochlorhydric persons, in those using antacids, and when gastric acidity is buffered by a meal. In endemic areas, the disease is more common in the summer and fall months. In endemic areas, children < 2 years of age are less likely to develop severe cholera than are older children, perhaps because of passive immunity acquired from breast milk.; those with type O blood are at greatest risk, while those with type AB are at least risk.
PATHOGENESIS - Contaminated food / water --- Adherence to the intestinal epithelium - mediated by the toxin-coregulated pilus (TCP) -- intestinal colonization --- produces CTX,[monomeric enzymatic moiety (the A subunit) and a pentameric binding moiety (the B subunit) ] -- B pentamer binds to GM1 ganglioside (toxin receptor) on the surface of jejunal epithelial cells & makes delivery of the A subunit to its cytosolic target -- activated A subunit (A1) irreversibly upregulates the cyclase catalytic subunit --- intracellular accumulation of high levels of cyclic AMP ---- cyclic AMP inhibits the absorptive sodium transport system in villus cells and activates the excretory chloride transport system in crypt cells ----- accumulation of sodium chloride in the intestinal lumen ---- water moves passively to maintain osmolality --- isotonic fluid accumulates in the lumen --- watery diarrhea results
Unless the wasted fluid and electrolytes are adequately replaced, shock (due to profound dehydration) and acidosis (due to loss of bicarbonate) follow.
Increasing evidence indicates that CTX also enhances intestinal secretion via prostaglandins and/or neural histamine receptors.
CLINICAL MANIFESTATIONS - incubation period - 24- to 48-h. Sudden onset of painless watery diarrhea & is often followed by vomiting. If fluids and electrolytes are not replaced, hypovolemic shock and death ensue. Fever is usually absent. Muscle cramps due to electrolyte disturbances are common. The stool has a characteristic appearance: a nonbilious, gray, slightly cloudy fluid with flecks of mucus, no blood, and a somewhat sweet, inoffensive odor -- "rice-water" stool . Clinical symptoms parallel volume contraction: At losses of 3 to 5% of normal body weight, thirst develops; at 5 to 8%, postural hypotension, weakness, tachycardia, and decreased skin turgor are documented; and at 10%, oliguria, weak or absent pulses, sunken eyes (and, in infants, sunken fontanelles), wrinkled ("washerwoman") skin, somnolence, and coma are characteristic. Complications derive exclusively from the effects of volume and electrolyte depletion and include renal failure due to acute tubular necrosis. Thus, if the patient is adequately treated with fluid and salt, complications are averted and the process is self-limited, resolving in a few days.
Laboratory data - elevated hematocrit ; mild neutrophilic leukocytosis; elevated levels of BUN and creatinine; normal Na /K /Cl; a markedly reduced HCO3 level (15 mmol/L); and an elevated anion gap (due to increases in serum lactate, protein, and phosphate). Arterial pH is usually low (about 7.2).
DIAGNOSIS - It can be detected directly by dark-field microscopy on a wet mount of fresh stool, and its serotype can be discerned by immobilization with Inaba- or Ogawa-specific antiserum. Culture media- thiosulfate-citrate-bile salts-sucrose (TCBS) agar
TREATMENT - Cholera is simple to treat; only the rapid and adequate replacement of fluids, electrolytes, and base is required.
It has been proved conclusively that fluid may be given orally (takes advantage of the hexose-Na+ cotransport mechanism). Since Na+ losses in the stool are high, a fluid containing Na+ at 90 mmol/L has been recommended by WHO
Severely dehydrated patients – IVF : RL - must be used with additional potassium supplements, preferably given by mouth. The total fluid deficit in severely dehydrated patients (10% of body weight) can be replaced safely within the first 4 h of therapy, half within the first hour. Thereafter, oral therapy can usually be initiated, with the goal of maintaining fluid intake equal to fluid output.
Antibiotic : reduces duration and volume of fluid loss and will hasten clearance of the organism from the stool. Single-dose tetracycline (2 g) or doxycycline (300 mg) / Ciprofloxacineither in a single dose (30 mg/kg, not to exceed a total dose of 1 g) or erythromycin (a total of 40 mg/kg daily in three divided doses for 3 days) is a clinically effective substitute. For children, furazolidone and trimethoprim-sulfamethoxazole
PREVENTION - Provision of safe water and facilities for sanitary disposal of feces.
Two types of oral cholera vaccines are under development.
1. killed : two formulations A. killed whole cell + nontoxic B subunit of CTX (WC/BS) and
B. composed solely of killed bacteria. The protective efficacy of WC/BS was superior to that of WC during the initial 8 months of follow-up (69 versus 41%) but equivalent or inferior thereafter. Immunity was relatively sustained in persons vaccinated at an age of 5 years but was not well sustained in younger vaccinees.
Strain CVD 103-HgR, an oral live cholera vaccine licensed for immunization of travelers in Europe, this vaccine is more effective against classical than against El Tor cholera.
Composition of World Health Organization ORS
Constituent Concentration, mmol/L
Na+ 90
K+ 20
Cl 80
Citratec 10
Glucose 110
If prepackaged ORS is unavailable, a simple homemade alternative can be prepared by combining 5 g NaCl (about 1 level teaspoon) with either 50 g precooked rice cereal or 40 g sucrose in 1 L of drinking water. In that case, potassium must be supplied separately (e.g., in orange juice or coconut water).
Cholera is an acute diarrheal disease that can, in a matter of hours, result in profound, rapidly progressive dehydration and death.
ETIOLOGY AND EPIDEMIOLOGY - V. cholerae -155 serogroups. Divided into those that agglutinate in antisera to the O1 group antigen (V. cholerae O1) and those that do not (non-O1 V. cholerae). Serogroup O1 was, until the emergence of serogroup O139, the exclusive cause of epidemic cholera. v. cholerae O139 (also called V. cholerae Bengal)
V. cholerae O1 exists in two biotypes, classical and El Tor,. Each biotype is further subdivided into two serotypes, termed Inaba and Ogawa.
Ingestion of water/food contaminated by human No known animal reservoir. ID50 is reduced in hypochlorhydric persons, in those using antacids, and when gastric acidity is buffered by a meal. In endemic areas, the disease is more common in the summer and fall months. In endemic areas, children < 2 years of age are less likely to develop severe cholera than are older children, perhaps because of passive immunity acquired from breast milk.; those with type O blood are at greatest risk, while those with type AB are at least risk.
PATHOGENESIS - Contaminated food / water --- Adherence to the intestinal epithelium - mediated by the toxin-coregulated pilus (TCP) -- intestinal colonization --- produces CTX,[monomeric enzymatic moiety (the A subunit) and a pentameric binding moiety (the B subunit) ] -- B pentamer binds to GM1 ganglioside (toxin receptor) on the surface of jejunal epithelial cells & makes delivery of the A subunit to its cytosolic target -- activated A subunit (A1) irreversibly upregulates the cyclase catalytic subunit --- intracellular accumulation of high levels of cyclic AMP ---- cyclic AMP inhibits the absorptive sodium transport system in villus cells and activates the excretory chloride transport system in crypt cells ----- accumulation of sodium chloride in the intestinal lumen ---- water moves passively to maintain osmolality --- isotonic fluid accumulates in the lumen --- watery diarrhea results
Unless the wasted fluid and electrolytes are adequately replaced, shock (due to profound dehydration) and acidosis (due to loss of bicarbonate) follow.
Increasing evidence indicates that CTX also enhances intestinal secretion via prostaglandins and/or neural histamine receptors.
CLINICAL MANIFESTATIONS - incubation period - 24- to 48-h. Sudden onset of painless watery diarrhea & is often followed by vomiting. If fluids and electrolytes are not replaced, hypovolemic shock and death ensue. Fever is usually absent. Muscle cramps due to electrolyte disturbances are common. The stool has a characteristic appearance: a nonbilious, gray, slightly cloudy fluid with flecks of mucus, no blood, and a somewhat sweet, inoffensive odor -- "rice-water" stool . Clinical symptoms parallel volume contraction: At losses of 3 to 5% of normal body weight, thirst develops; at 5 to 8%, postural hypotension, weakness, tachycardia, and decreased skin turgor are documented; and at 10%, oliguria, weak or absent pulses, sunken eyes (and, in infants, sunken fontanelles), wrinkled ("washerwoman") skin, somnolence, and coma are characteristic. Complications derive exclusively from the effects of volume and electrolyte depletion and include renal failure due to acute tubular necrosis. Thus, if the patient is adequately treated with fluid and salt, complications are averted and the process is self-limited, resolving in a few days.
Laboratory data - elevated hematocrit ; mild neutrophilic leukocytosis; elevated levels of BUN and creatinine; normal Na /K /Cl; a markedly reduced HCO3 level (15 mmol/L); and an elevated anion gap (due to increases in serum lactate, protein, and phosphate). Arterial pH is usually low (about 7.2).
DIAGNOSIS - It can be detected directly by dark-field microscopy on a wet mount of fresh stool, and its serotype can be discerned by immobilization with Inaba- or Ogawa-specific antiserum. Culture media- thiosulfate-citrate-bile salts-sucrose (TCBS) agar
TREATMENT - Cholera is simple to treat; only the rapid and adequate replacement of fluids, electrolytes, and base is required.
It has been proved conclusively that fluid may be given orally (takes advantage of the hexose-Na+ cotransport mechanism). Since Na+ losses in the stool are high, a fluid containing Na+ at 90 mmol/L has been recommended by WHO
Severely dehydrated patients – IVF : RL - must be used with additional potassium supplements, preferably given by mouth. The total fluid deficit in severely dehydrated patients (10% of body weight) can be replaced safely within the first 4 h of therapy, half within the first hour. Thereafter, oral therapy can usually be initiated, with the goal of maintaining fluid intake equal to fluid output.
Antibiotic : reduces duration and volume of fluid loss and will hasten clearance of the organism from the stool. Single-dose tetracycline (2 g) or doxycycline (300 mg) / Ciprofloxacineither in a single dose (30 mg/kg, not to exceed a total dose of 1 g) or erythromycin (a total of 40 mg/kg daily in three divided doses for 3 days) is a clinically effective substitute. For children, furazolidone and trimethoprim-sulfamethoxazole
PREVENTION - Provision of safe water and facilities for sanitary disposal of feces.
Two types of oral cholera vaccines are under development.
1. killed : two formulations A. killed whole cell + nontoxic B subunit of CTX (WC/BS) and
B. composed solely of killed bacteria. The protective efficacy of WC/BS was superior to that of WC during the initial 8 months of follow-up (69 versus 41%) but equivalent or inferior thereafter. Immunity was relatively sustained in persons vaccinated at an age of 5 years but was not well sustained in younger vaccinees.
Strain CVD 103-HgR, an oral live cholera vaccine licensed for immunization of travelers in Europe, this vaccine is more effective against classical than against El Tor cholera.
Composition of World Health Organization ORS
Constituent Concentration, mmol/L
Na+ 90
K+ 20
Cl 80
Citratec 10
Glucose 110
If prepackaged ORS is unavailable, a simple homemade alternative can be prepared by combining 5 g NaCl (about 1 level teaspoon) with either 50 g precooked rice cereal or 40 g sucrose in 1 L of drinking water. In that case, potassium must be supplied separately (e.g., in orange juice or coconut water).
Infectious Diseases: Typhoid Fever
TYPHOID FEVER
- 2300 serotypes; S.typh/paratyphi-enteric fever only in human. Non-typhoidal Salmonella –GIT of mammals, reptiles, birds.
- Typhoid: is a systemic disease characterized by fever and abdominal pain caused by dissemination of S. typhi or S. paratyphi.
ETIOLOGYGm –ive bacilli, family Enterobacteriaceae, facultatively anaerobic, motile-peritrichous flagella .
- Salmonella has three major antigenic determinants: the somatic O antigen [lipopolysaccharide (LPS) cell-wall components], the surface Vi antigen (restricted to S. typhi and S. paratyphi C), and the flagellar H antigen.
PATHOGENESIS (ID50) of S. typhi, 103 - 106 CFU, Host defenses- most important is the acidity of the stomach & integrity of SI epithelium.
- ↑ risk - age1 year, antacid ingestion, or achlorhydric disease,inflammatory bowel disease, history of gastrointestinal surgery.
- Contaminated food or water→ to colonize the small intestines→ cross the intestinal barrier→ phagocytosis by macrophages →dissemination throughout the reticuloendothelial system(liver, spleen, lymph nodes, and bone marrow. During this initial incubation stage, patients are relatively asymptomatic.
EPIDEMIOLOGY S. typhi and S. paratyphino known hosts except humans, the fecal-oral transmission via ingestion of contaminated food or water.
- Children 1 year of age appear to be most susceptible to initial infection and to the development of severe disease.
- Endemic in developing regions, many S. typhi strains contain plasmids encoding resistance to chloramphenicol, ampicillin, and trimethoprim
CLINICAL COURSE Incubation period - 3 -21 days.
- Symptoms: prolonged fever, headache, anorexia, cough, weakness, sore throat, dizziness, and muscle pains with either diarrhea or constipation; 20-30%with abdominal pain. Neuropsychiatric symptoms described as a "muttering delirium" or "coma vigil," with picking at bedclothes or imaginary objects.
- Signs: rash("rosespots"), hepato-splenomegaly, epistaxis, and relative bradycardia.
- Late complications,at 3-4th week - intestinal perforation and/or gastrointestinal hemorrhage. These complications can develop despite clinical improvement and presumably result from necrosis at the initial site of Salmonella infiltration in the Peyer's patches of the small intestine.
- Rare complications: pancreatitis, hepatic and splenic abscesses, endocarditis, pericarditis, orchitis, hepatitis, meningitis, nephritis, myocarditis, pneumonia, arthritis, osteomyelitis, and parotitis.
- Relapse rate~10% in immunocompetent hosts (with complete Rx).
- Chronic carriers:1 to 5% & is higher among women and among persons with gallstones, Ca-gallbladder & GI malignancies.
DIAGNOSIS
- TLC – N or ↓ed, rarely ↑.
- "Gold standard" is-culture positive for S. typhi or S. paratyphi --
- 1st week : blood culture, 2nd week bone marrow culture, 3rd week stool culture.
- Other Cultures : urine, rose spots, gastric/intestinal secretions (by a noninvasive duodenal string test)
- If blood, bone marrow, and intestinal secretions are all cultured, the yield of a positive culture is 90%
- Widal test : high rates of false-positivity and false-negativity
- TREATMENT
- 3rd gen CS: Ceftriaxone (1 to 2 g intravenously or intramuscularly) for 10 to 14 days; 5- to 7-day course of ceftriaxone +Cefixime 200BD for 7days
- Quinolones : Ciproflox – 500mg BD / Oflox – 200 -400mg BD for 10-14 days
- In cases of typhoid fever + alt. sensorium - Dexamethasone treatment should be considered
- Rx of Chronic carriers:Amox / Cotrimoxazole / Quinolone for 6 weeks (~80% effective). However, in cases of anatomic abnormality - requires surgical correction of the abnormalities.
PREVENTION AND CONTROL
- Good facilities for sewage disposal and water treatment
- Avoid uncooked food
- Consider vaccination
- Three vaccine are available:
- a heat-killed, phenol-extracted, whole-cell vaccine (two parenteral doses) - minimum age: 6 yrs
- Ty21a, L attenuated typhi vaccine (four oral doses); minimum age: 2 yrs
- ViCPS, consisting of purified Vi polysaccharide from the bacterial capsule (one parenteral dose) minimum age: 6 months
- All three vaccines have similar efficacy for the first year, the heat-killed whole-cell vaccine maintains its efficacy for 5 years, while Ty21a (4Yr) and ViCPS (2Yr).
- However, the whole-cell vaccine is associated with a much higher incidence of side effects than the other two vaccines
- 2300 serotypes; S.typh/paratyphi-enteric fever only in human. Non-typhoidal Salmonella –GIT of mammals, reptiles, birds.
- Typhoid: is a systemic disease characterized by fever and abdominal pain caused by dissemination of S. typhi or S. paratyphi.
ETIOLOGYGm –ive bacilli, family Enterobacteriaceae, facultatively anaerobic, motile-peritrichous flagella .
- Salmonella has three major antigenic determinants: the somatic O antigen [lipopolysaccharide (LPS) cell-wall components], the surface Vi antigen (restricted to S. typhi and S. paratyphi C), and the flagellar H antigen.
PATHOGENESIS (ID50) of S. typhi, 103 - 106 CFU, Host defenses- most important is the acidity of the stomach & integrity of SI epithelium.
- ↑ risk - age1 year, antacid ingestion, or achlorhydric disease,inflammatory bowel disease, history of gastrointestinal surgery.
- Contaminated food or water→ to colonize the small intestines→ cross the intestinal barrier→ phagocytosis by macrophages →dissemination throughout the reticuloendothelial system(liver, spleen, lymph nodes, and bone marrow. During this initial incubation stage, patients are relatively asymptomatic.
EPIDEMIOLOGY S. typhi and S. paratyphino known hosts except humans, the fecal-oral transmission via ingestion of contaminated food or water.
- Children 1 year of age appear to be most susceptible to initial infection and to the development of severe disease.
- Endemic in developing regions, many S. typhi strains contain plasmids encoding resistance to chloramphenicol, ampicillin, and trimethoprim
CLINICAL COURSE Incubation period - 3 -21 days.
- Symptoms: prolonged fever, headache, anorexia, cough, weakness, sore throat, dizziness, and muscle pains with either diarrhea or constipation; 20-30%with abdominal pain. Neuropsychiatric symptoms described as a "muttering delirium" or "coma vigil," with picking at bedclothes or imaginary objects.
- Signs: rash("rosespots"), hepato-splenomegaly, epistaxis, and relative bradycardia.
- Late complications,at 3-4th week - intestinal perforation and/or gastrointestinal hemorrhage. These complications can develop despite clinical improvement and presumably result from necrosis at the initial site of Salmonella infiltration in the Peyer's patches of the small intestine.
- Rare complications: pancreatitis, hepatic and splenic abscesses, endocarditis, pericarditis, orchitis, hepatitis, meningitis, nephritis, myocarditis, pneumonia, arthritis, osteomyelitis, and parotitis.
- Relapse rate~10% in immunocompetent hosts (with complete Rx).
- Chronic carriers:1 to 5% & is higher among women and among persons with gallstones, Ca-gallbladder & GI malignancies.
DIAGNOSIS
- TLC – N or ↓ed, rarely ↑.
- "Gold standard" is-culture positive for S. typhi or S. paratyphi --
- 1st week : blood culture, 2nd week bone marrow culture, 3rd week stool culture.
- Other Cultures : urine, rose spots, gastric/intestinal secretions (by a noninvasive duodenal string test)
- If blood, bone marrow, and intestinal secretions are all cultured, the yield of a positive culture is 90%
- Widal test : high rates of false-positivity and false-negativity
- TREATMENT
- 3rd gen CS: Ceftriaxone (1 to 2 g intravenously or intramuscularly) for 10 to 14 days; 5- to 7-day course of ceftriaxone +Cefixime 200BD for 7days
- Quinolones : Ciproflox – 500mg BD / Oflox – 200 -400mg BD for 10-14 days
- In cases of typhoid fever + alt. sensorium - Dexamethasone treatment should be considered
- Rx of Chronic carriers:Amox / Cotrimoxazole / Quinolone for 6 weeks (~80% effective). However, in cases of anatomic abnormality - requires surgical correction of the abnormalities.
PREVENTION AND CONTROL
- Good facilities for sewage disposal and water treatment
- Avoid uncooked food
- Consider vaccination
- Three vaccine are available:
- a heat-killed, phenol-extracted, whole-cell vaccine (two parenteral doses) - minimum age: 6 yrs
- Ty21a, L attenuated typhi vaccine (four oral doses); minimum age: 2 yrs
- ViCPS, consisting of purified Vi polysaccharide from the bacterial capsule (one parenteral dose) minimum age: 6 months
- All three vaccines have similar efficacy for the first year, the heat-killed whole-cell vaccine maintains its efficacy for 5 years, while Ty21a (4Yr) and ViCPS (2Yr).
- However, the whole-cell vaccine is associated with a much higher incidence of side effects than the other two vaccines
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