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EDYTA GRĄBCZEWSKA

Enteric (Typhoid) fever Epidemic (louse borne) typhus Leptospirosis. EDYTA GRĄBCZEWSKA. Nicolaus Copernicus University Ludwik Rydygier Collegium Medicum in Bydgoszcz. Enteric (Typhoid ) fever. Typhus abdominalis. Definition. a cute infectious disease i t occurs only in humans

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EDYTA GRĄBCZEWSKA

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  1. Enteric (Typhoid) fever Epidemic (louse borne) typhus Leptospirosis EDYTA GRĄBCZEWSKA Nicolaus Copernicus University Ludwik Rydygier Collegium Medicum in Bydgoszcz

  2. Enteric(Typhoid ) fever Typhusabdominalis

  3. Definition • acute infectious disease • it occurs only in humans • continuous febrile course • variety of symptoms • recurrences • dangerous complications

  4. Epidemiology worldwide occurrence 17-22 milion caseseachyearleading to 200 000-600 000 deaths • more frequently in the areas with poor public sanitation system, poorhygiene, inadequatesewagetreatment • the germ reservoir and source of infection is only a human - a sick person or a asymptomaticcarrier

  5. Epidemiology • infective material: mainly feces, less frequently urine, very seldom vomits • routes of spreading: • water (extent of outbreak depends on a number of people using the source of water) • food and milk (milk forms advantageous environment for the bacteria survival) • insects (flies) mechanical transfer of typhus rods from faeces onto food - sporadic cases • direct contact with the carrier (important role in spreading)or the sick person

  6. Epidemiology Carrier-state: • convalescents (after the sickness) – ends within three months after the illness course • chronic - can last for the lifetimeinflammatory states and diseases of bile ducts, urinarysystem and alimentary tract facilitate development and maintaining of the carrier state • healthy people can also be carriers (they have never been ill with clinically evident typhoid fever), they constitute the greatest epidemic threat

  7. Etiology • gram-negative rod of typhoid fever (Salmonella typhi) Enterobacteriacae family, • it grows well on ordinary bases, particularly those enriched with bovine bile • sensitive to disinfectants, heat and solar rays • dies after 20 minutes in the temperature of 60ºC • good tolerance of low temperature and drying out

  8. Etiology • it possesses three antigens: - ciliary- H - somatic - O - surfactant - Vi • antigens stimulate production of agglutinins that play fundamental role in serological diagnosis of typhoid fever

  9. Pathogenesis

  10. Phasesof clinicalcourse Endotoxindamage: CNS, heart, bonemarrow, vegetative system, liver, spleen 10-14 days Incubation period I week Increasing of symptoms II-III week Full development of the disease IV week Recovery

  11. Clinical course - I phase • average incubation period 10-14 days, in extreme case up to 7-28 days • phase I period – incubation/prodromes: • worsening of health condition and appetite • generally bad condition • occasional headaches • subfebrile temperatures

  12. Clinical course - II phase Phase II period – increasing of symptoms (stadium incrementi): • gradual increase of fever (after 3-7 days it reaches the level of 39-40) • severe headaches • unspecific muscles pains • bleeding from the nose – children often have vomits, catarrhal bronchitis, angina • meningeal symptoms • the patient becomes apathetic • characteristic stupor (inanity) up to the complete insensibility

  13. Clinical course - II phase In the physical examination: • tongue dry, covered in brown fur, sharply separated at edges and tip, • abdomen flatulent, painful, borborygm • enlargement of liver (tender) and spleen, • the circulatory system symptoms (lowered RR,pulse dicrotic, bradycardia - disproportionately slow to temperature)

  14. Clinical course - III phase • phase III period - full development of the disease (stadium acmes):in the second week - maximalintensity of symptoms • strong headaches, especially in the forehead area • stupor that disables consciousness of the patient, daze, raving, occasional mobility excitement (status typhosus) • strong thirst (the only stimulus that forces the patient to interact with other people) • Sleepless

  15. Clinical course - III phase In the physical examination: • dry and cracked lips • dry tongue • scarce and sticky saliva • dried up conjunctiva • facial features sharpened and hollowed • flatulent abdomen • diaphragm movements may be limited ( hepatosplenomegaly)

  16. Clinical course - III phase • phase III period - full development of the disease - continued - noticeable enlargement of painless spleen (continues till the end of the disease) • discrepancy between pulse and fever(conspicuous acceleration of the pulse may be an expression of complications) • in some case diarrhea can be infrequent (2-3 t./a day) or very frequent (10 or more) • continuous occurrence of bronchitis - sometimes its symptoms prevail (pneumotyphus)

  17. Clinical course - III phase • on the skin of the abdomen, lower part of the chest and in some exceptional cases on the limbs characteristic rash, the so called (roseola) – very scarce, sometimes only 3-4 pale pink spots, slightly raised above the skin, round approx. 1-4 mm in diameter, disappear when pressed • low RR • the daily amount of urine decreases • stools (without pain or tenesmus) constipated or loose, alkaline, with appearance of the pea soup

  18. Typhoid rash

  19. Clinical course - IV phase Phase IV – recovery (stadium sanationis): • improvement of the general well-being • lowering of the body temperature • symptoms of daze disappear • spleen diminishes • tongue clears • return of appetite -craving for food • diarrhea recedes,convalescents are weak, pale

  20. Complications

  21. Diagnosis • clinically - characteristic symptoms • epidemiologic- epidemiologic interview, traveler returning from a developing region (e.g. contact with a carrier) • in laboratory tests - leucopenia, eosinophilia, frequently thrombocytopenia, erythrocyte sedimentation rate – ESR - is usually normal) • microbiological - blood culture during the first days of the disease, in the period of bacteriaemia, stools • and urine culture, starting from the 2-3rd week of the disease • picture - ultrasound scan of the abdominal cavity, x-ray of the chest, x-ray of the abdomen - suspicion of perforation

  22. Diagnosis Serologic reaction – the classicVidal’s agglutination reaction. None of thesestestsissufficientlysensitiveorspecific to replaceculture-basedmethods for the diagnosisentericfever • in the second week of the disease, in the blood appear the antibodies that are specific for antigens H and O • reliable reaction: in the titre 1:200 and higher with antigen Oover 1:400 with antigen H • the day of the test is important, the previous incidence of typhus or vaccine against it • the reaction should be repeated several times with one week intervals, the increasing titre of the reaction is decisive • passivehaemagglutination reaction with antigen O Salmonella typhi - its value is equal to Vidal’s reaction value

  23. Differentiation • various infectious febrile diseases origins: common cold, influenza, paratyphoid fever, septicaemia, tuberculosis, brucellosis, tularemia, leptospirosis, EBV, CMV, viral hepatitis, malaria • non-infectious febrile diseases origins: endocarditis, lymphoma, proliferative diseases

  24. Treatment

  25. Treatment Symptomatic: • compensationof hydro-electrolyte disorders, • monitoringof circulation and renal system functions disorders • in case of shock symptoms - steroids for 3-5 days • recurrencesin 5-15% cases, most frequently 7-15 days after termination of antibiotic

  26. Prevention • common vaccinations only in the event of epidemic risk, also people travelling to the endemic areas (two types of vaccine Ty21a an oral live attenuated S.typhi vaccine given days 1,3,5,7 with booser every 5 years; and Vi CPS a parenteral vaccine consisting of purified Vi polysaccharide from the bacterial capsule, given in 1 dose with a booster every 2 years. • observing personal hygiene • proper water supply • appropriate utilization of waste • control of sanitary and working conditions in gastronomy and food industry • treatment and control of carriers • disinfection of premises and objects that the sick person had contact with examination of convalescents for the carrier-state

  27. Prevention Mary Mallon (September 23, 1869 – November 11, 1938), better known as Typhoid Mary, was the first person in the United States identified asanasymptomatic carrier of the pathogen associated with typhoid fever. She was presumed to have infected 49 people, three of whom died, over the course of her career as a cook.She was twice forcibly isolated by public health authorities and died after a total of nearly three decades in isolation.

  28. Leptospirosis

  29. Leptospirosis • itis a globallyimportantzoonoticdisease, caused by spirochetes of the genusLeptosira. Isalsoknown as Weil|’sdisaese, canicolafever, 7 day’sfever. Weil’sdiseasecame to signify, severeleptospirosischaracterized by diverseclinicalfindings: fever, jaundice, acuterenalinjury, refractoryshock, hemorrhageespeciallypulmonaryhemorrhage. • etiologic agent: • above250 pathogenicserotypes • in humanindentifyoften: L.caniola, L.icterohaemoragica, L.pomona, Grippotyhosa Leptospira icterohaemorrhagiae

  30. Leptospirosis • motile, Gram negative, Spirochaete: • to visualize the spirochetesdirectly in cultureor in clinicalspecimensdark-field orphase-contrastmicroscopy • leptospiresaredifficult to isolate in pureculture • susceptible: high temperature, disinfection • reservoir– rodents, small mamals, farm animals, dogs • animalseliminatebacteriawith urine. Leptospira icterohaemorrhagiae

  31. Epidemiology • the incidence of the disaeseis 3 – 21 cases per year (Poland) It is estimated that seven to ten million people are infected by leptospirosis a year.The number of deaths this causes is not clear.The disease is most common in tropical areas of the world but may occur anywhere

  32. Epidemiology Sources of infection: rats, dogs, cattle, pigs • Route of infection – (human-to-human transmission does not occur. It’s sporadic human infection. It can be occupation-related case, and case related enviromental exposure) • direct contact with sick animal • work on reclamation and sewer system • water containing animal urine (lake, swimmingpool) Contaminated agents; • contaminated water • contaminated soil • blood • Portal of entry • damage skin, mucosae membrane of nose • conjuctiva • respiratory tract – inhalation (laboratory-acquired infection rarely)

  33. Epidemiology

  34. Clinical symptoms Incubationperiod • on average 10 days (5-15), bacteriaspread to CNS, eyes, causevasculitis. Leptospiral infection in humans causes a widerange of symptomand some infected persons may have no symptoms at all

  35. Clinical symptoms Biphasiccourse of disaese • I phase (leptospiremia) lasts 3-10 days: at the beginingflu-likesymptoms (fever, chills, myalgia, intense headache, conjuctivalsuffusion, hepatosplenomegaly) The first phase (mild leptospirosis) resolves, and the patient is briefly asymptomatic until the second phase (severe leptospirosis) begins. 90 percent of cases of the disease are mild leptospirosis and without any specific treatment and the rest develop to severe leptospirosis • II phase (immunological) • affectedheart, liverdamage, renalfailure • affectedbrain, menigitis, encephalitis > 50% cases • opticneuritis, peripheralneuropathy

  36. Weil’s disease • Weil’sdiseaseischaracterized by variablecombinations of jaundice, acutekidneyinjury, hypotension, hemorrhage most commonlyinvolving the lungs, but alsopottentiallyafecting the gastrointestinaltract, pericardium and brain • othersymptomsinclude: • asepticmeningitis • uveitis • cholecystitis • acute abdomen • pancreatitis • myalgia • musclesweakness • loss of consciousness • myocarditis

  37. Weil’s disease Abnormalitiesin physicalexamination: • enlargedliver • splenomegaly(sometimes) • oliguria • pulmonary hemorrhage (cough, chest pain, hemoptysis without purulent sputum) • severe myalgia typically of the legs • petechiae, macular and maculopapule rash • conjuctival hemorrhage

  38. Diagnostic test • Laboratorytests: • leucocytosiswith increased of count of neutrophils • thrombocytopenia • hemolyticanemia mild to moderate • elevation: aminotransferase, creatinekinase, urea, alkalinephosphtase, creatinine, bilirubin • decline; INR • urinalysismay show abnormalitis of the sediment : leukocytes, erythrocytes, hyalin and granularcases. • CSF: • cytosis 10-1000 cells/ml • glucosaein normalrange • protein <100 mg/ml

  39. Diagnostic test • Etiologictests • culture – isolationbacteria from blood, urine, CSF • microscopicslide in dark-field orphase-contrastmicroscopy • PCR • serologicassays(ELISA, indirecthemagglutination, MAT –microscopicagglutination test) investigationsshould be repeatedafter 10-14 days

  40. Diagnostic test

  41. Treatment

  42. Prevention • no vaccineisavailable for humanleptospirosis • preventivestrategiesincludingprophylaxis with doxycyclinehavebeenvariablyeffective in differentsettings • antibioticprophylaxiscan be considered for anticipatedshort-term, well-definedexposuressuch as thoseincurredduringmilitarytrainingorspecificadventuretravel • long-term antibioticprophylaxishas not beenshown to be effective in preventinginfection in high-transmissionendemicsettings

  43. Epidemic (louse borne) typhus Thisis a form of typhus so named because the disease often causes epidemics following wars and natural disasters. The causative organism is Ricketssiaprowazeki transmitted by the human body louse (Pediculushumanuscorporis).Feeding on a human who carries the bacillus infects the louse. R. prowazekii grows in the louse's gut and is excreted in its feces. The disease is then transmitted to an uninfected human who scratches the louse bite (which itches) and rubs the feces into the wound. The incubation period is one to two weeks. 

  44. Epdemiology Typhus fever occurs in colder (i.e. mountainous) regions of Centraland Eastern Africa, Centraland South America, and Asia. In recent years, most outbreaks have taken place in Burundi, Ethiopia and Rwanda. Typhus fever occurs in conditions of overcrowding and poor hygiene, such as in prisons and refugee camps.

  45. Clinical symptoms Suddenonset: • fever, headache, musclepain, prostration, myalgia, cough • feverrisingrapidly to 38-40 º C • the 5-th or 7-th dayappearsrashwhichbegins on the uppertrunkthenbecomegeneralizedinvolving the entire body without face, palms and soles.Therashismacular, maculopapular, petechial and confluent. Skin necrosisand gangrena • potophobia, conjuctivalinjection, eyespain • interstitialpneumonia • patientwith untreatedinfectionsdeveloprenalinsufficiency, multiorganinvolvement in whichneurologicmanifestationsarefrequently prominent. • confusion, coma

  46. Clinical symptoms

  47. Rash and necrosis

  48. Diagnostic tests Serological reactions in rickettsial infections

  49. Treatment and prevention • doxycycline - 200 mg/d given in two divided doses 7-10 days • prevention of epidemic typhus • control of body lice • clothes should be changed regulary • insecticides should be used every 6 weeks to control the louse population

  50. Brill-Zinser disease • It is a recrudescentillnessoccuringyearsafteracuteepidemictyphus, probably as a result of wanigimmunity. R.prowazekiiremainslatent for years, itsreactivationresults in sporadiccases of disease in louse-freepopulationsor in epidemics in louse-infestedpopulation

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