Typhoid fever
Typhoid fever - the acute infectious disease caused by a salmonella (Salmonella typhi), is characterised by a fever, symptoms of the general intoxication, a bacteriemia, liver and lien augmentation, an enteritis and original morphological changes of the lymphatic apparatus of an intestine.
The typhoid fever originator (S. typhi) concerns family Enterobacteriaceae, sort Salmonella, kind Salmonella enterica, to subspecies enterica, serovar typhi and morphologicallies does not differ from other salmonellas. It is a Gram-negative mobile rod with it is peritrichous the located flagellas, dispute and capsules does not form, well grows on usual nutrient mediums. Biochemically differs from other salmonellas a fermentation of a glucose without formation of gas and the slowed down abjection of hydrogen sulphide. Antigenic structure S. typhi it is characterised by presence somatic O (9, 12, Vi) - a complex and flagellate antigen H (d). Depending on quantity and a Vi-antigen locating distinguish 3 variants of cultures:
- the V-form contains a Vi-antigen covering the O-complex, colonys of such cultures are opaque and not agglutinate O-whey
- the W-form does not contain a Vi-antigen, colonys are transparent, culture well agglutinate O-whey
- the VW-form has a nested locating of a Vi-antigen and agglutinate O - and Vi-Serums
Typhoid fever originators on sensitivity to sample bacteriophages are sectioned on 78 stable phagovar. The lysotypy represents a convenient label for an establishment of epidemiological communication between diseases and revealing of a source of an infection contamination. Typroid bacteria are capable to L-transformation, that, probably, grows out of originator evolutionary adaptation to a surviving in the conditions of an immune organism. S. typhi are moderately steady in an external environment - in bedrock, to water can remain till 1-5 months, in excrements - till 25 days, on linen - till 2 weeks, on foodstuff - from several days about one weeks, it is especially long - in milk, a mincemeat, vegetable salads where at temperature above 18оС they are capable to propagate. At warming quickly perish. (The lysol, Chloraminum, Phenolum, corrosive sublimate) in usual concentrations kill disinfectants of the originator within several minutes.
Epidemiology. The typhoid fever concerns intestinal anthroponoses. A unique source and the infection contamination reservoir is the human. An infection contamination source are chronic bacillicarriers of the originator of a typhoid fever who, remaining practically healthy more often, excrete salmonellas during long time (years and even tens years). Represent also danger of the person with easy and atypical forms of disease as they not always are in due time isolated, visit public places, continue to carry out official duties, including on objects of a food and water supply.
The mechanism of transfer of originators fecal-oral, i.e. infestation of humans descends at the use of the infected water or nutrition. The is contact-household path of transfer S. typhi it is observed was rarely, mainly among children. Water flashes arise at contamination of water sources by sewage, technical malfunction of water, sewer systems and constructions, and also owing to disturbance of a regimen of water treating. Danger of alimentary infestations consists that in some products (milk, cold meat snack) typhoid fever salmonellas can remain and even to propagate. The risk of occurrence of disease in these cases is enlarged owing to the big infecting dose of the originator.
The sensibility of humans to a typhoid fever is various, in spite of the fact that the originator possesses obligate pathogenicity and is evolutionary has adapted to a parasitizing in a human body. Immunity is usually caused by presence of specific immunodefence as a result of the tolerated disease, household immunization or bacterination. At mass infestation in the epidemic locuses can be ill to 40-50 % of humans.
Disease meets in all climatic regions and parts of the world. However in larger degree it is extended in the countries with a hot climate and low level of sanitary-municipal arrangement of the population.
Pathogenesis. The phase theory of a pathogenesis of a typhoid fever has remained as a whole till now. On its basis excrete following parts of a pathogenesis: originator introduction in an organism, lymphadenitis development, a bacteriemia, an intoxication, parenchymatous diffusion, abjection of the originator from an organism, formation of immunodefence and homeostasis restoration. The resulted scheme is conditional, as is experimentally proved, that, for example, penetration of originators into blood descends already within first two phases. Hence to speak about inter - the parts of a pathogenesis of a typhoid fever caused and often coinciding on time more correctly.
For disease occurrence hit in a gastrointestinal tract of a certain infecting dose of microbes-originators is necessary. In researches on volunteers the American authors have established, that it compounds from 10 million to 1 billion microbic cells. Originator introduction descends in a small bowel from which lumen of a salmonella inpour into solitary follicles and Peyer's glands, causing a lymphangitis. Then microbes get to mesenteric lymph nodes where they propagate, and, having broken through a lymphatic barrier, through a thoracal duct get to blood. There is a bacteriemia which coincides with the first clinical signs of a typhoid fever. As a result of bactericidal action of blood the part of microbes perishes with endotoxin abjection. The same process descends and in lymph nodes. The endotoxin circulating in blood causes an intoxication of an organism of various intensity.
The endotoxin has the expressed neurotropic an effect with a toxic lesion of nerve centres and development in them of inhibition processes. Clinically it is characterised by an infectious-toxic encephalopathy which shows in original retardation of patients, obnubilation. At serious disease it is most expressed and has received the name of a typhous condition (status typhosus). The endotoxin reacts also on sympathetic nerve terminations of a celiac nerve (in an abjection place) and on vegetative ganglions that leads to trophic and vascular disturbances in a mucosa and lymphatic formations of a small bowel. As a result there are intestinal ulcers, there is a meteorism, sometimes diarrhoeia. In favour of the similar mechanism of occurrence of cankers of a small bowel at a typhoid fever the facts of formation of similar ulcers on morphology at experimental animals testify at introduction of a typroid endotoxin in abdominal vegetative ganglions. Endotoxin S. typhi amazes also an osteal brain that shows a leukopenia.
The lesion a myocardium endotoxin causes its dystrophic changes, and in more serious cases - a toxic myocarditis. At serious disease the infectious-toxic shock can educe. Thus there is a disturbance of a tonus of peripheric pots (arterioles and sphincters of postcapillary venules). There is a blood deposition in a peripheric bed, an exit of its liquid part in extravasal space. The absolute hypovolemia with venous inflow reduction to heart educes in the beginning relative, and then. The hypoxia, a metabolic acidosis, disturbances of vodno-electrolytic balance accrue. Flow and the forecast of an infectious-toxic shock are in many respects defined by cardiovascular insufficiency, a lesion of nephroses ("a shock nephros"), lungs ("a shock lung") and a liver. In the conditions of a long brjushno-typhus endotoxemia there is an activation kinin-kallikrein system, that can promote development at a typhoid fever of an infectious-toxic shock, hemodynamic disorders, functional and morphological changes of an internals, hemostasis disturbances.
Hence, in a pathogenesis of a typhoid fever the leading part is played by an intoxication an endotoxin. However the great value has also the originator. Typhoid salmonellas are carried by a blood flow on all organism and fixed in various organs ("parenchymatous diffusion by microbes") where they are grasped by elements of mononuklearno-phagocytal system (MPS). Depending on a functional condition mononuclear - phagocytal system microbes in organs either perish, or cause various focal lesions (a meningitis, osteomyelites, pyelites, a pneumonia, abscesses).
Simultaneously with a dissimination of salmonellas purification of an organism by originator deducing by various organs of abjection (a nephros, alimentiry glands of an intestine, salivary, sudoral glands, a liver) begins.
Most intensively bacteria are deduced through a liver where their great bulk perishes, and the others are excreted with bile in an intestine lumen. Their part is deduced with excrements in an external environment, and the part again takes root into lymphoid formations of a small bowel. The hypothesis bound to this fact about an allergic genesis of formation of ulcers of a small bowel now is represented improbable as the expressed allergic responses are not inherent to a typhoid fever, and it is possible to explain intestine changes by toxic action of an endotoxin as on peripheric vegetative ganglions and the terminals, and is immediate on lymphatic formations of an intestine.
Organism defence reactions at a typhoid fever educe from the beginning of occurrence of infectious process. For 4-5th day of disease in blood it is possible to find the specific antibodies concerning to IgM. By 2-3rd week of disease the specific immunogenesis reaches the highest development (O-antibodies IgM prevail). During same time there are the IgG-antibodies which titer in the subsequent accrues, and antibodies IgM - decreases. Formation of cellular immunodefence is induced by antigens of salmonellas of a typhoid to a lesser degree, rather than humoral, that is a consequence of deep deficiency of a common pool T - cells and T - helpers, and also moderate depression T - suppressors.
Cyclic flow of a typhoid fever can show five seasons of pathogenetic changes in a small bowel, the colon is sometimes amazed also. The first season (1st week of disease) is characterised by an appreciable swelling of group lymphatic follicles; the second (2nd week) is accompanied by a necrosis of these formations. During the third season there is a sloughing and formation of ulcers. The fourth (3-4th weeks) name the season of pure ulcers. In the fifth season (5-6th week) there is a healing of ulcers. At treatment by antibiotics pathogenetic changes of an intestine can already educe against body temperature normalisation.
Postinfectious immunodefence at a typhoid fever is strictly specific and can is long to remain (15-20 years). However now there are observations of recurrent diseases by a typhoid fever through rather short time intervals (1,5-2 years), that bind to disturbance of an immunogenesis as a result of an antibioticotherapia more often.
Symptoms and flow. Clinical classification of a typhoid fever means its separation depending on clinical forms - typical, atypical (abortal, erased); severity levels - easy, moderately severe, serious; character of flow - cyclic, recurring; presence of complications - uncomplicated, complicated.
The incubation interval lasts more often 9-14 days (minimum - 7 days, maximum - 25 days), that depends on quantity of the microbes which have got to an organism. At a becoming infected sick of the big dose of the originator (at alimentary flashes) an incubation interval, as a rule, short, and disease proceeds more hardly, than at an infestation waterway.
In disease excrete following seasons:
- the initial
- height of disease
- fading of the basic clinical implications
- recover
In typical cases of a typhoid fever disease begins gradually, sometimes even it is difficult to establish day of the beginning of disease. At patients the expressed general delicacy, fast fatigability, an adynamia, a moderate headache educe, there can be small cold fits. Every day these phenomena strengthen, the body temperature raises and by 4-7 day of disease it reaches a maximum. The intoxication accrues, the headache and an adynamia strengthen, goes down or appetite disappears, the sleep (drowsiness in the afternoon, a sleeplessness at night) is broken. The chair is usually detained, there is a meteorism. By 7-9 day disease reaches full development.
At inspection of sick disease in an initial stage tap mainly symptoms of the general intoxication without distinct signs of organ lesions. Retardation of patients is observed, they are inactive, prefer to lay blindly, questions answer not at once, tersely. The person acyanotic, is less often slightly hyperemic, the conjunctivitis and a herpetic eruption usually does not happen. A skin dry, hot. In some cases the hyperemia of a mucosa of fauces is possible. Peripheric lymph nodes, as a rule, are not enlarged, though at some patients the augmentation and sensitivity of cervical and axillary lymph nodes become perceptible. The relative bradycardia is characteristic, at some patients the sphygmus dicrotism, a muting of cardiac sounds (or only I tint on an apex) are observed. Arterial pressure goes down.
Over lungs auscultate to absent-minded dry rhonchuses that regard as implication of a specific typroid bronchitis. The pneumonia in this season is taped in rare instances. Tongue usually dry, is imposed by serovato-brown scurf, is thickened (there are impresses of dens along the edges), an end and tongue edges are free from scurf. The gaste is blown moderately up. The shorting of a percussion note in right ileal ranges (Padalka's symptom) sometimes becomes perceptible. At a palpation the rasping rumble of a caecum and rising of painful sensitivity here are defined. From 3-5th day of disease the lien is enlarged, and to the extremity of 1st week it is possible to tap liver augmentation. Sometimes the typhoid fever begins in the form of an acute gastroenteritis or an enteritis without the expressed general intoxication when in the first days disturb a nausea, vomiting, a liquid chair without pathological admixings, diffuse abdominal pains, and in the subsequent there are characteristic symptoms of disease.
By 7-8 day of disease there comes the height season when there is a number of the characteristic signs facilitating clinical diagnostics. Appreciable intensifying of an intoxication shows in sharp retardation of patients, a stupefaction (an infectious-toxic encephalopathy).
On a skin there is a characteristic roseolous exanthema. It is usually a little elements of an eruption, they are localised on a skin of the top parts of a gaste and the inferior parts of a thorax. Roseolas monomorphism with accurate borders, tower over skin level (roseola elevata) a little. Elements exist from several o'clock till 3-5 days. On a roseola place there is hardly appreciable pigmentation. During the feverish season appearance of fresh roseolas can be observed. At serious forms of disease probably hemorrhagic impregnation of elements of an eruption that is an unfavorable prognostic sign. The relative bradycardia and a sphygmus dicrotism remain, arterial pressure even more goes down. Cardiac sounds become deaf persons. Approximately at 1/3 patients the myocardial dystrophy educes, and in some cases there can be a specific infectious-toxic myocarditis. In this season against a bronchitis the pneumonia can educe. It happens is caused both the originator, and the joined secondary flora, more often the coccal. Changes from digestion organs become even more expressed. Tongue dry, cracked, with impresses of dens, is covered by dense is dirty-brown or brown scurf (baked tongue), edges and a tongue end are free from scurf. The gaste is considerably ventricose, at some patients the chair is detained, at the majority diarrhoeia is observed. The rumble and morbidity are more accurately taped at a palpation in ileocecal range, and also a Padalka's symptom. The liver and a lien in this season are always enlarged.
In the season of fading of the basic clinical implications the body temperature lytic decreases, and then is normalised. Decrease and subsequently the phenomena of the general intoxication, a headache disappear. There is an appetite, tongue is cleared, the liver and lien dimensions decrease.
The reconvalescence season begins after normalisation of a body temperature and 2-3 weeks depending on disease severity level last. As a rule, undue fatigability and vascular lability at this time remain.
Besides typical clinical forms atypical forms of a typhoid fever can be observed. The abortal and erased clinical forms concern them. Abortal forms of disease are characterised by the beginning and expansion more or less characteristic signs of disease, but with fast (in 5-7 days, sometimes in 2-3 days), quite often critical, temperature depression, disappearance of symptoms and transition in a recover stage. To the erased forms carry cases of a typhoid fever with a short-term subfebrile fever, weak symptoms of an intoxication and absence of many characteristic signs. The body temperature on all extent of disease does not exceed 38оС, the intoxication insignificant, is not present a bradycardia, a meteorism, there is no eruption.
According to the affirmed representations, the haemogram at a typhoid fever is characterised short-term, in the first 2-3 days, a moderate leukocytosis which is replaced by a leukopenia with a deviation to the left, by an aneosinophilia or a hypoeosinophilia, a relative lymphocytosis. An ESR it is often moderately enlarged. The leukocytosis in the first days usually remains undetectable.
Now the clinical picture of a typhoid fever has essential variated, that in a certain measure speaks frequent application of antibiotics and preventive engraftings against typhus - paratyphoid diseases. Easy forms of a typhoid fever at which the phenomena of the general intoxication are expressed weakly have become frequent, many symptoms of classical disease are absent. The fever proceeds only 5-7 days (sometimes 2-3 days) even without use of antibiotics. There is an acute beginning of disease (at 60-80 % of patients), and also a hyperadenosis is more often. Difficulties in diagnostics represent also atypically current cases, for example, a typhoid fever with a clinical picture of an acute gastroenteritis and a short-term fever (1-3 days). In a reconvalescence against a normal body temperature there can come complications in the form of punching of an intestinal ulcer; such patients arrive in surgical hospitals. Have undergone changes as well results of laboratory researches. So, almost at half of patients the normocytosis is observed, in blood eosinocytes remain, serological tests during all disease can remain negative.
Paratyphoids A and B - the acute infectious diseases caused by salmonellas and proceeding as a typhoid fever.
The originator of paratyphoid A is Salmonella enterica subs. enterica serovar paratyphi A, paratyphoid B - Salmonella enterica subs. enterica serovar paratyphi B. As well as typroid bacteria, they contain O - and H-antigens, but have no Vi-antigens, possess identical morphological properties, are sectioned into phagotypes. Infection contamination sources at paratyphoid A are sick humans and bacillicarriers, and at paratyphoid B them can be and animals (large horned livestock, pigs, poultry). Pathogenetic and patologo-anatomical disturbances at paratyphoids A and B same, as well as at a typhoid fever.
Paratyphoids A and B are very similar to the clinical signs and have some clinical features. To differentiate them among themselves and from a typhoid fever practically probably only bacteriologically - on originator abjection. Note only some signs of paratyphoids distinguishing them from a typhoid fever.
Paratyphoid A. There is less often, than a typhoid fever and paratyphoid B. Proceeds in the form of moderately severe diseases is more often, but can give and serious forms of disease. In an initial stage the hyperemia of the person, an injection of pots of scleras, a herpetic eruption on labiums, a cold, tussis are observed. The eruption appears early - for 4-7th day of disease, happens polymorphic (roseolous, macular, macula-papular and even petechial). The basic method of acknowledgement of the diagnosis - bacteriological. Widal reaction usually negative during all disease (in some cases - positive in very low caption). Complications and relapses are observed now a little bit less often, than at a typhoid fever.
Paratyphoid B. Clinically paratyphoid B proceeds easier, than a typhoid fever though there are also serious forms purulent septic complications. Disease often begins subitaneously with the phenomena of an acute gastroenteritis and only then the symptoms similar to clinical implications of a typhoid fever join. The temperature curve differs the big daily scope, often wavy. The eruption appears for 4-6th day of disease, roseolous, but more abundant, than at a typhoid fever. The diagnosis proves to be true originator abjection, however it is possible to use and serological tests, especially at their statement in dynamics.
Complications. The most dangerous complications of tifo-paratyphoid diseases are punching of intestinal ulcers, an intestinal bleeding and an infectious-toxic shock. The pneumonia and a myocarditis are quite often observed, is rarer - other complications: cholecystocholangitis, a thrombophlebitis, a meningitis, a parotitis, arthritises, pyelonephrites, an infectious psychosis, a lesion of peripheral nerves.
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