YERSINIAL INFECTION

Main Statements

Yersiniosis is anthropozoonotic infection; the causative agent is transmitted by wild and domestic animals, and the source of infection is human being.

The third representative of genus Yersinia is Yersinia pestis, the causative agent of plague. Y. enterocolitica produces termostable toxin, Y. enterocolitica and Y. pseudotuberculosis produce lypopolysaccharide endotoxin.

Yersinia causes diseases with fever, abdominal syndrome, rash (sometimes with typical localization), diarrhea. Clinical presentation can resemble acute appendicitis.

Majority of yersiniosis cases are moderate, but with quite prolonged course, not requiring antibacterial therapy.

Patients with increased ferrum level of the body (chronic liver diseases, hemochromatoses, talassemias) have increased risk of Yersinia invasion with development of septic forms.

There is no specific prophylaxis.

The term “Yersinia infection” includes two acute infectious diseases:

pseudotuberculosis and intestinal yersiniosis caused by bacteria of Yersinia genus (Y.

pseudotuberculosis and Y.enterocolitica), which are characterized by general

intoxication, exanthema, involvement of liver, spleen, gastro-intestinal tract, joints and

other organs and systems.

Pseudotuberculosis

Pseudotuberculosis (Far East scarlet fever-like disease, pasterellosis, acute

mesenterial lymphadenitis, etc.) is an acute infectious disease from zoonotic group

which is characterized by general intoxication, fever, scarlet fever-like rash, as well as

involvement of other organs and systems.

Etiology. The causative agent of pseudotuberculosis is Y. pseudotuberculosis, a

gram-negative rod, situated in long chains in culture, not forming spores, encapsulated,

weakly motile. The bacteria are sensitive to drying and action of sun light. At heating till

600С and at action of UVR the bacteria is inactivated in 30 min, at boiling in 10 sec.

Usual disinfection (2% chloramines solution, lysol solution, sulema, etc.) kills the

bacteria during 1 minute.

The particularity of Y. pseudotuberculosis is the ability to grow at low

temperatures (1-40С), while the optimal growth temperature is 22-280С. The bacteria

actively replicates in boiled, tap, river water. Microbes are preserved during 2-8 months 1

in water, 5 months in butter, till 3 weeks in sugar, till 150 days in bread, during 30 days

in milk, about a year in soil at favorable conditions.

Epidemiology. The disease belongs to group of zoonotic infections. The sources of

infection are wild and domestic animals. The microbe is found in 60 types of mammals

and 29 types of birds. The main reservoir of the infection is rodents. They infect food

with their excretions; during storage in fridges and in vegetable storages bacteria

reproduction and massive accumulation occurs. It is considered that the reservoir of

bacteria can be not only rodents and other animals but outer environment and soil,

where the bacteria can reproduce and survive for a long time.

The role of human as a source of infection is not proved yet. Infection occurs by

alimentary route while eating infected food (salads, beetroot salad, fruits, milk products,

water, etc.) without thermal processing. Children and adults are susceptible to

pseudotuberculosis.

Children under 6 months of age are commonly unsusceptible to

pseudotuberculosis; children from 7 months till 1 year of age seldom develop the

disease, which is explained by their character of feeding.

The disease is registered during the whole year; its maximum is during winter and

spring period, which is explained by wide usage of vegetables and fruits from vegetable

storages.

Pathogenesis. The causative agent enters the mouth with infected food and water

and, overcoming gastric barrier, penetrates enterocytes and extracellular spaces of small

intestine wall (enteric phase), which results into inflammatory changes of small intestine

mucosa. From bowel the bacteria penetrates regional mesenteric lymph nodes and

causes development of lymphadenitis (phase of regional infection). Massive penetration

of bacteria and its toxins from primary sites of localization into blood leads to

appearance of the next stage of pathogenesis, generalized infection stage (bacteremia

and toxinemia). It coincides with development of clinical signs of the disease. Further

progression of the process is connected to bacteria fixation by reticuloendothelial cells

predominantly in liver and spleen (parenchymatous phase). Clinically it presents with

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enlargement of liver and often spleen and disturbance of their function. Recurrent

generalization of the process and development of exacerbations and relapses is possible.

Finally stable fixation and elimination of the bacteria occurs due to activation of cellular

factors of immunological defense, as well as production of specific antibodies. Clinical

recovery follows.

Allergic component plays a certain part in pathogenesis of pseudotuberculosis.

Presence of allergic rash, arthralgias, nodular erythema and other allergic signs confirms

the role of allergy in disease pathogenesis.

Accumulation of specific humoral antibodies occurs slowly, and they often do not

posses prominent protective properties. In a number of cases specific antibodies only

appear after disease relapses. Weak production of specific antibodies is probably

explained by insufficient antigenic stimulation. Phagocytosis and other non-specific

protective factors play a big role in bacteria elimination. Length of immunity is not

definitely determined yet, but it can be considered long-term. Repeated cases of the

disease are seldom seen.

Clinical manifestations.

Incubational period is from 3 till 18 days. The disease begins acutely with fever;

only in rare cases the disease onset is gradual or subacute. From the first days of the

disease children develop general weakness, headache, sleeplessness, decreased appetite,

sometimes chills, muscle and joint pains. Mild catarrhal signs such as nasal stiffness and

cough, pain at swallowing and tickling in the throat can be observed.

Patients present with prominent primary intoxication symptoms: dizziness, nausea,

vomiting, abdominal pain, predominantly in right iliac area or in epigastrium. In some

cases diarrhea of enteritis type can be seen 2-3 times a day. Edematous and hyperemic

face and neck are observed, in contrast with pale nasolabial triangle. Conjunctival

hyperemia, sclera injections, more seldom herpetic rash on lips and nasal wings are

seen. Majority of patients also develop hyperemia of tonsils, soft palate, sometimes very

bright and separated from hard palate. Oral mucosa is edematous, sometimes enanthema

is seen. During the primary period the tongue is covered with thick grayish-whitish

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cover, with the third day of the disease it starts to clean and becomes strawberry-like,

with papilles. From the first days of the disease in some cases joint pain and enlarged

liver and spleen are seen.

Disease symptoms progress and on the 3-4th days reach its maximum. At this time

the height period of disease begins. It is characterized by worsening of condition,

prominent symptoms of intoxication, high fever, involvement of inner organs and skin.

Some patients develop at this period face and neck hyperemia with cyanotic tint,

“gloves” symptom (limited pink-bluish color of hands), “socks” symptom (limited pink-

bluish color of feet).

Rash at pseudotuberculosis is localized on the lower parts of abdomen, on axillary

areas and on lateral surfaces of trunk; stable white dermographism is seen. It can appear

from the first days of the disease, but often develops during disease height. The rash

appears simultaneously; by character it can be pointed, scarlet fever-like or macular.

The color of rash is from pale pink till scarlet. Background skin color can be hyperemic

or unchanged. Large rash elements are situated around large joints, where they form

continuous erythematous color. Combination of scarlet fever-like and macular rash is

seen in approximately half of patients. The rash is sometimes accompanied by slight

itching. At persistent course or at relapses elements of nodular erythema appear on legs,

more seldom on buttocks.

Pastia’s symptom (intensity of skin folds, linear hemorrhages), pinch and bandage

signs are usually positive. The rash is present not longer than 3-7 days, sometimes, if

mild, it can only be seen during several hours. After disappearance of rash sometimes

scaled desquamation appears on hands and feet and branny desquamation on back,

thorax and neck.

Changes in cardiovascular system present with relative bradycardia, more seldom

by tachycardia, muffled heart sounds, sometimes systolic murmur, in severe cases

arrhythmias. Arterial pressure is moderately decreased. ECG reveals changes of

myocardium contraction function, disturbances of conductivity, extrasystoles, depressed

T wave, widening of ventricular complex.

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Appetite is considerably decreased; nausea, sometimes vomiting, often abdominal

pain and diarrhea are seen. The abdomen is moderately distended. At palpation half of

the patients reveal tenderness and rumbling in right ileac area. Sometimes in caecum

projection enlarged and tender mesenteric lymph nodes are detected.

Changes of gastrointestinal tract in some patients can be prominent with

development of signs of terminal ileitis or acute appendicitis.

At pseudotuberculosis enlarged liver and spleen are seen, sometimes skin and

sclera jaundice. In blood serum the levels of direct bilirubin and hepatocellular enzyme

activity (ALT, AST, P-1-PA, etc.) are increased, sedimentary probes are positive.

Clinical presentations of acute cholecystitis or angiocholecystitis are sometimes seen.

At the disease height lumbar pain and decreased diuresis can be observed. In urine

sediment albuminuria, microhematuria, cylindruria and pyuria are detected. These

changes are explained as infectious-toxic kidneys. In some cases signs of diffuse

glomerulonephritis can develop.

The length of the disease is seldom longer than 1-1 ½ months. In 16-22% of

patients development of relapses is possible, which present by exacerbation of disease

symptoms, appearance of allergic and joint symptoms, nodular erythema. Single relapse

is more commonly seen; more seldom 2-3 and more relapses are observed. The relapse

course is milder than the one of the first episode. In these cases the disease is prolonged;

complete recovery is seen in 2-3 months after disease onset.

Diagnosis. Clinical criteria:

- incubational period from 3 till 18 days;

- acute onset;

- febrile wave-like fever with mean duration of 7-11 days;

- intoxication syndrome;

- enteritis, more seldom gastroenteritis or enterocolitis;

- exanthema is scarlet fever-like, macular-papular, petechial-hemorrhagic or

nodular erythema. The rash appears on the 2-4th days of the disease; it is situated on

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hyperemic skin background of the face (including nasolabial triangle), trunk, extensor

surfaces of extremities, around joints; the symptom of “gloves”, “socks”, “hood”;

- “strawberry” tongue;

- white dermographism;

- scaled desquamation on hands and feet;

- liver and spleen enlargement;

- conjunctiva hyperemia and sclera injections;

- joint pain – migrating arthralgias, predominantly involving wrist, elbow, knee

and interphalangeal joints; the joints are edematous and painful;

- muscle pain;

- mild catarrhal signs;

- acute tonsillitis;

- probable hepatitis;

- can be abdominal syndrome;

- possible development of myocarditis;

- can be symptoms of peritoneal irritation;

- possible development of “infectious-toxic kidney”.

In 16 - 22% of cases relapses of the disease can develop with exacerbation of

disease symptoms or appearance of allergic, joint symptoms and nodular erythema.

Laboratory methods:

1) Complete blood count: leukocytosis, neutrophilia with young forms,

eosinophilia, accelerated ESR.

2) Bacteriological method: revealing of causative agent in feces and other

physiological media of the body (urine, blood, sputum, contain of abscesses).

3) Serological method: reaction of agglutination and indirect hemagglutination on

the 3-4th week of the disease and during disease course. Diagnostic titer is 1:200

and higher.

Immune enzyme analysis reveals specific IgM in blood.

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Complications. At pseudotuberculosis the following complications can develop:

carditis, biliary tract dyskinesia, inflammation of biliary tract, acute renal insufficiency,

acute hepatic insufficiency, DIC syndrome.

Treatment. Mild form of the disease can be treated symptomatically, without

antibacterial drugs. Children with moderate and severe forms should be obligatory

hospitalized.

Etiotropic therapy is given at bacteremia (confirmed bacteriologically).

Chloramphenicol, cephalosporins of III - IV generations and aminoglycosides are used.

However, mortality at septicemia caused by Y. pseudotuberculosis in children reaches

75%, independently of performed antibacterial therapy. Mean length of the course is 14

days; the antibiotics are given parentherally.

Desintoxication therapy at mild forms includes increased amount of alkaline fluid

by mouth; at moderate and severe forms it includes infusions of salt and glucose

solutions. At prominent joint involvement non-steroid anti-inflammatory drugs should

be given.

Prophylaxis. The main point in prophylactic activity is eradication of rodents.

Organization of appropriate storage of vegetables, fruit and other food with exclusion of

infection contamination is of great importance. It is necessary to perform strict sanitary

control of technology of food preparation, especially of those foods which are not

treated with heat before eating (salads, beetroot salads, fruit, etc.), as well as control of

water supply in village areas. Anti-epidemic activities in infection nidus in general

should be the same as the ones at bowel infections. After hospitalization final

disinfection is performed. Specific prophylaxis is not developed.

Yersiniosis (Intestinal yersiniosis)

Intestinal yersiniosis (Yersiniosis enterocolitica) is an acute infectious disease

caused by Yersinia enterocolitica and characterized by symptoms of intoxication and

involvement of gastrointestinal tract, liver, joints and other organs and systems.

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Etiology. The causative agent of yersiniosis is Yersinia enterocolitica from genus

Yersinia, enterobacteria family. They are short Gram-negative rods. Mobility is due to

fimbria all over the cell. It is a facultative aerobe. By biochemical features 5 biovars are

described; III, IV and more seldom II biovars are more pathogenic for humans.

According to somatic О-antigen, 34 serovars of Yersinia are described, among which

the most pathogenic for humans are 0:3; 0:9; 0:5, 0:27; 0:8 and 0:6, 0:30. There is

antigenic similarity of Yersinia 0:3 Y.pestis with salmonellas; 0:9 with О antigen of

Brucella, Vibrio cholerae, as well as common antigens with Rickettsia, Shigella,

Escherichia and Proteus.

Majority of revealed virulence factors of Yersinia are temperature dependent. So,

at 250C the microbes are quite motile but unable to express majority of virulent proteins;

whereas at 370C they lose ability to move but produce actively virulent factors. At

temperature 300C Yersinia actively produce enterotoxin, but it does not belong to critical

virulent factors. Phenomenon of production of different proteins in different temperature

conditions allows the causative agent to survive both in macroorganism and outside.

Epidemiology. The source of infection can be human (sick or carrier) and different

domestic (cows, pigs, dogs, cats) and wild animals (rodents, hares, foxes, etc.).

The route of transmission is alimentary and contact. Watery route is not excluded

(Yersinia 0:3, 0:9 are revealed from water reservoirs near stock-farms).

Transmission factors can be food infected with Yersinia without thermal treating

(meat, vegetables, fruit, milk, cream, ice-cream). Secondary infection of prepared food

through kitchen devises is possible. Realization of food factor of bacteria transmission is

due to bacteria accumulation during long-term storage at low temperatures and absence

or insufficiency of their thermal processing. Infecting dosage for human is 3.5 x109

microbes. The most susceptible are early age children who are the most sensitive to

enteropathogenic bacteria.

The source of infection can be human (sick person or carrier). Cases of children

infection in the age of several weeks are described, as well as family outbreaks with

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consequent infection of adults and children afterwards. Yersiniosis is registered as a

cause of nosocomial outbreaks and group outbreaks in children institutions.

Typical feature of acute yersiniosis includes long-term excretion of bacteria with

feces after disappearance of the symptoms. So, according to different investigators,

bacteria excretion is described with mean duration within 40-45 days; children are prone

to more prolonged persistence of Yersinia excretion than adolescents or adults.

In countries with moderate climate the disease in children mostly develops in cold

seasons.

Pathogenesis. Infection occurs at ingestion of infected food, water, or by contact

route. The amount of ingested bacteria plays a great role at infection development.

Passing through stomach, the bacteria is localized in small intestine, where it begins to

proliferate. The most common localization is the area between small intestine and

caecum (terminal part of small intestine and appendix). Possessing enterotoxigenic and

invasive properties, Y. enterocolitica incorporates and destroys epithelial cells of

intestinal mucosa. The character of inflammatory process can be different, from

catarrhal till ulcerative necrotic. Infection is spread to regional lymph nodes which are

enlarged due to hyperplasia of lymphoid tissue; foci of necrosis and microabscesses can

be formed there. The process can involve liver and pancreas.

The disease can terminate with enteral or regional stage. However, in more severe

cases bacteria breaking into blood is possible with subsequent generalization of

infection and appearance of pathological foci: abscesses of liver, spleen, lungs and

bones.

The causative agent can persist for a long time in lymph nodes, causing repeated

exacerbations of the disease or being transformed into chronic forms. Development of

different infectious and allergic signs at yersiniosis, such as rash, poly- and

monoarthrites, arthralgias, myalgias, tendovaginites, myosites, heart damage, nodular

and other erythemas, Reiter syndrome, some authors connect to antigenic similarity of

Y. enterocolitica and histocompatibility antigen HLA В-27, which is seen in these

patients in 90% of cases in comparison to 14% in general population.

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Clinical manifestations. The disease begins with fever till 39-400С; chills, fatigue

and adynamia develop. Early age children can present with changing episodes of

adynamia and restlessness, tremor, seizures, not motivated crying.

Hemodynamic disturbances rapidly develop: paleness, cyanosis, mottled skin,

tachypnea, tachycardia; endotoxic shock can develop. Intoxication continues from 3 till

7 days and sometimes longer.

Abdominal pain is intense, prolonged, appears from the first day of the disease and

later, is localized around umbilicus and in right iliac area, more seldom all over the

abdomen. The pain is permanent, increases with movement, sometimes it is so intense

that “acute abdomen” can be suspected. Patients can present with positive Blumberg’s

symptom. Real Yersinia appendicitis is also described. Abdominal pain in first year of

age children present with severe restlessness, crying, rapid movement of the legs, pain

reaction to abdominal palpation.

Localization of pathological process is determined by symptoms of gastroenteritis

and enteritis in children older than 1 year of age and gastroenterocolitis in first year of

age children.

Vomiting is a common sign in majority of patients. It appears on the first day of

the disease, can be repeated and multiple, often persistent. Vomiting in first year old

children is a sign of intoxication; in older children it is a symptom of gastritis,

sometimes pancreatitis.

Diarrhea in most patients is seen from the first day of the disease, but it can be

moderate (frequency is 2-5 times per day). The stool is abundant, foamy, with

unpleasant odor, of brownish-green color with undigested food. Later stool becomes

enterocolitic in character: foamy, with unpleasant odor, of brownish-green color,

sometimes cloudy mucus and short-term bloody admixture appears. Diarrhea continues

longer than 2 weeks, as a rule; in some cases it can persist for several months.

At palpation tenderness of large intestine (ascending part), rumbling, splash

sounds and flatulence are observed. Unlike dysentery, there is no distal colitis; unlike

salmonellosis, there are no long-term admixtures of mucus and blood in stool.

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Exanthema (macule-papule rash, more seldom petechial hemorrhages) is an

allergic rash with scalloped borders, annular, confluent. Localization of the rash is on

trunk and extremities, more seldom on face. Rash on palms and soles is typical; these

areas can be hyperemic and edematous. The rash appears on the 2-4th days of the

disease, increases during 1-2 days and disappears in 2-5 days. On the 2nd week scaled

desquamation of palms and soles is observed.

Besides described signs the patients can present with muscle and joint pain,

enlarged liver, more seldom spleen, sometimes jaundice.

At yersiniosis development of appendicitis (catarrhal, phlegmonous, gangrenous),

terminal ileitis, mesenterial lymphadenitis and pancreatitis is possible. Clinical picture

of “acute abdomen” is accompanied by vomiting and diarrhea. This form of yersiniosis

is diagnosed in children older than 5 years of age. In some cases local or total peritonitis

can develop, as well as interintestinal abscesses and peritoneal adhesions.

Yersinia hepatitis is accompanied by long-persistent fever, intoxication, pain in

right subcostal area. On the 3-5th day dark urine, hypocholic stool and jaundice appear.

Liver is hardened to palpation, enlarged. Direct fraction of bilirubin and enzyme activity

are increased but to a lesser degree than at viral hepatitis. In pre-jaundice period there

can be foamy feces with unpleasant odor, rash, scleritis, conjunctivitis. Signs of

hepatitis disappear in 10-14 days, but liver enlargement is present till one month and

longer.

Arthralgia and arthritis can also develop. They are more often seen in older

children. 1-3 weeks before development of arthritis children present with enteritis signs

and fever. Knee and elbow joints are involved, more seldom small joints of feet and

hands. Joint damage can develop both at acute phase and at recurrences. Arthritis is

accompanied by rash and abdominal syndrome. Described duration of arthritis can be

up to 2 – 3 years. Reiter syndrome can be observed at yersiniosis (arthritis, urethritis,

uveitis, iridocyclitis and conjunctivitis).

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Complications of yersiniosis can be the following: prolonged hyperthermia,

granulomatous hepatitis, osteomyelitis, liver abscesses, polymyositis, pneumonia,

urinary tract infection and kidney abscess.

Patients with yersiniosis can develop kidney involvement (proteinuria,

leukocytouria, microhematuria, isosthenuria, decreased diuresis). At septic forms acute

renal failure can develop.

Frequent complication is myocarditis. Endocarditis can develop very seldom. The

course of yersinia myocarditis is benign.

Nodular erythema at yersiniosis appears by the end of the first – second week of the

disease and is more often seen at recurrence. Simultaneously with high fever and

intoxication, on the anterior surface of legs and sometimes thighs and forearms blue-

purple hardened painful lesions appear, till 2-3 cm in diameter. New lesions later appear

and resolve with pigmentation. These lesions are often accompanied by arthritis and

myocardial damage. Such patients are often hospitalized into cardiologic departments.

The course of yersiniosis can be acute (1-4 weeks) and prolonged (1 month - 1

year). According to the course: cyclic (recovery after acute period), wave-like (new

exacerbations and foci develop during incomplete recovery) and recurrent. Relapses are

seen in 10-15% of children and develop 1-3 weeks after clinical recovery. Sometimes

several relapses can develop. During them allergic signs and arthritis prevail.

Complications. Imbalance of electrolyte metabolism, carditis, acute renal failure,

acute hepatic failure, intestinal perforation, peritonitis, bowel obstruction, megacolon,

mesenterial thrombosis and intestinal wall gangrene can develop.

Diagnosis. Clinical criteria:

- acute onset;

- prolonged fever till 1-2 weeks;

- rash is macular-papular, small pointed, situated in skin folds, on thorax and

around joints;

- rash can be hemorrhagic or nodular erythemal; it is preserved during 6-14 days;

- symptom of “hood”, “socks”, “gloves”;

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- liver enlargement;

- possible jaundice syndrome;

- extended abdominal pain, more often in lower part of abdomen;

- rumbling and tenderness in ileocecal area;

- diarrhea of enteritis or gastroenteritis type;

- “strawberry” tongue;

- arthralgia and arthritis;

- spleen enlargement.

Laboratory methods:

1) Complete blood count shows leukocytosis, neutrophilia, young forms,

accelerated ESR, eosinophilia.

2) Bacteriological method reveals bacteria in feces, urine, pus, oral mucus, lymph

nodes (if required).

3) Serological methods: agglutination reaction and indirect hemagglutination

reaction with live or inactivated culture of yersinia in dynamics. Diagnostic

titers in agglutination reaction are 1:40 - 1:160, in indirect hemagglutination

reaction are 1:200.

High agglutinin titer appears in children on the 2-4th weeks of the disease.

Immunoenzyme analysis reveals specific IgM in blood.

Treatment. Uncomplicated enteritis, ileitis and mesenteric lymphadenitis do not

require antibacterial therapy. Treatment should include adequate hydration and

supportive therapy in these cases. Majority of strains are highly susceptible to co-

trimoxazole, 3rd generation cephalosporins, aminoglycosides and doxycycline.

Prophylaxis of yersiniosis is the same as for bowel infections of other etiology. At

the same time prophylactic activities coincide with those at pseudotuberculosis.

Questions for self-control:

1. What does the term “Yersinia infection” include?2. Causative agents of pseudotuberculosis and intestinal yersiniosis.3. The source of infection at pseudotuberculosis and intestinal yersiniosis.4. Main transmission routes at pseudotuberculosis and intestinal yersiniosis.

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5. Main clinical signs of pseudotuberculosis.6. Leading clinical presentation of intestinal yersiniosis.7. Laboratory methods of yersiniosis diagnosis.8. Complications of pseudotuberculosis and intestinal yersiniosis.9. Etiotropic therapy of yersiniosis.10. Main methods of prophylaxis of pseudotuberculosis and intestinal yersiniosis.

Tests for self-control

1. Which antibiotics are not used at pseudotuberculosis?A. cephalosporins of III generation B. chloramphenicol C. aminoglycosides D. carbapenems E. penicillin2. Laboratory diagnosis of pseudotuberculosis includes:A. pharyngeal swab for flora B. immunofluorescence reaction C. immune-enzyme analysis D. reaction of complement fixation E. stool and urine culture 3. In peripheral blood at pseudotuberculosis the following changes are seen:A. neutrophilia with young forms, considerable acceleration of ESRB. leucopenia with lymphopenia C. lymphocytosis, eosinophilia, considerable acceleration of ESRD. lymphocytosis, monocytosis, presence of virocytes E. prominent eosinophilia 4. The causative agent of pseudotuberculosis is a bacteria of Enterobacteriaceae family, genus Yersinia:A. Y.pestisB. Y.enterocoliticaC. Y.fredericseniaD. Y.kristenseniaE. Y.pseudotuberculosis5. Typical forms of pseudotuberculosis are the following:A. exanthemal B. joint C. abdominal D. septic E. all the answers are correct 6. Which antibiotics are used for treatment of intestinal yersiniosis in children:A. tetracyclines B. cephalosporins of III generation C. penicillins D. quinolones E. carbapenems 7. Mean duration of incubational period at intestinal yersiniosis:A. 1-3 daysB. 21 daysC. 1 – 3 month

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D. 5 – 7 daysE. 3 – 6 months8. For joint involvement at intestinal yersiniosis it is typical:А. it is seen in older age children В. large joints are affected С. lumbosacral joint, toe joint are affected D. arthralgias prevail С. all the answers are correct 9. The source of infection at pseudotuberculosis is not:A. human B. pigs C. domestic birds D. wild pigsE. cattle10. Main reservoir of infection at pseudotuberculosis is the following:A. human B. pigs C. domestic birds D. mouse-like rodentsE. cattle

Test answers:

1-Е, 2-C, 3-А, 4-E, 5-E, 6-B, 7-D, 8-D, 9-А, 10-D.

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