Monday, February 25, 2013

Awareness Campaign On Yersina Pseudotuberculosis




Infection due to Y. pseudotuberculosis is most often seen as a pseudoappendicitis syndrome without diarrhea.

ETIOLOGY. Y. pseudotuberculosis is differentiated biochemically from Y. enterocolitica on the basis of ornithine decarboxylase activity, fermentation of sucrose, sorbitol, cellobiose, and other tests, although some overlap between species may be seen. Antisera to somatic O antigens and sensitivity to yersinial phages may also be used to differentiate the two species. Subspecies-specific DNA sequences have been isolated that allow direct probe- and primer-specific differentiation of Y. pestis, Y. pseudotuberculosis, and Y. enterocolitica.

EPIDEMIOLOGY. Less is known of the epidemiology of Y. pseudotuberculosis infections than for Y. enterocolitica or Y. pestis. The seasonal incidence in humans parallels that in wild and domestic animals. Transmission from cats and cat-contaminated substances is established. There is a low reported incidence in the 5–12-yr age range.

PATHOLOGY AND PATHOGENESIS. The pathology is similar to that described for Y. enterocolitica, with ileal and colonic mucosal ulceration and mesenteric adenitis. Necrotizing, epithelioid granulomas are seen in the mesenteric nodes. The appendix is frequently grossly and microscopically normal. Mesenteric nodes are frequently the only source of positive cultures. Y. pseudotuberculosis antigens bind directly to HLA class II molecules and function as superantigens, which may partly explain the clinical syndromes resembling Kawasaki syndrome caused by this organism.

CLINICAL MANIFESTATIONS. Children usually present with fever and abdominal pain that is diffuse or localized to the right lower quadrant. Frequently, there is tenderness over the McBurney point and strong clinical suspicion of appendicitis. At surgery, the terminal ileum is thickened and shiny with enlarged mesenteric nodes, which may appear necrotic. The appendix is normal or only mildy inflammed.

Presentations resembling scarlet fever or Kawasaki syndrome are reported.

DIAGNOSIS. Mesenteric adenitis should be suspected in children with unexplained fever and abdominal pain. A characteristic picture of enlarged mesenteric lymph nodes, thickening of the terminal ileum, and no image of the appendix may appear on ultrasound. Y. pseudotuberculosis is rarely isolated. It is almost never isolated from stools, and the best source is an involved mesenteric node. Culture conditions are the same as for Y. enterocolitica.

Serologic tests have been described, but commercially available tests or standardized antigens are not available.

DIFFERENTIAL DIAGNOSIS. Appendicitis is the most common diagnosis. Inflammatory bowel disease and nonspecific intra-abdominal infections are also considered.

PREVENTION. Specific preventive measures other than avoiding exposure to potentially infected animals and careful food-handling practices are not apparent. Vaccines for prevention of Y. pseudotuberculosis have not been developed.

TREATMENT. Uncomplicated mesenteric adenitis due to Y. pseudotuberculosis is a self-limited disease, and antimicrobial therapy is not required. Culture-confirmed bacteremia should be treated with an aminoglycoside in combination with another agent, as for infections due to Y. enterocolitica.

Short statement of the material
Pseudotuberculosis is an acute infectious disease that is characterized by the expressed polymorphism of clinical symptoms with predominance of toxic-allergic syndrome, rashes like in scarlet fever, the damage of gastro-intestinal tract, liver; quite often has relapsed motion.

Etiology: Yersinia pseudotuberculosis, gram-negative bacillus

Epidemiology:
• Source of infection-wild and home animals (rats, dogs, foxes, cats and other);
• Way of transmitting – alimentary;
• Susceptible organism – children (not infants), adults.

Pathogenesis:
1. Entering the bacilli to gastrointestinal tract. An entrance gate is a thin bowel (terminal department and appendix)
2. Enteral phase: invasion of bacteria in enterocytes, development of local inflammation, diarrhea, enterotoxin secretion.
3. Regional lymphadenitis (regional infection).
4. Generalization (bacteriemia, toxemia) in severe cases.
5. Parenhymatous phase: hematogenous distribution of bacteria with forming of the secondary focus (lungs, liver, spleen, bones).
6. Immunological response, recovering from disease.
7. May be secondary bacteriemia (exacerbations and relapses), because of possible persistency in lymph nodes.

Clinical criteria
Incubation period is 3-18 days. Beginning is acute with high temperature, intoxication.
• Polymorphism of complaints: malaise, fatigue, headache, sleepless, anorexia, arthralgias, muscle pain, sore throat, nausea, abdominal pain, dyspepsia.
• Rashes: maculopapulous (like in scarlet fever), may be erythematosus or even erythema nodosum may developed (photo 56a, 56b);
- The eruption is characterized by dusky red, tiny papules;
- The rashes are present on face, intensified periorbitally, on the neck (“glasses” symptom, “hood” symptom (photo 56));
- On the body the rashes are intensified in skin folds (photo 57), at the sites of pressure (red dermographysm), on the hands, feet, (“gloves”,”socks” symptom), round the joints;
- The exanthema usually lasts 4 to 5 days and then begins to desquamate, first on the face, other parts of the body (photo 58) and last on the palms and soles (photo 59, 60).
• Pharyngeal and tonsilar erythema without the exudates, erythema of the soft palate, conjunctivitis, corryza demonstrate catarrhal syndrome.
• “Strawberry” tongue also simulates the scarlet fever (photo 61).
• Abdominal syndrome; tenderness during the palpation of abdomen, may be acute appendicitis.
• Dyspepsia: nausea, vomiting, liquid feces.
• Hepatomegaly, rare – splenomegaly, lymphadenopathy.
• Arthritis of knees (photo 62), elbows, foot and hand small joints or arthralgia.
• Hepatitis with or without the jaundice.
• Toxic myocarditis.
• Toxic nephritis, pyelonephritis.
• Bronchitis or pneumonia may also develop.

IMG_56
”hood” symptom

IMG_57
Rashes are intensified in skin folds (Pastia lines)

socks” symptom

IMG_58
Skin desquamation

IMG_59
Desquamation on palms

IMG_60
Desquamation on palms

IMG_61
Strawberry tongue

IMG_62
Arthritis
 
Nodular erythema in case of relapsed course

Clinical forms classification

Type
Severity 
Course 
Typical forms
Like Scarlet fever
Abdominal
Arthralgic
Icteric (jaundice)
Combined
Generalized (septic)

Atypical  forms
Catarrhal
Effaced
Subclinical  

Mild
Moderate
Severe

Indexes of severity:
Meningoencephalitic  syndrome
Hemorrhagic syndrome
Considerable damage of liver
Abdominal syndrome
Damage of joints
Signs of process generalization

Smooth 

Uneven with exacerbations and relapses

Uneven with complications


Diagnosis example:
Pseudotuberculosis, typical combined (Scarlet fever like + arthralgic) form, moderate severity, uneven prolonged duration with exacerbation.

Features of pseudotuberculosis at the children of early age
• high and prolong fever;
• expressed hepatolienal syndrome;
• systemic increase of lymphnodes;
• dyspeptic syndrome;
• damage of respiratory tract, development of pneumonia (very often);
• rarely: scarlatina rashes, damage of joints;
• prolong, undulating duration with exacerbation and relapses;
• frequent complications.

Laboratory findings
·        Complete blood analyses: leucocytosis, neutrophilia with left shift, eosynophilia, ERS is enlarged.
·        Bacteriological: Yersinia Pseudotuberculosis may be found in feces, urine, blood and mucus.
·        Serologically: increasing of special antibodies 4 times and more in paired sera (AR, IHAR with diagnostic titles 1:200 and more).
·        Immune-enzyme analysis (ELISA test): Specific antibodies Ig M are positive in an acute phase of the disease.

Differential diagnosis should be performed among scarlet fever, measles, viral hepatitis, typhoid fever, paratyphoid fever, sepsis, enterovirus infection, bacterial diarrhea.

Sign
Pseudotuberculosis
Scarlet fever
Infectious mononucleosis
Typhoid fever
Enterovirus infection
Viral hepatitis
Beginning
Acute
Acute
Acute
Acute
Acute
Acute,
subacute
Initial signs
Toxic,  dyspeptic and different other
signs
Sore throat, toxic
Lymphoproliferative, toxic
Toxic
Catarrhal, toxic
Catarrhal,dyspeptic, arthralgicasthenic
Rashes
Pin-point, maculous-papulous, erythema
Pin-point, sand paper
maculous-papulous, erythema
Single reseals
Small maculous
Rare
(in case of B hepatitis)
Catarrhal sign
Typical
Absent
Absent
Rare
Typical
In the initial period
Changes in the throat
Hyperemia of the back pharyngeal wall
Tonsillitis
Tonsillitis Hyperemia of the back pharyngeal wall, posterior rhinitis
Hyperemia of the palatal arch, back pharyngeal wall
Herpangina
Absent
Joints’ damage
Arthritis, arthralgias
Not typical
Absent
Absent
Absent
Arthralgias in the initial period
Abdominal pain
Around the navel
Absent
Absent
In the right inguinal region
Around the navel
In the right hypochondria
Dyspeptic syndrome
Typical

Rare
Absent
Constipation, rare - diarrhea
Typical
More intensive in prodromal period

Hepatitis
Л
May be
Absent
May be
Absent
Absent
Typical

Lymphoproliferative
May be
Regional lymphadenitis
Typical
Hepato- and splenomegaly
Absent
Hepato-, rare - splenomegaly
Tongue
Coated, strawberry from the 4th-5th day
Coated, strawberry from the 4th-5th day
Coated
Coated with grey,
teeth excavation on its’ borders
Coated
Coated
Damage of the nervous system
May be
Not typical
Not typical
Delirium, sopor
May be serous meningitis,
encephalitis
(rare)
Hepatic encephalopathy in severe case

Treatment
Children with mild form of pseudotuberculosis may be treated at home symptomatically without the etiological medicine.
Hospitalization is obvious for:
• Children with moderate form of pseudotuberculosis;
• Children with severe form of pseudotuberculosis.
Regimen
• half-bed regimen in mild cases;
• bed regimen in moderate cases;
• straight bed regimen in severe cases.
Diet:
• Icteric (jaundice) form – N 5;
• Abdominal (intestinal) form – N 4;
• Other forms – N 15.

Etiological:
• Chloramphenicol (orally) 10-15 mg/kg 3 or 4 times per day during all period of pyrexia
and plus 3 days (average duration is 14 days).
• Alternative antibiotics (Reserve): cefalosporins of the 3rd or 4th generation (IM, IV),
• In severe cases combination together with aminoglycosides of the 3rd generation (IM, IV).
Pathogenetical:
• Disintoxication: oral with large amount of alkaline fluids (in mild cases), or parenteral with glucose-saline solutions (in moderate, severe cases);
• Glucocorticoids 1-3 mg/kg (in equivalent to prednisolone) as a short course 3-5 days (in severe cases), for 2-4 wks in case of myocarditis;
• Control of fever and myalgia (when the temperature is more than 38.5-39 °C); in children before 2 mo and in case of perinatal CNS damage, seizures in the history, severe heart diseases – when the temperature is up to 38 °C with acetaminophen (paracetamol 10-15 mg/kg not often than every 4 hours (not more than 5 times per day) or ibuprophen 10 mg/kg per dose, not often than every 6 hours;
• Antihistamines (in average doses) – pipolphen, suprastin, claritin, cetirizin;
• NSAIDs in case of arthritis, carditis, nodular erythema (ibuprophen, aspirin, voltaren,
indomethacin in average doses).

Prophylaxis:
1.     Deratization, disinfection.
2.     Right keeping of products.
3.     Looking after people from the epidemic focus for 18 days with bacteriological investigation.

No comments:

Post a Comment