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COURSE OF DYSENTERY WITH PATHOGENIC FUNGI AND TREATMENT
APPROACHES IN CHILDREN
Bobojonova Nilufar Ismoilovna
Fergana Medical Institute of Public Health
Department of Microbiology, Virology, and Immunology
Abstract:
The dynamics of the pathogen’s biological properties, infection conditions, and the
biological state of the host organism determine the constant evolution of clinical manifestations
and outcomes of infectious diseases (Pokrovsky V.I. et al., 2003). The previously held view of
dysentery as a disease with a mild course and decreasing lethality, prevalent by the mid-1980s,
was revised due to a sharp worsening during the epidemic spread of Shigella flexneri 2a in the
1990s (Solodovnikov Yu.P., 1992; Kartsev A.D., 1992; Pokrovsky V.I., Yushchuk N.D., 1994;
Belyaeva T.V., 1995, 2003; Kondrasheva L.N. et al., 2003). Literature analysis indicates that
Shigella dysentery caused by Flexner bacilli in recent years has been marked by an increased
proportion of severe cases and unfavorable outcomes (Brodov L.E. et al., 1996; Rakhmanova
A.G. et al., 1996).
Keywords:
Shigellosis in children, Flexner dysentery, Candida infection, intestinal microbiota,
dysbiosis, antibiotic-associated diarrhea (AAD), pathogenic fungi, antimicrobial resistance,
coprological analysis, immunological response
Dysentery (shigellosis) is an acute intestinal infection caused by bacteria of the genus Shigella,
transmitted via the fecal-oral route. It manifests as anatomical and functional damage to the large
intestine and systemic intoxication, sometimes with primary neurotoxic syndrome. According to
estimates, around 140 million shigellosis cases occur globally each year. Susceptibility to the
infection varies by age group, with children under 2–3 years being most vulnerable. One factor
determining the severity, duration, outcome, and pathogen clearance is the state of the intestinal
microbiocenosis (Nisevich N.I.; Mazankova L.N.). The intestinal flora forms during the early
days of life and includes anaerobes (bifidobacteria, lactobacilli, bacteroides), aerobes (E. coli –
indigenous flora), facultative flora (staphylococci, fungi), and transient (allochthonous) flora
(Klebsiella, Clostridia, etc.) (Bondarenko V.M.; Parfenov A.I.). This flora comprises 1–4% of
the intestinal microbial biomass (N.I. Nisevich; V.F. Uchaikin; D.J. Hentges; G.W. Elmer; F.
Bäckhed).
The structure, prevalence, and dynamics of dysentery among children in Uzbekistan in recent
years show the persistent circulation of dysentery and outline its modern clinical features.
Pathogen sensitivity patterns reveal that Shigella flexneri 2a and Shigella sonnei are highly
susceptible to 3rd and 4th generation cephalosporins, ciprofloxacin, and amikacin, but resistant
to kanamycin, gentamicin, tetracycline, chloramphenicol, and ampicillin.
Comprehensive clinical-immunological studies of invasive intestinal infections in children
revealed early predictors of disease severity and outcomes. Laboratory diagnosis prioritizes
bacteriological analysis. Fecal sampling is advised before initiating antibiotics, ideally bedside,
with delivery to the lab within 2 hours. Results may be negative by day 3–5 or positive by day 5–
7 post-sampling.
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Modern treatment standards have encouraged widespread use of antibacterial agents, which
raises the problem of antibiotic-associated diarrhea (AAD). AAD is defined as three or more
episodes of loose stool over two or more days during or after antibiotic therapy (1). Most
antibiotic classes reduce beneficial gut flora and increase pathogenic flora. Dysbiosis may persist
and become pathogenic (Seredina E.Yu., 2002; Rozhanets A.N., 2002; Dmitrachkov V.V., 2000;
Gorelov A.V., 2005). Candida, Klebsiella, Enterobacter, and resistant strains often increase after
antibiotics (Kharchenko G.A., 1997).
Objective:
To optimize comprehensive therapy for shigellosis in children based on modern
clinical characteristics, regional pathogen profiles, and immune response patterns.
Research Objectives:
1.
To study the clinical features and structure of invasive dysentery over the past decade in
children of different ages in Uzbekistan.
2.
To analyze regional Shigella strains in dysentery cases complicated by fungal infection,
with attention to antibiotic resistance.
3.
To evaluate cellular and humoral immunity parameters by age, severity, and clinical
outcome.
4.
To investigate coprological and bacteriological parameters in children with fungal-
associated dysentery.
5.
To analyze the clinical course of Candida co-infection in Shigella flexneri 2a dysentery.
Materials and Methods:
40 children aged 1–14 were studied: 20 with acute dysentery hospitalized in Infectious Disease
Hospital No. 4, Fergana, and 20 with Candida-associated dysentery (control). Diagnosis was
confirmed by bacteriological culture (mostly Shigella flexneri). Based on disease severity, they
were divided into two groups: 10 with Flexner dysentery, and 10 with fungal dysentery. Acute
dysentery showed signs of intoxication and colitis in 80.7%, with hemorrhagic colitis in 70.2%.
Patients received traditional treatment including etiological, pathogenetic, and symptomatic
therapies.
Results and Discussion:
Monooxygenase system activity correlated with disease severity (see Table 1). Amidopyrine
demethylation decreased significantly in patients, indicating impaired detoxification. Post-
treatment, recovery of biotransformation was noted only in mild cases, with acetylation levels
still below normal. The monooxygenase system showed no full restoration even after treatment.
This indicates an ongoing deficit in xenobiotic biotransformation, limiting chemical homeostasis
in recovering children.
Conclusions:
1.
Dysentery with Candida in children suppresses intestinal flora function, especially
evident in dysbiosis severity correlating with disease severity.
2.
Standard therapy improves gut microbiota, yet flora remains below normal during
recovery. Restoration lags behind Candida reduction, disrupting microbial balance.
3.
Targeted pathogenetically justified therapy is needed to reduce toxic load during fungal
and bacterial dysentery.
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Gastrointestinal involvement in shigellosis was marked by severe colitis (abdominal pain,
tenesmus,
spastic
sigmoid
colon,
loose
stools
with
mucus
and
blood).
Treatment includes bed rest, rehydration, dietary management, pathogenetic therapy (sorbents,
probiotics, prebiotics, enzymes), etiotropic therapy (antimicrobials, oral immunoglobulins), and
symptomatic agents (antipyretics, spasmolytics, hemostatics).
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