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EVIDENCE-BASED MEDICINE: CASE SCENARIOS
Year : 2017  |  Volume : 15  |  Issue : 2  |  Page : 114-120

Common infections in children


Pediatric Infectious Diseases, Department of Paediatrics, Christian Medical College, Vellore, Tamil Nadu, India

Date of Web Publication18-May-2017

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cmi.cmi_33_17

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How to cite this article:
Chacko A. Common infections in children. Curr Med Issues 2017;15:114-20

How to cite this URL:
Chacko A. Common infections in children. Curr Med Issues [serial online] 2017 [cited 2020 Jul 3];15:114-20. Available from: http://www.cmijournal.org/text.asp?2017/15/2/114/206523




  Introduction Top


Infections are common presentations of children in the outpatient settings of most general practitioners and pediatricians. A good history of the illness and clinical examination, with the support of laboratory investigations, can guide the physician to a diagnosis without much trouble in most cases. Having a list of differential diagnoses for each case helps in choosing the right investigations. A few case scenarios of infections in children are discussed.

Case 1: Fever with nonspecific symptoms

A 12-year-old boy was admitted with daily intermittent fever, progressively increasing for 12 days. He had a frontal headache along with the onset of the fever for 1 week, epigastric pain for 5 days, loose stools, and vomiting for 1 day. He had been treated by his family physician with injection cefoperazone-sulbactam for 3 days as outpatient.

On examination, he was febrile (103°F) and looked ill, but not in shock. There was tachycardia (150/MT); his systemic examination was otherwise normal. There was no eschar or skin rash.

Questions

  1. What are the possible differential diagnoses?
  2. What investigations will help in making a diagnosis?


Case 2: Fever with chills, headache, and vomiting

A 6-year-old girl presented with fever with chills, headache, and vomiting for 4 days, multiple generalized tonic-clonic seizures at presentation, and one episode of epistaxis. On examination, she was drowsy with heart rate 120 beats/min, blood pressure 116/70 mmHg, temperature 99.1°F, Glasgow coma scale score 12/15 (postictal), pupils equal and reacting. She was pale with no neck stiffness and Kernig's sign was negative.

Questions

  1. What are the possible differential diagnoses?
  2. What investigations will help in making a diagnosis?


Case 3: White patch on throat

A 9-year-old boy presented with high-grade fever, throat pain, cough, and cold for 4 days and vomiting, headache, and noisy breathing for 1 day. He was incompletely immunized – last vaccination was given at 1½ years and he missed his 5-year booster. On examination, he was febrile and toxic. Throat examination revealed bilateral enlarged tonsils with a grayish white membrane over the tonsils. There were multiple enlarged cervical lymph nodes.

Questions

  • What are the possible differential diagnoses for a white patch on the throat?
  • What is the treatment of this condition?



  •   Answers Top


    Case 1 – Typhoid Fever

    1. Differential diagnosis for a child with fever with no specific signs and symptoms


    • Enteric fever
    • Rickettsial fever
    • Malaria
    • Pneumonia
    • Urinary tract infection
    • Tuberculosis (should have fever for 2 weeks, to consider the possibility of tuberculosis)
    • Noninfectious causes – Possible malignancy, rheumatological disorder.
    • The investigations performed in this individual are shown in [Table 1].
    Table 1: Investigations

    Click here to view



      Discussion Top


    Typhoid fever

    The diagnosis of this child was typhoid fever.

    Enteric fever is caused by Salmonella enterica serotype Typhi (formerly S. typhi), which causes typhoid fever, and Salmonella serotypes S. paratyphi A, Salmonella schottmuelleri (S. paratyphi B), and Salmonella hirschfeldii (S. paratyphi C) which cause paratyphoid fever. Enteric fever is associated with overcrowding, poor sanitation, and poverty. Humans are the only reservoir for S. enterica serotype Typhi.[1] Children between the ages of 2 and 4 years are most susceptible to the illness.

    The incubation period for Salmonella typhi is 4–14 days. The infective dose of enteric organisms is 10[5]–10[9]. The higher the infective dose, the shorter is the incubation period.[2]

    After ingestion of the bacteria, the organisms penetrate the terminal ileum through M-cells which lie on the top of the Peyer's patches and through the enterocytes. The organisms proliferate in the submucosa, go to the Peyer's patches, and are carried into the lymphatics and finally into the bloodstream (primary bacteremia). The organisms then get seeded in tissue macrophages in the liver, gall bladder, spleen, and bone marrow. These sites act as sanctuary sites and sources for relapsing infection and complications such as osteomyelitis and abscesses. This period is the incubation period, which lasts around 15 days. A secondary bacteremia occurs with the start of clinical symptoms.[3]

    Chronic Salmonella carriage is excretion of Salmonella in stool or urine >1 year after acute infection.[1] This is seen more frequently in women and patients with cholelithiasis or other biliary tract abnormalities [Box 1].



    The common clinical features associated with typhoid in children in decreasing order are as follows - high-grade fever 95%, coated tongue 76%, anorexia 70%, vomiting 39%, hepatomegaly 37%, diarrhea 36%, toxicity 29%, abdominal pain 21%, pallor 20%, and splenomegaly 17%.[3] Intestinal hemorrhage and perforation occur in the 3rd week of illness.[4]

    High-grade fever and a coated tongue are the most common clinical manifestations. Relative bradycardia may be seen along with the fever (relative bradycardia is a clinical sign where the pulse rate is less than that expected for a given temperature. This is a poorly defined term and the underlying mechanisms are unknown. Some authors define it as for every degree rise in Fahrenheit, the heart rate increases by 10 beats/min) splenomegaly, though considered a classical feature of typhoid fever is not as prevalent.

    Intestinal hemorrhage and perforation tend to occur in the 3rd week of illness.[4] Dietary advice to ensure that the patient takes in adequate nutrition is therefore important in the management of typhoid, in addition to antibiotics.

    Natural history of the disease

    Typhoid is a prolonged illness with a duration of approximately 4 weeks. Without treatment, there is a high case fatality rate of >10%. With treatment, the case fatality rate is <1%, with 2%–4% relapse and <2% going on to become chronic carriers (in the pediatric population).

    Investigations

    The investigations that are useful in the diagnosis of typhoid fever in chronological order are given in [Table 2]. Knowing this helps the clinician to send the appropriate test at the right time.
    Table 2: Diagnostic investigations in typhoid fever at different stages of the illness

    Click here to view


    Serological tests

    The Widal test detects antibodies against antigens O-somatic and H-flagellar in the blood. Although this is widely available and is relatively inexpensive, it has poor sensitivity and specificity, with a false-negative result in up to 30% of cases (as in the case discussed). Widal is usually done in the 2nd week of a febrile illness.

    The dot-enzyme immunoassay – typhidot – is a serologic test that detects the presence of IgM and IgG antibodies to a 50 kDa outer membrane protein antigen on S. typhi. These typhoid rapid antibody tests are simple and rapid with a reported sensitivity of 79%–92.3%* and a specificity of 79%–89% in the 2nd week of febrile illness.[5],[6] However, they appear to correlate poorly with blood culture results in various studies.

    Management

    Nalidixic acid-resistant S. typhi serves as a marker for reduced susceptibility to fluoroquinolones. Multidrug-resistant typhoid fever refers to resistance simultaneously to first-line drugs – chloramphenicol, cotrimoxazole, and ampicillin.[7]

    Sensitivity patterns in South India showed that >90% of isolates are sensitive to the first-line drugs. Fluoroquinolone resistance is prevalent in Asia [8] and these drugs (ciprofloxacin, nalidixic acid) should not be used as first-line drugs for the treatment of typhoid in children.

    Treatment regimens

    The Indian Academy of Pediatrics (IAP) guidelines [7] recommend a third-generation cephalosporin such as cefixime for 14 days as the first-line drug for uncomplicated enteric fever. Ensure that there are 5 afebrile days at the end of the course, if not give the antibiotics for a few more days. Azithromycin can be added as a second-line drug. Ceftriaxone or cefotaxime are recommended for severe enteric fever [Table 3] and [Table 4].
    Table 3: Treatment of uncomplicated enteric fever-Indian Academy of Pediatrics guidelines7

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    Table 4: Treatment of severe enteric fever-Indian Academy of Pediatrics guidelines7

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    For patients with suspected or known typhoid fever with delirium, obtundation, stupor, coma, or shock-adjunctive dexamethasone (3 mg/kg followed by 1 mg/kg every 6 h for a total of 48 h) under controlled setting and strict supervision should be given.[9]

    Chronic carriage is usually associated with cholelithiasis, increasing age and is more common in females. It is uncommon in children. Chronic carrier state may be eliminated using antibiotics which are concentrated in bile-ciprofloxacin and norfloxacin for 4 weeks. Cholecystectomy may be indicated if antimicrobial therapy fails.[9]

    Treatment of typhoid fever - Key points

    • The Indian Academy of Pediatrics guidelines state that a third-generation cephalosporin is to be used as first line treatment for typhoid
    • More than 90% of isolates are sensitive to the first-line drugs. Fluoroquinolone resistance is prevalent in Asia and these drugs (ciprofloxacin, nalidixic acid) should not be used as first-line drugs for treatment of typhoid in children
    • Typhoid fever with delirium, obtundation, stupor, coma, or shock-adjunctive dexamethasone (3 mg/kg followed by 1 mg/kg every 6 h for a total of 48 h)
    • Adequate nutritional intake is as important as antibiotics in the treatment of typhoid fever.


    Typhoid vaccines

    Indian Academy of Pediatrics (IAP) primary schedule

    There are two typhoid conjugate vaccines (Typbar-TCV and PedaTyph), available and licensed in the country (efficacy >90%). According to the IAP schedule [10], the first dose is given at 9–23 months followed by a booster at 2 years of age. The other vaccine available in India for children is the Vi polysaccharide vaccines: single dose at 2 years with revaccination every 3 years (efficacy 70%–80%).

    Case 2 – Malaria

    1. The investigations and the results are given in [Table 5].
    2. Differential diagnoses considered in this child, considering the history of fever, headache, and seizures, are as follows
    Table 5: Laboratory investigations and results

    Click here to view


    1. Encephalitis - dengue, rickettsial, other viral etiology
    2. Cerebral malaria
    3. s



      Discussion Top


    Severe mixed malarial infection with glucose-6-phosphate dehydrogenase deficiency

    The diagnosis in this case was severe mixed malarial infection with glucose-6-phosphate dehydrogenase (G6PD) deficiency.

    Tests for diagnosis of malaria

    Blood smear for malarial parasites

    This is the confirmatory test for malaria; however, this requires training and smears may be negative if the parasite load is low. Three positive smears are necessary for the diagnosis of malaria.

    Rapid diagnostic tests

    These rapid tests are based on the detection of antigens such as histidine-rich protein II (HRP-II) and Plasmodium lactate dehydrogenase (PLDH) released from the parasitized erythrocytes.

    HRP-II is a protein produced by asexual stages and young gametocyte of Plasmodium falciparum. This can remain positive for up to 3 weeks after treatment even when malaria parasite (MP) smears are negative. PLDH is a marker protein for the intraerythrocytic form of the MP. The test becomes negative within 3–5 days of treatment. These tests are effective and rapid, but the diagnosis needs to be confirmed by a blood smear examination for parasites.

    What is “severe malaria?”

    Cerebral malaria, severe normocytic anemia (Hb <5 g/dL), renal failure (creatinine >3 mg/dl), pulmonary edema, hypoglycemia, circulatory collapse/shock, spontaneous bleeding/disseminated intravascular coagulation, repeated generalized convulsions, acidosis, and macroscopic hemoglobinuria all constitute severe malaria.[11] Other manifestations are impaired consciousness but rousable, prostration, extreme weakness (inability to stand or sit), hyperparasitemia (>5% red blood cell infected), jaundice (bilirubin >3 mg/dL), and hyperpyrexia (axillary temperature >39.5°C).

    Management of malaria in children

    The regimens for the treatment of malaria based on the National Drug Policy on Malaria 2013 and the guidelines for diagnosis and treatment of malaria in India 2014 are given in [Table 6],[Table 7],[Table 8].[12],[13],[14]
    Table 6: Treatment regimen for Plasmodium vivax infection

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    ,
    Table 7: Treatment regimen for uncomplicated plasmodium falciparum infection and mixed malarial infection

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    ,
    Table 8: Management of severe malaria

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    Antimalarial treatment in glucose-6-phosphate dehydrogenase deficiency

    • The WHO guidelines 2015[15] for P. falciparum states that clinically significant hemolysis is not expected to occur in either G6PD-normal or -deficient individuals given a single 15-mg adult dose (0.25 mg base/kg) of primaquine. There is no need for systematic testing for G6PD deficiency before administering a single dose of 0.25 mg/kg primaquine base
    • A single 0.25 mg base/kg primaquine dose should be given to all patients with parasitologically confirmed P. falciparum malaria on the 1st day of treatment in addition to an artemisinin-based combination therapy (ACT), except for pregnant women and infants <6 months of age.[16]


    Prevention of relapse (Plasmodium vivax and Plasmodium ovale) in malaria

    • Adults and children (except pregnant women, infants <6 months of age, lactating women who are breastfeeding infants) – 14 days course (0.25–0.5 mg/kg daily) of primaquine
    • Preventing relapse in G6PD deficiency: In addition, the WHO guidelines [16] for treatment of relapse states that for people with G6PD deficiency to prevent relapse, a once weekly dose of primaquine 0.75 mg/kg for 8 weeks may be given with close medical supervision to prevent hemolysis (conditional recommendation, very low-quality evidence)
    • Preventing relapse in pregnant women: The other option mentioned for pregnant and breastfeeding mothers is once weekly prophylaxis with chloroquine until delivery is completed (conditional recommendation, moderate quality evidence),[16] hence chloroquine is another option we can consider even in G6PD deficient children if primaquine is not an option.


    Case 3 – White Patch in Throat

    Differential diagnoses for white patch on the throat



    What did we do for our child?

    The child in the case scenario discussed had a mixed malarial infection. He was treated with ACT, doxycycline, and weekly primaquine 0.6 mg/kg once weekly as per IAP for 6 weeks with close monitoring. There was no hemolysis.

    Investigations showed total white cell count of 21,000/ccmm with immature forms (metamyelocytes and bandforms) and 20% lymphocytes. Throat swab showed Gram-positive bacilli which on culture and polymerase chain reaction showed Corynebacterium diphtheriae (sensitive to penicillin and erythromycin).


      Discussion Top


    Diphtheria

    Diphtheria can manifest as:

    • Respiratory diphtheria - anterior nasal, pharyngeal, tonsillar, and laryngeal diphtheria
    • Cutaneous diphtheria
    • Life-threatening complications: Respiratory tract obstruction, toxic cardiomyopathy (usually in 2nd–3rd weeks), and toxic cranial neuropathy (5th week) in the form of ocular and palatal palsies and symmetric polyneuropathy (2nd–12th weeks).


    Treatment of Diphtheria

    Diphtheria antitoxin

    Diphtheria antitoxin (DAT) should be administered without delay (even before culture reports are available) to:

    1. All cases of respiratory diphtheria with laboratory-confirmed toxigenic C. diphtheriae
    2. Probable cases - In a patient in whom diphtheria is suspected and who:


    • Is toxic in appearance and is without another clearly established diagnosis
    • And/or has rapidly worsening illness
    • And/or has history of recent contact with dairy animals
    • And/or has history of recent travel to a country where diphtheria is endemic or epidemic
    • And/or was never vaccinated or is not up to date with diphtheria toxoid vaccination.


    The dose of DAT to be administered depends on the type of diphtheria that is suspected and is shown in [Table 9].[17]
    Table 9: Dose ranges for diphtheria antitoxin

    Click here to view


    Antimicrobial therapy

    Erythromycin orally for 14 days (or) injection penicillin G for 14 days (or) injection procaine penicillin for 14 days.

    Isolation

    Standard and droplet precautions for pharyngeal diphtheria until two cultures from both nose and throat collected 24 h after completing antimicrobial treatment are negative for C. diphtheriae.

    Management of contacts

    Individuals who come into contact with an individual with diphtheria are recommended to take antimicrobial prophylaxis with erythromycin.

    Vaccination is recommended for asymptomatic contacts with a booster vaccine (DTaP, DT, Tdap, or Td) if not vaccinated within 5 years and complete immunization (for those who have not completed the immunization schedule).[17]

    Financial support and sponsorship

    Nil.

    Conflicts of interest

    There are no conflicts of interest.



     
      References Top

    1.
    Pegues DA, Miller SI. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 8th ed., Ch. 225. Elsevier Inc. Philadelphia: USA; 2015. p. 2559-68.  Back to cited text no. 1
        
    2.
    Glynn JR, Hornick RB, Levine MM, Bradley DJ. Infecting dose and severity of typhoid: Analysis of volunteer data and examination of the influence of the definition of illness used. Epidemiol Infect 1995;115:23-30.  Back to cited text no. 2
    [PUBMED]    
    3.
    Reller ME. Salmonella species. In: Long SS, Pickering LK, Prober CG, editors. Principles and Practice of Pediatric Infectious Diseases. 4th ed., Ch. 146. Edinburgh; New York: Elsevier Churchill Livingstone; 2012. p. 814-9.  Back to cited text no. 3
        
    4.
    Bitar R, Tarpley J. Intestinal perforation in typhoid fever: A historical and state-of-the-art review. Rev Infect Dis 1985;7:257-71.  Back to cited text no. 4
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    5.
    Olsen SJ, Pruckler J, Bibb W, Nguyen TM, Tran MT, Nguyen TM, et al. Evaluation of rapid diagnostic tests for typhoid fever. J Clin Microbiol 2004;42:1885-9.  Back to cited text no. 5
    [PUBMED]    
    6.
    Jesudason MV, Sivakumar S. Prospective evaluation of a rapid diagnostic test Typhidot for typhoid fever. Indian J Med Res 2006;123:513-6.  Back to cited text no. 6
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    7.
    Kundu R, Ganguly N, Ghosh TK, Yewale VN, Shah RC, Shah NK; IAP Task Force. IAP Task Force Report: Management of enteric fever in children. Indian Pediatr 2006;43:884-7.  Back to cited text no. 7
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    8.
    Medalla F, Sjölund-Karlsson M, Shin S, Harvey E, Joyce K, Theobald L, et al. Ciprofloxacin-resistant Salmonella enterica serotype Typhi, United States, 1999-2008. Emerg Infect Dis 2011;17:1095-8.  Back to cited text no. 8
        
    9.
    American Academy of Pediatrics. Red Book: 2015 Report of the Committee on Infectious Diseases. 30th ed. Elk Grove Village, IL, USA: American Academy of Pediatrics; 2015. p. 695-702.  Back to cited text no. 9
        
    10.
    Vashistha VM, Choudhary J, Jog P, Yadav S, Unni JC. Indian Academy of Pediatrics (IAP) recommended immunization schedule for children aged 0 through 18 years – India, 2016 and updates on immunization. Indian Pediatr 2016; [E-pub ahead of print].  Back to cited text no. 10
        
    11.
    Kundu R, Ganguly N, Ghosh TK, Choudhury P, Shah RC. Diagnosis and management of malaria in children: Recommendations and IAP plan of action. Indian Pediatr 2005;42:1101-14.  Back to cited text no. 11
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    12.
    National Drug Policy on Malaria; Directorate of National Vector Borne Disease Control Programme. Directorate General of Health Services. New Delhi. 2013. Available at http://nvbdcp.gov.in/Doc/National-Drug-Policy-2013.pdf. [Last accessed on 2017 Mar 15].  Back to cited text no. 12
        
    13.
    Guidelines for Diagnosis and Treatment of Malaria in India; National Institute of Malaria Research. National Vector Borne Disease Control Programme. New Delhi. 2014. Available at http://nvbdcp.gov.in/Doc/Guidelines-Malaria-Diagnostic-Treatment-2014.pdf. [Last accessed on 2017 Mar 15].  Back to cited text no. 13
        
    14.
    Infectious Diseases Chapter, Indian Academy of Pediatrics, Kundu R, Ganguly N, Ghosh TK. Management of malaria in children: Update 2008. Indian Pediatr 2008;45:731-5.  Back to cited text no. 14
        
    15.
    Policy Brief on Single-dose Primaquine as a Gametocytocide in Plasmodium falciparum Malaria January, 2015 by WHO. Available from: http://www.who.int/malaria/publications/atoz/policy-brief-single-dose-primaquine-pf/en/. [Last accessed on 2017 Mar 15].  Back to cited text no. 15
        
    16.
    World Health Organization. Guidelines for the Treatment of Malaria. 3rd ed. Geneva: World Health Organization; 2015. p. 9, 11, 43. Available from: http://www.apps.who.int/iris/bitstream/10665/162441/1/9789241549127_eng.pdf. [Last accessed on 2017 Mar 15].  Back to cited text no. 16
        
    17.
    American Academy of Pediatric Committee on Infectious Diseases. Red Book: 2015 Report of the Committee on Infectious Diseases. 30th ed.: Elk Grove Village, IL, USA. American Academy of Pediatric Committee on Infectious Diseases; 2015. p. 325-9.  Back to cited text no. 17
        



     
     
        Tables

      [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9]



     

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