|Year : 2014 | Volume
| Issue : 2 | Page : 232-235
Case of severe Friedlander's pneumonia with review of the literature
Prasanna K Satpathy1, Pradnya M Diggikar1, Rabindra Nath Misra2, Mukund Sudhakar Wasekar1
1 Department of Medicine, Padmashree Dr. D. Y. Patil Medical College, Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth, Pune, Maharashtra, India
2 Department of Microbiology, Padmashree Dr. D. Y. Patil Medical College, Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth, Pune, Maharashtra, India
|Date of Web Publication||4-Feb-2014|
Mukund Sudhakar Wasekar
Department of Medicine, Padmashree Dr. D. Y. Patil Medical College, Hospital & Research Centre, Dr. D. Y. Patil Vidyapeeth (Deemed University), Pimpri, Pune - 411 018, Maharashtra
Source of Support: None, Conflict of Interest: None
Friedlander's bacillus (Klebsiella pneumoniae) is among the most common Gram-negative bacteria encountered by physicians world-wide. Here, we report 31 years immunocompetent male who presented with fever, productive cough, hemoptysis, breathlessness and multi-organ failure with radiological evidence of total right upper lobe consolidation. Sputum microscopy, culture and blood culture - all confirmed Friedlander's bacillus as the etiology of this severe community acquired pneumonia with fatal outcome.
Keywords: Community acquired pneumonia, Friedlander′s pneumonia, Klebsiella pneumonia
|How to cite this article:|
Satpathy PK, Diggikar PM, Misra RN, Wasekar MS. Case of severe Friedlander's pneumonia with review of the literature. Med J DY Patil Univ 2014;7:232-5
|How to cite this URL:|
Satpathy PK, Diggikar PM, Misra RN, Wasekar MS. Case of severe Friedlander's pneumonia with review of the literature. Med J DY Patil Univ [serial online] 2014 [cited 2019 Sep 20];7:232-5. Available from: http://www.mjdrdypu.org/text.asp?2014/7/2/232/126365
| Introduction|| |
Friedlander's pneumonia (FP) is a severe form of community acquired pneumonia (CAP) caused by Friedlander's bacillus (Klebsiella pneumonia [KP]), with a predilection for upper lobes of the lungs and liable to suppurate and form abscesses.  KP is a Gram-negative, non-motile, encapsulated, facultative anaerobic, rod shaped bacillus often involves in severe CAP and nosocomial infections. It has been proved to be an independent risk factor for mortality in CAP.  Its distribution as a CAP pathogen is uneven across the world with a highest incidence in developing countries and in Asia.  This geographical variation in incidence is attributed to virulence of strains, host defenses and self-antibiotic medication.  KP is naturally resistant aminopenicillins an antibiotic that is commonly used as the first line therapy in CAP in many developing countries. This raises serious concerns since a recent multicenter prospective study conducted in several Asian countries showed KP accounted for 15.4% of the pathogens responsible for CAP, next to Streptococcus pneumonia.  Emerging resistances among Gram-negative bacilli due to production of extended-spectrum beta-lactamases (ESBL) are increasingly recognized as a major public health issue in both developed and developing countries. 
| Case Report|| |
This 30-year-old male patient who apparently in good health 4 days prior to the illness when he developed high grade fever with chills. Soon this was followed by productive cough with a moderate amount of rusty color sputum. This was associated with mild breathlessness without chest pain or wheeze. He has mild diffuse colicky abdominal pain associated with 3-4 episodes of small volume watery stool without blood and mucous. Furthermore, he had daily 3-4 vomiting, small quantity containing food particles, with small streaks of blood on few occasions. There was no history of recent travel, he did not consume alcohol, illicit drugs nor have a high risk sexual behavior. He occasionally smoked cigarettes. He did not suffer from tuberculosis, diabetes mellitus, bronchial asthma and hypertension.
Clinically, he had a very ill look, accessory muscles of respiration were active, respiratory rate was 40/min, patient was conscious, temperature was 102°F, pulse 160/min, regular, feeble, low volume, blood pressure (BP) 70/50 mmHg, SpO 2 97% while breathing oxygen enriched air (O 2 8 L/min), periphery cold, normal jugular venous pressure, mild jaundice, no lymphadenopathy. Mean arterial pressure was 57 mmHg. Trachea was central, apex beat was normally located; right axillary, supraclavicular, suprascapular regions had diminished movements, increased vocal fremitus was, there was dull percussion note, tubular bronchial breath sound with egophony and whispering pectoriloquy were present with fine inspiratory crepitations and generalized bronchospasm. Abdomen was soft abdomen there was soft non-tender liver 2 cm below the costal margin. Bowel sounds were normal. Patient was conscious, oriented, with no neurological deficit or signs of meningeal irritation. Urgent chest X-ray revealed homogenous opacity involving whole of right upper lobe with bulging of transverse fissure and air bronchogram, normal tracheal position [Figure 1].
|Figure 1: Chest radiograph showing right upper lobe consolidation with air bronchogram with bulging of inter lobar fissure|
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He was admitted to intensive care unit as severe CAP of right upper lobe and treated by intravenous (IV) tigecycline, IV ceftazidime, Tab Tamiflu, hourly nebulization, crystalloid as per the requirement.
Hb 13.3 g%, therapeutic life-style changes 2200/cm normal DLC, peripheral smear normal, platelets 40,000/cm. Total bilirubin 4.2 mg/dl, direct 2.4 mg/dl, serum alanine aminotransferase 69 U/dl, serum alkaline phosphatase 20 U/dl. Blood urea 52 mg/dl, serum creatinine 1.7 mg/dl. Serum protein 5.7 g/dl, serum albumin 3.7 g/dl, serum Na 129 mEq/L, serum k 3.0 mEq/L. Arterial blood gas - pH 7.54, PCO 2 17.8 mmHg, PO 2 90 mmHg, HCO 3 15.3 mg/dl. H 1 N 1 - Negative. Sputum Gram-negative bacilli and Gram-positive cocci acid fast bacillus absent, pus cells present. Sputum culture - KP isolated sensitive to: Norfloxacin, cefotaxime, amikacin, ceftazidime, imipenem, ceftazidime + tazobactam, ceftazidime + clavulanic acid. Resistant to ampicillin [Figure 2] and [Figure 3]. Blood culture - KP isolated sensitive to above antibiotics, resistant to ampicillin [Figure 4]. Urine: Albumin: 2+, Sugar: Nil, Pus cells: Nil, microscopic - NAD. Human immunodeficiency virus: Negative. Hepatitis B surface antigen: Negative.
|Figure 2: Blood culture and antibiotic sensitivity test. Norfloxacin-zone size: 25 mm, cefotaxime-zonesize: 32 mm, ceftazidime-zonesize: 25 mm, ceftazidime + tazobactam-zonesize: 25 mm, ceftazidime + clavulanic acid-zone size: 24 mm, amikacin zone size: 22 mm, ampicillin zone size: 8 mm|
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Within 6 h of hospitalization, he became more tachypnoeic, SpO 2 <60% with unrecordable BP, put on pressure and respiratory support. Within next 4 h, he developed repeated cardiac arrest and failed to respond to cardio-respiratory resuscitative measures and expired.
| Discussion|| |
Pneumonia due to KP was first described by Friedlander's in 1882 and was believed to be the most common cause of bacterial CAP;  subsequently, pneumococcus proved to be most common cause.  We present here a young non-immunocompromised patient with severe CAP due to KP pathogen. KP is responsible for severe CAP in many studies throughout the world and also an independent mortality factor. ,, At present there are two sets of criteria to assess the severity of CAP - pneumonia severity index (PSI) and CURB-65 criteria. ,,, PSI is less practical in an emergency situation because of 20 variables. The CURB-65 criteria include five variables-confusion (C), urea >7 mmol/L (U), respiratory rate >30/min (R), BP systolic <90 mmHg or diastolic <60 mmHg (B), age >65 years (65); one point for each criteria. Three or more points indicate severity. Our patient had three points at the time of admission to intensive care units (ICU). Hemoptysis (currant jelly sputum) is important features of FP, but rarely described in the literature.  Our patient had classical hemoptysis as red currant jelly sputum, classical radio graphical description of bulging of interlobar fissure was present in this case, an uncommon feature in many large series of KP. , Bacteriologically, there are two types of KP - classic KP and hypervirulent (hypermucoviscous) (hvKP), the latter causing severe CAP.  The hypermucoviscosity of hvKP has been semiquantitatively defined by a positive string test, in which there is the formation of a viscous string >5 mm in length when bacterial colonies on an agar plate are stretched by an inoculation loop  [Figure 5]. The viscous string reflects increased capsule production, which determines the virulence of the organism. This particular virulent strain is sensitive to a large number of antibiotics in contrast [Figure 2]. Recent acquisition of ESBL and carbapenemases by this organism has resulted in multi-drug/pandrug resistant strain including virtual distortion method-1.  The ESBL resistance varies from 0% (South Korea, Malaysia) to 36.4% (India) among community acquired infections. ,
|Figure 5: Mucoid colony seen in MacConkey medium with positive "stringe" sign|
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The mortality rate in FP is very high. Several factors attribute this high mortality: Virulent and multi-drug resistant KP, immunocompromised state, neutropenia, CURB-65>3, alcoholism, inappropriate and delayed antibiotic therapy. ,, The mortality reported in various literatures varies from 33% to 72%. ,, CURB-65 Score 3-4 points was associated 31% mortality.  Time to first antibiotic dose for CAP has recently received significant attention from a quality of care perspective study; statistically significant lower mortality was demonstrated among patients who received early antibiotic therapy.  Infectious Disease Society of America/American Thoracic Society Committee recommends that antibiotic therapy should be administered as soon as possible after the diagnosis is considered.  Our patient had neutropenia, CURB-65 Score of three points, significantly delayed (4 days) initiation of appropriate antibiotic therapy, a very virulent non ESBL organism causing pneumonia, septicemia and multi-organ failure. All these factors resulted in a fatal outcome within few hours of ICU admission.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]