Unexplained pneumonia and pleural effusion, suspecting Acinetobacter pneumonia

47/M driver by occupation came with complaints of fever since 1 week high grade , associated with chills and rigors ,dry cough since 1 week
And also complained of Burning micturition

H/o chest pain ,diffuse type,severe type , intermittently ,since 5-6months
3 episodes in last month
Generalised bodypains since 5-6months 

No high risk behavior 

K/c/o T2 DM since 1 yr on metformin 

Chronic smoker-beedi/cigarette 1 pack /day since 30 yrs 

Chronic gutka chewer since 3-4 yrs 

Occasional alcoholic 

On auscultation:- RS- bae+ ,cvs- s1 S2+ 

O/e. Temp: 99      BP: 130/80 mm hg, PR:  78/min

On  the day of admission patient had severe chest pain on left side with shortness of breath 

Ecg was done and that showed normal finding
Initial x Ray showed pleural effusion on left side 

Our provisional diagnosis: was 

Urinary tract infection 

pleural effusion 

After sending sputum and urine samples 

We started him on amoxicillin and clavum

Patient shortness of breath and cough gradually increased,and clinically we could appreciate crepts over left infraxillary area

,that gradually progressed to decreased air entry on left side of lung except the apical area

Fever chart 

Laboratory investigations :

Hemogram shows increase in total leucocyte count that rose from 12700 to 14700 

Sequential x Ray's showed increasing in    left lung consolidation with pleural effusion 

ultrasound of chest showed left side mild to moderate pleural effusion with loculations and consolidation

Usg chest

Complete urine examination showed 5-6 pus cells and

Urine culture showed no growth

Sputum for AFB came negative 

Gram Stain showed plenty of pus cells with few epithelial cells and gram negative bacilli

Sputum report

Sputum culture isolated Acinetobacter species (probable colonizers) .

Pleural fluid analysis: 

Sugars- 220

Protien -4.1

Ldh-205

Pleural fluid cytology

Pleural fluid /serum  LDH--1.5 

Pleural fluid /serum protien -0.7 

Cytology lymphocyte predominant -Likely exudative

Pleural fluid microbiology reports are awiated 

Sputum for CBNAAT is negative 
Sputum for AFB also negative 
We repeated sputum for c/s so as to isolate the organism but after starting of antibiotics - so the Report showed growth of commensal -candida species 
And repeat pleural fluid analysis was planned but usg chest showed only minimal pleural fluid that couldn't be accessed ,it was not done 

So the patient got discharged and kept on follow 

Discussion : 

Acute onset ,rapidly progress pneumonia clinically as well as radiologically with sputum grown  Acinetobacter (probably coloniser)

We reviewed the literature to see Acinetobacter causing  rapidly progressing pneumonia 

There are studies showing Acinetobacter baumannii causing  pneumonia mostly during months of April to October ,male

predominant with illness ,alcoholics (reference articlehttps://www.ncbi.nlm.nih.gov/pubmed/11591541/

So as in our case that showed Acinetobacter but we are not sure whether it was colonizers or pathogenic,review of literature gave us some clues 

(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367029/)-isolation, identification of Acinetobacter species and antibiotic Resistance

We found a case study that showed of 3298 infected samples, 111 (3.36%) were found to be Acinetobacter. The most predominant species was Acinetobacter calcoaceticus-A. baumannii (Acb) complex (72%). 

species were predominantly isolated from blood samples 41 (36.9%) followed by pus 25 (22.5%), respiratory samples 16 (14.4%), urine 13 (11.7%), other body fluids 10 (9%) and various catheter tips 6 (5.4%). 

High incidence of resistance was recorded for piperacillin (55%), followed by ceftriaxone (46%) and ceftazidime (46%). 

A high level of antibiotic resistance was observed in our study and maximum isolation rate of Acinetobacter was in the ICUs. 

Acb complex was the most predominant and most resistant species. The analysis of susceptibility pattern will be useful in understanding the epidemiology of this organism in our hospital setup, which will help in treating individual cases and controlling the spread of resistant isolates to other individuals.

Isolation rate and antibiotic resistance was higher in the Intensive Care Units (ICUs) of the hospital. ESBL and MBL production was detected in 31.5% and 14.4% of the isolates respectively.

Acinetobacter emerged as an important nosocomial pathogen due to its ability for survival in the hospital environment on a wide range of dry and moist surfaces.

Acinetobacter species obtained were maximum during July to September period, which is consistent with previous reports.[25,26,27] The reason for this seasonality correlated with atmospheric temperature changes (high isolation rates especially in regions where temperature is hot and humid). 

Conclusion::: occurrence of Acinetobacterspecies among nonfermenters is high in hospital settings. Rationale use of antibiotics is important and necessary to prevent microbial resistance catastrophe

 Some Common  misconceptions:

Many misconceptions concerning acinetobacter still

appear repeatedly in the scientific and medical liter-

ature. Chief among these are the statements that

A. baumannii is (i) ubiquitous or highly prevalent in

nature, (ii) that it can be recovered easily from

soil, water and animals, and (iii) that it is a frequent

skin and oropharyngeal commensal of humans. While

these statements certainly apply to members of the

genus Acinetobacter when considered as a whole,

A. baumannii (and its close relatives of clinical

importance) are not ubiquitous organisms. While it

is certainly true that A. baumannii can be isolated

from patients and hospital environmental sources

during outbreaks, this species has no known natural

Follow up :
Patient came for follow-up ,his shortness of breath decreased but complained of shortness of breath intermittently associated with cough , dysphagia,loss of appetite
So repeat x ray done showing cavity in left upper lobe region and he is being admitted