Introduction to Opportunistic Infections Flashcards
opportunistic pathogens:
Organisms of – intrinsic virulence that are not normally –
May cause — in certain circumstances, e.g:
– in an — patient
– where a — is present ( – risk)
low
harmful
serious infections
immunocompromised
foreign body
biofilm
features of opportunistic pathogens:
1. Low— & sometimes — , e.g.
Pneumocystis jirovecii (Pneumocystis carinii), Candida albicans, S. epidermidis, P. aeruginosa
2. May be part of — , e.g. S. epidermidis, Candida
3. – to host & circumstances, e.g. – production
4. Often difficult to completely — / may — , e.g.CMV
5. Variable – presentation
6. Absent normal — response; — serology
pathogenicity
ubiquitous
normal flors
adapt
biofilm
eradicate and it may relapse
clinical
immune
-ve
where do opportunistic pathogens come from:
1. Endogenous (aka – )
- —
- —
2. Exogenous
- —
- —
microbiome
GIT
skin
environment
healthcare staff
general term:
any patient compromised by virtue of their underlying condition is known as –
* e.g. multiple trauma patient in ICU
non-specific
Specific term:
A patient with a recognised deficiency of one or more immune parameters is known as—-
refers to specific categories of patients
1. Primary immunodeficiency
2. Secondary immunodeficiency ( – e.g. — , – ,— )
immucompromised patient
drugs as serious , malignancy , HIV
importance of opportunistic infections:
* Increased numbers of — patients
* Increased use of indwelling —-
(increasing risk of — formation & —)
* Significant cause of — &—
* May be — & —
* Bacteria often —-
* Variable — presentation – atypical, fever often absent. May be difficult to diagnose
- the categories of ooportunstic pathogens are:
immocompromised
medical devices
biofilm and infection
morbidity ad mortality
poly microbial and complex
multi antibiotic resistance
clinical
bacteria viruses fungi n protozoa
1- bacteria:
- endogenous organisms are — , — , —- which includes —
- exogenous organisms which include:
2- viruses :
* Herpes viruses: Latency leading to —
– Herpes — virus 1 & 2
– —- -zoster virus
–—
* Polyomaviruses: Latent in — & —
tissue
– — virus Progressive mutlifocal Leukoencephalopathy
(PML)
– – virus (stem cell and renal transplant recipients)
* Parvovirus B19: Can cause profound —
– Persistent — in immunocompromised / persistent —
* Hepatitis B: – carriage or – of— infection
endo:
* S. epidermidis
* S. aureus
* Gut flora
– E. coli
– Enterococci, including
vancomycin-resistant
enterococci (VRE)
exo:
* S. aureus, including
MRSA
* Enterobacterales
* P. aeruginosa
* Listeria
* Atypical mycobacteria &
M. tuberculosis
reactivation
herpes simplex
Marcella
Cytomegalovirus
kidney n lymphoid
JC virus
BK virus
red cell aplasia
presistant infection n anaemia
chronic
reactivation
latent
3- fungi:
* — spp.
– Mucositis, oesophagitis,
candidaemia
* — fumigatus
– Lower respiratory tract
infection
* — neoformans
– Meningitis or meningo-
encephalitis
* — jirovecii–PJP
– Pneumonia
4- protozoa:
* Toxoplasma gondii
– — toxoplasmosis
* Cryptosporidium
parvum
– Severe —
candida
asperiglus
cryptococcus
pneumocystis
cerebral
diarrhoea
- — is defined as a neutrophil count of <500 cells/mm3 (<0.5 x109/L) or a neutrophil count that is expected to decrease to <500 cells/mm3 during the next 48h1
- Low numbers of neutrophils mean patients are vulnerable to a variety of —, including those caused by — pathogens
- immunosuppressive causes of this:
- Due to use of —
- Especially, if severe & prolonged neutropaenia:
– increased risk of — and — - Common sources of microbial invasion of the blood
– chemotherapy-induced–
– breaks in the — lining - Bacterial / fungal—
– – lines
neuropenia ( while neorphilia can be from steroid n bacterial sepsis )
infections
opportunistic
myelosuppressive chemotherapy
bloodstream infections (BSI) & respirator infections
mucositis
gastrointestinal
translocation
intravascular
neutropenic sepsis pathogens:
* Gram- — i (e.g. coagulase-negative
staphylococci, S. aureus, streptococci/ enterococci) in about 55-60%
* Gram- – (e.g. E. coli, P. aeruginosa) in about 40-45%
* — such as Aspergillus spp. & Candida spp.
Sites of infection:
* — cavity, the – , – & — areas, — , —— etc
+ve cocci
-ve bacili
fungi
oral , skin , perirectal , genital , bsi , lungs ndwelling intravascular catheters or other foreign bodies
IV line infection ( if the patient has picc line) ;
Pathogens:
* *Coagulase —- most
common
* — / Gram- —
Diagnosis
* – cultures (at least two sets – – and –)
Management
* — control: Often the prosthesis must come out for effective treatment ( — )
* — line
* — is usual empiric treatmen
negative staphylococci
S. aureus / Gram-negative bacilli
blood
line and peripheral
source
biofilm
culture iv
vancomycin
NEUTROPAENIC ENTEROCOLITIS (TYPHLITIS):
More commonly in neutropaenic patients with —
* Usually due to a combination of :
– chemotherapy-induced —
– — neutropenia,
– impaired host defences to — by – organisms (which leads to — of various layers of the bowel wall).
Pathogens:
* Various including gram — , gram – , — ,
* —- infection frequent.
Clinical:
* In addition to – , patients may present with abdominaldistension, tenderness, nausea, vomiting and/or diarrhoea.
* – or – common
haematological malignancies
mucosal injury,
profound
invasion
bowel
necrosis
gram -ve bacili , gram +ve cocci , anaerobes as (Clostridium septicum) , candida spp
Polymicrobial
fever
bacteremia or fungemia
candida:
Major disease of— hosts
Risk factors:
* — (including — therapy)
* Intravenous — / TPN (parenteral – )
* – therapy,
* — -operative – GI surgery
* —
Diagnosis:
* Clinical suspicion: – + no response to — (sometimes multi-site colonisation)
Treatment:
* Antifungal resistance = need to – and do — tests
* – (e.g., fluconazole)
* — (eg caspofungin)
- lab diagnosis:
* specimen :
– Blood, sterile site samples, tissue
* Microscopy :
– –
– Gram – - –
– — tube test
* Culture:
– Grow — on – and —
agar (Sabouraud dextrose agar)
– Need to do — tests!
* Identification:—
* NAAT: –
immunocompromised
immunsopressitn as steriod therpau
iv catheter and paternal nitrites
antibiotic
post operative
diabetes mellitus
fever + no response to broad-spectrum antibiotics
ID and susepcitibility test
azoles
echinocandin
budding yeast
gram +ve large
germ tube
aerobically on blood n selective agar
suscepiitbiltiy test
MALDI-TOF
18S PCR
asperigillus is — infection and A. fumigatus — common
Environmental – , survives in – & –
– prognosis
Risk factors:
* — (> 14 days)
* high dose –
Pathogenesis:
* Primary site usually — – — inhaled
* Widespread — growth in tissue: Invasion of — (haemoptysis/catastrophic bleeding)
* Dissemination to other sites (liver, spleen, kidney,CNS)
Diagnosis:
* CXR/CT thorax: cavitation, ‘—’ sign
* – antigen (BAL, serum)
Treatment
*— (e.g., voriconazole – need to monitor
levels / posaconazole)
* — B
- prophylaxis (prevention)
*—
* Infection – and – : hospital
building works
invasive
most
mould services in soil n dust
poor
prolonged neutropenia
high dose steroids
lungs
spore
destructive
blood vessels
halo
galactomannan
azoles
amphotercin b
posaconzole
prevention n control
PNEUMOCYSTIS (CARINII) JIROVECII (PJP/PCP):
-Incidence has greatly declined since introduction of—
-Risk factors:
* – (especially low – counts)
* High dose –
* — (solid organ especially lung /
haematopoetic stem cell)
-Diagnosis:
* Clinical - –
* CXR/ High-resolution – thorax
Ground – infiltrates
* NAAT: —- lavage
* B D Glucan: —
-Treatment:
— dose – co-trimoxazole
Prevention
Co-trimoxazole –
prophylaxis
HOV low CD4
steroids
transplantation
hypoxia
CT
glass
bronchoalveolar
serum
high iv
PO
CRYPTOCOCCUS NEOFORMANS:
* — ( — )
* Soil, avian faeces, rotting vegetation
* Inhaled into – – generally –
- – and – in immunosuppressed patients
-Risk factors
– —
– —
– –
– —
-Diagnosis
* – detection in blood & CSF
* Culture of – , –
* — on tissue samples
* Microscopy (—-ink) rarely used now
Treatment: includes —
yeast ( encapsulated )
lungs
no symptoms
meningitis and pneumonia
HIV
organ transplant
steriods
malignancy
antigen detection
CSF and blood
18s PCR
india
Amphotericin B
patient management:
* High index of —
* Repeated – assessments
* Appropriate investigations that may need to be –
* Knowledge of likely – , both
common & less common
* – & — basis for antibiotic use
* +/- remove all –
investigation:
1-History: Any clues as to the infection site?
2-Examination:Don’t forget: skin, oral cavity, oropharynx, lungs, abdomen, perianal area This will help you figure out what investigations to do
next
3-Blood cultures :X two sets: one peripheral and one from IV catheter
4-Microbiologic testing from
suspected site(s) of infection:
Your investigations will depend on the potential site of
infection and likely pathogen
Many tests may be negative e.g. serological tests due to
immunosuppression
5-Radiology: Computed tomography (CT) scans are generally more
useful than plain radiographs
- Often don’t have pulmonary infiltrates during
neutropenia (only upon neutrophil recovery)
- thickened bowel walls with neutropenic enterocolitis
suspeciion
clinical
repeated
pathogens
logical n rational
devieces
treatment of neutropenic fever:
Stage 1 : Include an – with activity against – :
—-/–+ —
Stage 2: Cover gram – pathogens:
- Add — , e.g. –
Stage 3: Add an — , e.g. –
Stage 4 : Consider adding — therapy,
antibiotic
pseudomonas
Piperacillin/tazobactam + gentamicin
gram +ve
glycopeptide as vancomycin
anti fungal as caspofungin
anti-viral/PJP therapy
ongoing pyrexia bc:
1. Occult –
2. Antibiotic – organism
3. Intravascular – infection (or other device)
4. — infection
- — infection pneumonitis, gastrointestinal or
CNS symptoms (Ganciclovir)
- Herpes — virus (HSV) and varicella zoster(VZV) can present as vesicular or ulcerative lesions (Aciclovir)
- — viruses eg. RSV, COVID, influenza,
adenovirus etc.
5. – infection
6. Invasive — (—) disease
7. Profound—
absess
resistant
catheter
viral
CMV
simplex
respiratory
protozal
fungal aka mould
neutropenia
prevention:
* High standards of – and —
– Patient and carer education also NB
* Appropriate —
– –
– – prophylaxis
* Protective –
summary :
* Population susceptible to opportunistic infections is
increasing
* Opportunist pathogens refer to microbes of – grade low virulence that do not cause infection in normal hosts
* Predisposing conditions include neutropenia, HIV/AIDS,
solid & stem cell transplants, certain medications, burns& the presence of foreign bodies
* Patients require— assessments & often — agents
asepsis and antisepsis
prohylaxis
vaccination or antimicrobial prophylaxis
isolation
low
repeated and multiple
anti-microbial
