Bacterial meningitis
Transcript of Bacterial meningitis
NEISSERIAE MENINGITIDIS
Dr. Uzma Mussarat
LEARNING OBJECTIVES
Enlist the bacterial causes of meningitis Describe the morphological features,virulence
factors and diagnosis of following bacteria Neisseria meningitides Listeria monocytogenes Haemophilus influenzae Streptococcus agalactae streptococcus pneumonia
Meningitis
Meningitis means inflammation but usually implies serious infection of the meninges
Microorganism reach the meninges either by direct extension from the ears, nasopharynx, cranial injury or congenital meningeal defect, or by bloodstream spread.
Non infectious causes of inflammation include malignant cells, drugs and blood following subarachnoid hemorrhage
Meningococcal Meningitis
Is inflammation of the meninges- meningitis, caused by the bacteria Nesseria meningitidis.
Neisseria meningitidis,Streptococcus pneumoniae and Haemophilus influenzae are the most common agents of bacterial meningitis.
Meningococcal Meningitis
Less common bacterial causes of Meningitis, such as Staphylococci, enteric bacteria, group B streptococci and Listeria, occur in sub-populations like the immunocompromised, neonates, or head trauma patients.
Patients with Meningococcal Meningitis present with sudden onset of fever, intense headache, nausea, vomiting, stiff neck and, frequently, a petechial rash with pink macules or, very rarely, vesicles. Delirium and coma often appear.
Case fatality rate is between 5% and 15%.
Pathology
In acute bacterial meningitis, the pia arachnoid is congested with polymorphs. A layer of pus forms. This may organize to form adhesions, causing cranial nerve palsies and hydrocephalus.
In chronic infection (e.g. TB), the brain is covered in a viscous grey green exudates with numerous meningeal tubercles. Adhesions are invariable. Cerebral edema occurs in any bacterial meningitis.
In viral meningitis there is a predominantly lymphocytic inflammatory CSF reaction without pus formation, polymorphs or adhesions, there is little or no cerebral edema unless encephalitis develops.
Neisseria meningitides
General Characteristics of Neisseria spp.
Aerobic Gram-negative cocci often arranged in pairs
(diplococci) with adjacent sides flattened (like coffe beans)
Oxidase positive Most catalase positive Nonmotile Acid from oxidation of carbohydrates, not
from fermentation
Neisseria gonorrhoeaeNeisseria meningitidis
Important Human Pathogens
Other species normally colonize mucosal surfaces of oropharynx and
nasopharynx and occasionally anogenital mucosal membranes
Neisseria Associated Diseases
(ophthalmia neonatorum)
Encapsulated small, gram-negative diplococci
Second most common cause (behind S. pneumoniae) of community-acquired meningitis in previously healthy adults; swift progression from good health to life-threatening disease
Introductionof Neisseria meningitidis
Meningococcal meningitis
Humans only natural hosts Person-to-person transmission by
aerosolization of respiratory tract secretions in crowded conditions
Close contact with infectious person (e.g., family members, day care centers, military barracks, prisons, and other institutional settings)
Epidemiology of Meningococcal Disease
Highest incidence in children younger than 5 years and particularly those younger than 1 year of age as passive maternal antibody declines and as infants immune system maturesCommonly colonize nasopharynx of healthy individuals; highest oral and nasopharyngeal carriage rates in school-age children, young adults and lower socioeconomic groups
Occurrence Infections can occur through the year, but are more
common in late winter to early spring.
Mode of Transmission By direct contact- respiratory droplets from nose and
throat of infected people. Infection usually causes subclinical infection, severe
systemic infection is rare. Carrier prevalence can be as high as 25%.
Pathogenicity:
Pili-mediated, receptor-specific colonization of nonciliated cells of nasopharynx
Antiphagocytic polysaccharide capsule allows systemic spread in absence of specific immunity
Toxic effects mediated by hyperproduction of lipooligosaccharide
Serogroups A, B, C, Y, W135 account for about 90% of all infections
Specific receptors (GD1 ganglioside) for bacterial fimbriae on nonciliated columnar epithelial cells in nasopharynx of host
Organisms are internalized into phagocytic vacuoles, avoid intracellular killing in absence of humoral immunity and complement system (patients with late complement deficiencies are particularly at risk)
Replicate intracellularly and migrate to subepithelial space where excess membrane fragments are released
Pathogenesis of Meningococcal Disease
Hyperproduction of endotoxin (lipid A of LOS) and blebbing into surrounding environment (e.g., subepithelial spaces, bloodstream) mediates most clinical manifestations including diffuse vascular damage (e.g., endothelial damage, vasculitis (inflammation of vessel walls), thrombosis (clotting), disseminated intravascular coagulation (DIC)
Following dissemination of virulent organisms from the nasopharynx: Meningitis Septicemia (meningococcemia) with or
without meningitis Meningoencephalitis Pneumonia Arthritis Urethritis
Diseases Associated with Neisseria meningitidis
Meningitis Clinical findings
Clinically: rapid deterioration of flu like illness
Headache, neck stiffness, +ve kerning’s sign, fever,
Diagnosis: CSF + blood cultureCSF: WBC , RBCsGram stain: bacteria & cells
Neisseria meningitidis in Cerebrospinal Fluid
Skin Lesions of Meningococcemia
NOTE: Petechiae have coalesced into hemorrhagic bullae.
Neck rigidity
Haemorrhagic rash
Large numbers (e.g., >107cells/ml) of encapsulated, small, gram-negative diplococci (flattened along adjoining side) and polymorphonuclear leukocytes (PMN’s) can be seen microscopically in cerebrospinal fluid (CSF)
Laboratory Characterization of Neisseria meningitidis
Contd…
Transparent, non-pigmented nonhemolytic colonies on chocolate blood agar with enhanced growth in moist atmosphere with 5% CO2
Oxidase-positiveAcid production from glucose and
maltose but not from other sugars
Diagnosis Isolation of the organism
from CSF or blood.
2. Streptococcus pneumoniae (G+,Lancet shaped diplococci Alpha- haemolytic colonies on blood agar Quelling Test +ive Optochin –sensitive Bile solubility test +ive (bile soluble) Capsular polysaccharide Antigen detection
from CSF by Latex agglutination method
Streptococcus pneumoniae
General characteristics Inhabits the nasopharyngeal areas of healthy
individuals Possess C substance
Virulence factors Polysaccharide capsule
Clinical infections pneumonia meningitis bacteremia sinusitis/otitis media
The quellung reaction (swelling reaction) forms the basis of serotyping and relies On the swelling of the capsule upon binding of homologous antibody. The test consists of mixing a loopful of colony with equal quantity of specific antiserum and then examining microscopicallyfor capsular swelling
Contd…
Pneumoccus grow only in enriched media. (blood agar, glucose broth)
aerobes, facultative anaerobes optimal temperature – 37C (25-42C) optimal pH – 7.8 (6.5-8.3) increased growth in 5-10% CO2
Laboratory Diagnosis:Streptococcus pneumoniae
Colony morphology Smooth,
glistening, wet-looking, mucoid
a-Hemolytic CO2enhances
growth
Laboratory Diagnosis: Streptococcus pneumoniae
Identification Catalase
negative Optochin-
susceptibility-test–susceptible
Bile-solubility-test–positive
Alpha & Beta Haemolysis
S. pneumoniae
Pus cells and S. pneumoniae in sputum gram stain
Neutrophil & Red Cells
3. Haemophilus influenzae
Aerobic , Small, pleomorphic gram-negative coccobacilli Polysaccharide capsule Six different serotypes (a-f) of polysaccharide capsule(based on
the antigenicity of capsular polysacchrides)
Contd… 95% of invasive disease caused
by type b The type b capsule is composed of polyribitol phosphates Unencapsulated and untypeable strains can cause sinusitis and otitis media
but are usually noninvasive Growth in culture requires heme (X factor) and/or nicotinamide adenine
dinucleotide (NAD) (V factor) for adequate energy production
H.INFLUENZAE IS THE LEADING CAUSE OF MENINGITIS IN YOUNG CHILDREN
Important cause of URTI(otitis media,sinusitis and epiglottitis) and sepsis in children
It causes pneumonia in adults particularly in those having COPD (chronic obstructive pulmonary disease)
LABORATORY DIAGNOSIS
Specimens: Oral swab: avoid contamination with oral secretions Sputum from LRT Direct needle aspiration Cerebrospinal fluid (CSF) and blood (>107 bacteria/ml)
Microscopy: both sensitive & specific; G(-) bacilli in CSF in >80% cases before antibiotics treatment
LABORATORY DIAGNOSIS Heated blood (chocolate) agar for isolation(to inactivate nonspecific inhibitors of
H.influenzae growth) Growth require heme (x factor) and nicotinamide adenine dinucleotide, NAD (v
factor)
Contd..
Definitive identification can be made by biochemical tests or the capsular swelling “QUELLUNG “reaction
Fluorescent-antibody staining of the organism and counterimmunoelectrophoresis or latex agglutination tests detect the capsular polysacchride.
Streptococcus agalactiae
Streptococcus agalactiae
Gram +ive cocci in small chains Beta haemolytic colonies on blood agar Lance-field gouping ---group B (specific antiserum) Hippurate Hydrolysis test +ive CAMP – TEST +ive (Chtist,Atkin,Mouch,Peterson) Bacitracin Disk ----Negative
FIG. 6. CAMP-positive Streptococcus agalactiae (group B) inoculated at right angles to the test organism Staphylococcus aureus. Note the arrow-shaped zones of enhanced hemolysis.
FIG. 7. CAMP-negative Streptococcus pyogenes (group A) inoculated at right angles to the test organism Staphylococcus aureus. Note the absence of arrow-shaped zones of enhanced hemolysis.)
Listeria Monocytogenes
Gram +ive , motile rod. Coccobacillus , Non –capsulated
Motile at 18 – 20 C°, non motile at 37 C° Tumbling/ Rotating motility Grows at Refrigerating temp 2-8 C°also Can cross placenta Causes meningitis in new born and pregnant women
Listeria Monocytogenes
Laboratory Diagnosis
Gram staining----G+ive rods Small grey coloured colonies
with narrow zone of beta hemolysis on blood agar
Motile nature differentiate it from corynaebacteria
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