Difference between revisions of "Haemophilus pertussis (Whooping Cough)"

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# [http://cmr.asm.org/content/18/2/326/T2.expansion.html Cherry J.D. and Mattoo S. Molecular Pathogenesis, Epidemiology, and Clinical Manifestations of Respiratory Infections Due to Bordetella pertussis and Other Bordetella Subspecies. ASM. 2005 Apr. (online table)]
 
# [http://cmr.asm.org/content/18/2/326/T2.expansion.html Cherry J.D. and Mattoo S. Molecular Pathogenesis, Epidemiology, and Clinical Manifestations of Respiratory Infections Due to Bordetella pertussis and Other Bordetella Subspecies. ASM. 2005 Apr. (online table)]
 
# [http://www.ncbi.nlm.nih.gov/pubmed/24227794 Weyrich LS, Feaga HA, Park J, Muse SJ, Safi CY, Rolin OY, Young SE, Harvill ET. Resident microbiota affect Bordetella pertussis infectious dose and host specificity. PubMed. 2013 Nov.]
 
# [http://www.ncbi.nlm.nih.gov/pubmed/24227794 Weyrich LS, Feaga HA, Park J, Muse SJ, Safi CY, Rolin OY, Young SE, Harvill ET. Resident microbiota affect Bordetella pertussis infectious dose and host specificity. PubMed. 2013 Nov.]
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# [http://www.cdc.gov/pertussis/clinical/features.html Pertussis: Clinical Features from CDC]
  
 
[[Category:Written by Teresa Vu, student of Tyrrell Conway at the University of Oklahoma]]
 
[[Category:Written by Teresa Vu, student of Tyrrell Conway at the University of Oklahoma]]
 
[[Category:Pages edited by students of Tyrrell Conway at the University of Oklahoma]]
 
[[Category:Pages edited by students of Tyrrell Conway at the University of Oklahoma]]

Revision as of 01:49, 28 July 2014

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Microbiology in Italy[1]
Haemophilus pertussis[2]

Etiology/Bacteriology

Taxonomy

| Domain = Bacteria | Phylum = Proteobacteria | Class = Betaproteobacteria | Order = Burkholderiales | Family = Alcaligenaceae | Genus = Bordetella | species = pertussis

NCBI: Taxonomy Genome: [4]

Description

Pertussis, more commonly known as “whooping cough,” had its first epidemic in Paris, France in 1578. Thomas Sydenham named it “pertussis,” meaning “violent cough.” The organism that causes this disease is called Heamophilus pertussis or Bordetella pertussis. It was first isolated in 1906 by Jules Bordet. B. pertussis is an aerobic, non-spore forming, Gram-negative ccoccobacillus bacterial pathogen that is strict to infecting and residing in the mouth, nose, and throat of humans[4][5].

Pathogenesis

Transmission

Transmission of B. pertussis occurs via airborne respiratory droplets from other people’s coughs and sneezes [4] [5]. Adults and adolescents serves as reservoirs for transmission of B. pertussis to infants and children [4].

Infectious dose, incubation, and colonization

There are four important steps relating to infection, colonization, and disease due to B. pertussis: (i) attachment, (ii) evasion of host defenses, (iii) local damage, and (iv) systemic manifestations. Infection is initiated by the attachment of B. pertussis to the cilia of epithelial cells of the upper respiratory tract with the aid of protein adhesins. Evasion of host defenses is facilitated by adenylate cyclase toxin (CyaA) and PT. Specifically, CyaA enters neutrophils and catalyzes the excessive production of cAMP, which intoxicates the cells such that phagocytosis is compromised. Like CyaA, PT also adversely affects phagocytosis and killing of organisms by inhibiting migration of lymphocytes and macrophages to areas of infection. Local tissue damage of the ciliated epithelial cells may be due to TCT, DNT, and perhaps CyaA. Systemic manifestations results in the common clinical features exhibited by pertussis patients[5].

B. pertussis's infectious dose is < 100 CFU [7]. The incubation period is 7-10 days long with the exceptions of household secondary cases being 28 days longer than primary cases [5].

Virulence factors

Ahesins

Filamentous hemagglutinin (FHA) is required for B. pertussis’s tracheal colonization. To make sure the tracheal colonization is persistent, the assistance of Fimbriae (FIM) is also available. This is required for protective immunity to infections[6]. B. pertussis inhibits T-cell proliferation to exogenous antigens in vitro in an FHA-dependent manner. Interactions of FHA with receptors on macrophages results in suppression of the proinflammatory cytokine, interleukin-12 (IL-12), via an IL-10 dependent mechanism [5]. Both FHA and FIm are some of the main components of the acellular pertussis vaccines [6].

Autotransporters

Pertacin (PRN) mediates eukaryotic cell binding to enhance protective immunity. BrkA is a putative adhesion that confers serum resistance and protection against antimicrobial peptides. SphB1 allows FHA maturation [6].

Toxins

The primary component of pertussis vaccines is the Pertussis toxin (PT), which is associated with pertussis-associated lymphocytosis. Adenylate cyclase (CyaA) acts as an anti-inflammatory and antiphagocytic factor during infections. Other toxins include Type III secretion, dermonectrotic toxin, and tracheal cytotoxin [6].

Others

The LPS of Bordetella pertussis is pyrogenic, mitogenic, and toxic and can activate and induce tumor necrosis factor production in macrophages[5]. Locus wlb consists of 12 genes that are required for LPS biosynthesis [6].

A siderophore, called Alcaligin, complexes iron internally through outer membrane receptors. This is important for B. pertussis’s survival in its host [6].

Clinical features

Infant with pertussis[3]

According to CDC, clinical course of the illness is divided into three stages: catarrhal, paroxysmal and convalescent

Diagnosis

The classical method for identifying pertussis is to culture a nasopharyngeal sample. Yet, this method is not preferred due to the disease’s nature to disappear early in its process [1]. It is difficult to get an early diagnosis in adults due to the fact that intense coughing could be a result of other factors such as asthma, smoking, GERD, and medical treatments. It is also difficult to detect in young children unless severe symptoms like coughing occurs before vaccination. The most useful test for a diagnosis of a Bordetella pertussis infection is bacterial DNA tests performed on a nasal swab or wash specimen [3]. Other methods include antigen detection by direct fluorescent antibody and PCR [1].

Diagnosis can also be done serologically through complement fixation, agglutination tests, toxin neutralization, and enzyme-linked immunosorbent assay. The last method being the most commonly used today [1].

Another quick test consists of using monoclonal antibodies against the bacterium’s virulence factors: lipo-oligosaccharide and peroxidase conjugate. The test dries cells of Bordetella pertussis in a formalin-saline onto a nitrocellulose disk, the disk is placed in a filtration device, and then the monoclonal antibodies are added. Afterwards, disk is washed in a peroxidase substrate solution and Bordetella pertussis is identified using a direct fluorescent-antibody assay [5].

Treatment

Apnoeic or cyanotic cases of infants under 6 months should be taken care of in hospitals. Any suspicion of symptoms of whooping cough should be a sign to excuse children from school and receive antibiotic treatments within 3 weeks of illness. Clarithromycin and azithromycin are the preferred antibiotics for babies from birth to 1 year old. Adults can also take these antibiotics. However, co-trimoxazole can be used if the individual who cannot tolerate macrolides. Pregnant women who already has the disease are treated with erythromycin to prevent transmission to infant. Spasms are treated with mild sedation, and cyanosis is treated with administration of oxygen. [2]

Prevention

The key to preventing pertussis is vaccination, in infants as well as teenagers and adults. Booster vaccinations were recommended by the Advisory Council on Immunization in 2006 to increase immunity. Many developed countries now administer the DTap vaccine to reduce pertussis and its circulation among human populations [4]. Pregnant women are also vaccinated a month before giving birth to decrease the chances of the infant getting infected [3]. Primary vaccinations today are presented as pertussis antigens contained in pentavalent childhood vaccine, administered as a “before preschool” immunization requirement [1].

Host Immune Response

References

  1. Oakley S, and Kilcoyne A. The whooping cough epidemic: prevention and treatment. Practice Nursing. 2012 Oct. 604-7
  2. Treatment of Whooping Cough. General Practice Notebook (online)
  3. Pluta R.M. Pertussis. JAMA. 2010 Aug. (online)
  4. Cherry J.D. and Mattoo S. Molecular Pathogenesis, Epidemiology, and Clinical Manifestations of Respiratory Infections Due to Bordetella pertussis and Other Bordetella Subspecies. ASM. 2005 Apr. (online)
  5. Clyburn M. Pertussis.(online)
  6. Cherry J.D. and Mattoo S. Molecular Pathogenesis, Epidemiology, and Clinical Manifestations of Respiratory Infections Due to Bordetella pertussis and Other Bordetella Subspecies. ASM. 2005 Apr. (online table)
  7. Weyrich LS, Feaga HA, Park J, Muse SJ, Safi CY, Rolin OY, Young SE, Harvill ET. Resident microbiota affect Bordetella pertussis infectious dose and host specificity. PubMed. 2013 Nov.
  8. Pertussis: Clinical Features from CDC