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2009- 2015, 0 number of reported cases in Malaysia (repersented by flat green line in the graph)

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Macrolides (antibiotic) for treatment of H ducreyi infection in sexually active adults

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Macrolides (antibiotic) for treatment of H ducreyi infection in sexually active adults

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There was no difference between the types of antibiotics in sexually active adults with genital ulcers compatible with chancroid. Erythromycin is usually the first choice for treatment but low quality evidence suggested that azithromycin (as a single dose, oral (by mouth) administration) had similar safety and effectiveness.

Because of sparse evidence about the safety and effectiveness of macrolides to treat Haemophilus ducreyi infection in people with HIV, these results should be taken with caution.

Macrolides are antibiotics that could be effective and safe for treating H ducreyi infection.

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Simplified PCR for detection of Haemophilus ducreyi and diagnosis of chancroid.
Straightforward chloroform extraction sample preparation method.
A one-tube nested PCR to minimize contamination risks, and a colorimetric method for detection of products.
Primers were designed from published nucleotide sequences of the 16S rRNA gene of H. ducreyi. A pair of primers was selected from sequences of an anonymous fragment of DNA cloned from H. ducreyi.The primers were tested in amplification reactions with both purified DNA and lysed organisms for their ability to detect H. ducreyi, and with DNA from a variety of different bacteria for their specificity.
With longer outer primers for annealing at a higher temperature and shorter inner primers labelled with biotin and digoxigenin for binding with avidin and colorimetric detection.
The adaptations of this simplified PCR strategy, at the sensitivity and specificity levels obtained, mean it will be useful for detection of H. ducreyi in areas where the organism is endemic, particularly where testing by culture is difficult or impossible.
Additional studies demonstrated that the failure of PCR to detect H. ducreyi in all of the culture-positive specimens probably resulted from inhibitors of the Taq DNA polymerase that were present in the nucleic acids extracted from the clinical specimen.

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The genome of an H. ducreyi strain that is virulent in humans

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The genome of an H. ducreyi strain that is virulent in humans

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The genome is composed of a single 1.7-Mb chromosome.Although there is substantial homology observed for many genes, there is little long-range conservation of the order of genes or operons in the chromosome when H. ducreyi is compared to these related species.
*Additional info
Chancroid vaccine may help reduce the transmission of HIV

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Genetic manipulation for vaccines development.

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Genetic manipulation for vaccines development.

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The Haemophilus ducreyi trimeric autotransporter adhesin DsrA is an effective vaccine immunogen in the experimental swine model of chancroid.The passenger domain of DsrA (rNT-DsrA) was tested as a vaccine against chancroid.rNT-DsrA protected against a homologous challenge.High titered DsrA antisera bound the surface of viable Haemophilus ducreyi.Anti-DsrA IgG partially blocked fibrinogen binding by viable bacteria. Protection by the rNT-DsrA vaccine may involve a novel mechanism.
Adherence of pathogens to cellular targets is required to initiate most infections. Defining strategies that interfere with adhesion is therefore important for the development of preventative measures against infectious diseases. As an adhesin to host extracellular matrix proteins and human keratinocytes, the trimeric autotransporter adhesin DsrA, a proven virulence factor of the Gram-negative bacterium Haemophilus ducreyi, is a potential target for vaccine development. A recombinant form of the N-terminal passenger domain of DsrA from H. ducreyi class I strain 35000HP, termed rNT-DsrAI, was tested as a vaccine immunogen in the experimental swine model of H. ducreyi infection. Viable homologous H. ducreyi was not recovered from any animal receiving four doses of rNT-DsrAI administered with Freund's adjuvant at two-week intervals. Control pigs receiving adjuvant only were all infected. All animals receiving the rNT-DsrAI vaccine developed antibody endpoint titers between 3.5 and 5 logs. All rNT-DsrAI antisera bound the surface of the two H. ducreyi strains used to challenge immunized pigs. Purified anti-rNT-DsrAI IgG partially blocked binding of fibrinogen at the surface of viable H. ducreyi. Overall, immunization with the passenger domain of the trimeric autotransporter adhesin DsrA accelerated clearance of H. ducreyi in experimental lesions, possibly by interfering with fibrinogen binding.
Reference:
https://www.sciencedirect.com/science/article/pii/S0264410X14006987

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Generally, the global epidemiology of chancroid is poorly documented, and it is not included in World Health Organization estimates of the global incidence of curable sexually transmitted infections (STIs).

Key challenges in interpreting data on the epidemiology of H. ducreyi as a causative agent of genital ulcer diseases (GUD):

*genital herpes cases are easily misdiagnosed as chancroid on clinical examination (reports based only on clinical diagnosis can be invalid)

* laboratory culture is technically difficult, and the highly sensitive and specific nucleic acid amplification tests, such as PCR, are rarely available outside national reference laboratories or specialized STI research settings (makes it difficult to confirm clinical diagnoses)

Determining the true global incidence of chancroid is made more difficult due to widespread adoption of syndromic management for bacterial GUD without microbiological confirmation in many countries.
*Example; treatment with antimicrobial drugs effective against syphilis and chancroid.
Hence, countries often report only the total number of GUD cases.

Also, identification of GUD etiology is rarely conducted in resource-poor countries to validate syndromic management for which chancroid could also be common.

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Abstract

The global epidemiology of Haemophilus ducreyi infections is poorly documented because of difficulties in confirming microbiological diagnoses. We evaluated published data on the proportion of genital and nongenital skin ulcers caused by H. ducreyi before and after introduction of syndromic management for genital ulcer disease (GUD). Before 2000, the proportion of GUD caused by H. ducreyi ranged from 0.0% to 69.0% (35 studies in 25 countries). After 2000, the proportion ranged from 0.0% to 15.0% (14 studies in 13 countries). In contrast, H. ducreyi has been recently identified as a causative agent of skin ulcers in children in the tropical regions; proportions ranged from 9.0% to 60.0% (6 studies in 4 countries). We conclude that, although there has been a sustained reduction in the proportion of GUD caused by H. ducreyi, this bacterium is increasingly recognized as a major cause of nongenital cutaneous ulcers.

Keywords: Haemophilus ducreyi, bacteria, epidemiology, chancroid, genital ulcer disease, genital ulcers, skin ulcers, nongenital cutaneous infections, sexually transmitted infections

Haemophilus ducreyi, a fastidious gram-negative bacterium, is the causative agent of chancroid, a genital ulcer disease (GUD). The organism is usually spread during sexual intercourse through microabrasions, and the disease usually manifests as multiple painful superficial ulcers associated with inguinal lymphadenitis (). As a result of the painful nature of the lesions, patients usually seek immediate treatment, and asymptomatic carriage is therefore uncommon (). In addition to causing GUD, H. ducreyi has been found in several recent studies to be a major cause of chronic skin ulceration in children from developing countries (-).

The global epidemiology of chancroid is poorly documented, and it is not included in World Health Organization estimates of the global incidence of curable sexually transmitted infections (STIs). There are some key challenges in interpreting data on the epidemiology of H. ducreyi as a causative agent of GUD. First, genital herpes cases are easily misdiagnosed as chancroid on clinical examination. Thus, reports based only on clinical diagnosis can be erroneous. Second, laboratory culture is technically difficult, and the highly sensitive and specific nucleic acid amplification tests, such as PCR, are rarely available outside national reference laboratories or specialized STI research settings, which makes it difficult to confirm clinical diagnoses.

Determination of the true global incidence of chancroid is made more difficult by widespread adoption of syndromic management for bacterial GUD (i.e., treatment with antimicrobial drugs effective against syphilis and chancroid) without microbiological confirmation in many countries. Therefore, countries often report only the total number of GUD cases. In addition, identification of GUD etiology is rarely conducted in resource-poor countries to validate syndromic management for which chancroid could also be common.

Earlier studies of tropical skin ulcers did not generally test for H. ducreyi, with the exception of a small number of case reports ( -). There are major limitations in describing the prevalence of causative agents in tropical skin lesions that typically occur in children in rural areas where there is no access to laboratory facilities. Pathogens such as Fusobacterium fusiforme, Staphylococcus aureus, and Streptococcus pyogenes have been reported from Gram staining of exudative material collected from tropical ulcers (). However, cultures or PCR testing for definitive identification of fastidious pathogens involved has not been traditionally conducted. The purpose of this study was to improve our understanding of the epidemiology of H. ducreyi infection through a systematic review of published data on the proportion of genital and skin ulcers caused by this bacterium.

Methods

Search Strategy and Selection Criteria

A systematic review was conducted to identify all relevant studies that examined the etiology of GUD and nongenital skin ulcers involving H. ducreyi. We searched the National Library of Medicine through PubMed for " H. ducreyi," "chancroid," "genital ulcer," OR "skin ulceration" AND "proportion" OR "prevalence." The search was limited to studies published during January 1, 1980-December 31, 2014. In addition, we searched references of identified articles and other databases for other articles, and we reviewed abstracts, titles, and selected studies potentially containing information on chancroid epidemiology. We contacted researchers who were working with H. ducreyi to identify unpublished literature for inclusion. No language restrictions were set for searches.

The decision tree for inclusion or exclusion of articles is shown in . We included studies if the proportion of etiologic agents in genital ulcers and nongenital skin ulcers, including H. ducreyi, was confirmed by laboratory techniques. Clinical diagnosis of chancroid is often based on the appearance of the ulcer, which is characteristically painful, purulent, and deep with ragged, undermined edges (). However, because the appearance of these ulcers is similar to ulcers caused by other bacteria, clinical diagnosis can be nonspecific or insensitive and often requires laboratory confirmation (). In addition, microscopy identification of typical morphologic features and serologic detection lack sensitivity and specificity (,). Thus, we only considered the following diagnostic methods as providing acceptable evidence of H. ducreyi infection: 1) isolation and identification by culture; or 2) PCR/real-time PCR.

Data Extraction and Synthesis

For all qualifying studies, extracted data included study country, year of study, diagnostic test used for confirmation, total number of H. ducreyi-positive cases, and sample size. Descriptive analyses of extracted data were conducted, and the number of H. ducreyi-confirmed cases was divided by the total number of cases to calculate the proportion of cases caused by H. ducreyi. Studies qualifying for data extraction were grouped into 2 categories: studies conducted before 2000 and studies after 2000. This date separates studies before and after widespread implementation of syndromic management of GUD. Study sites were also plotted by geographic region. No quantitative metaanalysis was undertaken.

Results

We identified 277 records in which we found 46 articles describing 49 studies on GUD that met our inclusion criteria (, ; Technical Appendix). All identified studies were based on cohorts of patients attending STI clinics, including 3 studies that enrolled only commercial sex workers. The age group for all cases was adults >18 years of age, except for 3 studies in Zambia, South Africa, and China, which included patients >16 years of age, and 1 study in Madagascar, which included patients >14 years of age. A total of 9 published studies and 2 unpublished reports that described nongenital skin ulcers caused by H. ducreyi were also included in our systematic review.

Table 1

Table 2

Laboratory confirmation of chancroid by PCR or culture was reported in 33 (67%) and 16 (32%) of the 49 studies, respectively. Of 16 studies that used culture, 7 (43%) used Mueller-Hinton agar with a nutritional supplement (e.g., IsoVitalex; Becton Dickinson, Franklin Lakes, NJ, USA), 1% used hemoglobin, and 5 (31%) used chocolate agar-based media; the remaining studies used other culture media. Five (31%) of 16 studies incubated agar plates at low temperatures (33°C-35°C), and 2 (12%) incubated plates at 36°C. Remaining articles did not specify incubating temperature.

Different PCR primer targets were used to amplify DNA sequences, including the 16S rRNA gene, the groEL gene, and the hemolysin gene. In addition to herpes simplex virus (HSV) PCR, 23 studies used a multiplex PCR that could simultaneously detect the 3 major causes of GUD ( H. ducreyi, Treponema pallidum, and HSV types 1 and 2) (). Studies encompassed 33 countries: 17 in Africa, 4 in Southeast Asia, 3 in Europe, 2 in the Middle East, 3 in South America, and 2 in the Caribbean, 1 in the United States, and 1 in Australia.

Incidence of Chancroid

Of 49 studies on chancroid analyzed, 35 were published during 1980-1999 () and 14 during 2000-2014 (). In general, data showed a clear decrease in the proportion of chancroid during 1980-2014 in all areas analyzed ().

During 1980-1999, the proportion of genital ulcers caused by H. ducreyi in these studies ranged from 0.0% in Thailand and China to 68.9% in South Africa (). Eleven (31.4%) studies reported high proportions (>40%) of cases of infection with H. ducreyi. All of these studies were conducted in countries in Africa (Côte d'Ivoire, Gambia, Kenya, Lesotho, Senegal, South Africa, and Swaziland). Slightly lower proportions (20%-40% of cases) were observed in 15 (42%) studies: 10 in countries in Africa, 2 in the United States during localized outbreaks, 1 in Jamaica, 1 in the Dominican Republic, and 1 in India.

Only a few countries reported low proportions (<10%) of genital ulcers infected with H. ducreyi, including Singapore (8.3%), Peru (5%), Greece (4.6%), the Netherlands (0.9%), United States (3.1%), and Saudi Arabia (2.1%). The study in Saudi Arabia was conducted during 1995-1999; a total of 27,490 patients were examined for STIs. Chancroid was diagnosed by culture and was reported as the least common STI during this survey. The only studies that reported no cases of chancroid were conducted in Thailand in 1996 and China in 1999; both studies used multiplex PCR for detection of GUD cases.

During 2000-2014, the proportion of H. ducreyi infections was low (<10%) in all studies analyzed, except for 1 study in Malawi (15%) (). Studies in 5 countries (Kenya, Namibia, Zambia, Brazil, and Australia) did not report any cases of infection with H. ducreyi. Other studies reporting proportions of infections <10% were conducted in Botswana, Mozambique, South Africa, Uganda, Pakistan, and France. No reports were found for studies in North America, Southeast Asia, or the Caribbean.

Nongenital Skin Infections with H. ducreyi

During 1988-2010, several case reports described 4 children and 4 adults with nonsexually transmitted infections with H. ducreyi that manifested as lower leg lesions but no genital lesions. The reported case-patients were travelers who had been to Fiji ( 7), Samoa ( 8), Vanuatu ( 9), or Papua New Guinea ( 10) (). Outside the south Pacific region, a 5-year-old refugee from Sudan who had lower leg ulceration was also given a diagnosis of infection with H. ducreyi ( 11).

A cohort study conducted in Papua New Guinea in 2014 showed evidence that H. ducreyi is a major cause of chronic skin ulceration; H. ducreyi DNA was identified by PCR in 60.0% of skin lesions in children (). Similar studies in other areas reported laboratory-confirmed skin ulcers in children caused by H. ducreyi in Papua New Guinea (), Solomon Islands (), Vanuatu (C.Y. Chen, pers. comm.), and Ghana () ().

Discussion

Our review confirmed 2 major findings. First, reduction in the proportion of genital ulcers caused by H. ducreyi has been sustained for the past decade and a half. Second, there is increasing evidence that H. ducreyi is a common and newly recognized causative agent of chronic skin ulceration in children from developing countries.

In the 1990s, the global prevalence of chancroid was estimated to be 7 million (). Chancroid was one of the most prevalent GUDs, particularly in resource-poor countries in Africa, Asia, Latin America, and the Caribbean (; reference 51 in Technical Appendix). Recommendations to introduce syndromic management for treatment of GUD caused by bacteria were published by the World Health Organization in 1991 and fully implemented by 2000 (reference 61 in Technical Appendix). Since that time, global incidence of GUDs, particularly chancroid, has decreased substantially, and genital herpes viruses (HSV-1 and HSV-2) have become the predominant cause of GUD (reference 53 in Technical Appendix). Currently in Europe and the United States, chancroid is restricted to rare sporadic cases. Transmission of H. ducreyi remains ongoing in only a few countries that have limited access to health services (,).

Our data show marked decreases in the proportion of GUD caused by H. ducreyi in several countries. Spinola et al. reported similar conclusions obtained from 25 PCR-based studies (reference 62 in online Technical Appendix). For example, in Botswana (), Kenya, (), and South Africa (), the proportion of GUD caused by H. ducreyi decreased from 25%-69% to negligible (0.0%-1.2%) levels (; references 48, 52 in Technical Appendix). Studies in Zambia (reference 56 in Technical Appendix), Namibia (reference 51 in Technical Appendix), and China () did not report any cases of chancroid during 2000-2009. A study in Thailand reported elimination of chancroid by introduction of a condom use program in the 1990s (reference 63 in Technical Appendix). Similar decreases have been reported from Cambodia and Sri Lanka, with rapid elimination of chancroid and congenital syphilis in most settings (reference 63 in Technical Appendix). However, these findings should be interpreted with caution because, given the short duration of infectivity, even a low prevalence of H. ducreyi in a population with GUD implies that a reservoir of infected persons with a high rate of sex partners is present.

Recent research has identified H. ducreyi as a previously unrecognized cause of nongenital skin ulcers in tropical areas. In 2013-2015, six studies in Papua New Guinea (,), the Solomon Islands (), Vanuatu (C.Y. Chen et al., pers. comm.), and Ghana ( 5; C.Y. Chen et al., pers. comm.) showed that a high proportion of laboratory-confirmed skin ulcers were caused by H. ducreyi. Nearly half of the 690 enrolled patients with ulcers in these 6 studies had H. ducreyi detectable by PCR, whereas other bacteria, such as T. pallidum subsp. pertenue, the causative agent of yaws, were detected in 25% of patients.

These cases of infection with H. ducreyi confirmed by molecular analysis suggest that clinicians should be more aware of this newly recognized bacterium in skin ulcers of persons in tropical areas. In the context of new efforts to eradicate yaws, mass treatment with azithromycin in Papua New Guinea reduced the absolute prevalence of ulcers not caused by yaws, which were mainly caused by H. ducreyi, from 2.7% to 0.6% (prevalence ratio 0.23, 95% CI 0.18-0.29) at 12 months after treatment (). However, persistence of H. ducreyi at low levels after mass treatment in Papua New Guinea () and Ghana () suggest that 1 round of mass treatment might not be successful in eradicating H. ducreyi skin ulcers.

Our review has several limitations. First, the increase in HSV-related GUD as a result of immunosuppression by HIV infection would result in a decrease in the proportion of chancroid among all GUD case-patients. Second, the lack of sequential studies performed in similar clinical settings at multiple time points precludes an optimal interpretation of the apparent decrease. Third, results might be affected by poor-quality data from many developing countries and might be inflated by publication bias. Fourth, PCR is more sensitive than culture. Therefore, increasing diagnostic yield might have partially masked the scale of the decrease in H. ducreyi as a cause of GUD.

In summary, we observed a quantitative and sustained reduction in cases of chancroid as a result of antimicrobial drug syndromic management and major social changes. In addition, data from several research groups indicate that H. ducreyi can cause nongenital skin lesions in persons residing in different regions. Further studies of this newly described pathogen skin disease association are required, and appropriate policies are needed that include the routine practice of managing tropical skin ulcers.

Technical Appendix. Additional references on epidemiology of Haemophilus ducreyi infections.

Acknowledgments

M.M. is supported by a Wellcome Trust Clinical Research Fellowship (WT102807).

Biography

Ms. González-Beiras is a predoctoral fellow at Instituto de Higiene e Medicina Tropical, Lisbon, Portugal. Her primary research interests are strategies for elimination of neglected tropical diseases.

Footnotes

Suggested citation for this article: González-Beiras C, Marks M, Chen CY, Roberts S, Mitjà O. Epidemiology of Haemophilus ducreyi infections. Emerg Infect Dis. 2016 Jan [ date cited]. http://dx.doi.org/10.3201/eid2201.150425

References

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Epidemiology of Haemophilus ducreyi Infections

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The global epidemiology of Haemophilus ducreyi infections is poorly documented because of difficulties in confirming microbiological diagnoses. We evaluated published data on the proportion of genital and nongenital skin ulcers caused by H. ducreyi before and after introduction of syndromic management for genital ulcer disease (GUD).

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Detection of Pathogen Using Immunology Method

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Detection of Pathogen Using Immunology Method

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1) IMMUNOCHROMATOGRAPHIC LATERAL FLOW ASSAYS:
Requiring only the dilution of the test agent in a sample buffer and applying several drops (∼200 μl) to the test strip.

A capture antibody is applied in a line on the strip and dried. To perform the test, a specimen is suspended in buffer and added to the pad containing the colloidal gold-labeled antibody.  The antibody specifically binds to antigen present in the specimen, and the resulting complex wicks down the membrane where it binds to the capture antibody.

A positive reaction is visualized as a red line created by the bound colloidal gold.

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How Immunochromatographic Lateral Flow Assays work.

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How Immunochromatographic Lateral Flow Assays work.

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Detection of Pathogen Using Immunology Method

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Detection of Pathogen Using Immunology Method

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2) ELISA
combine the specificity of antibodies with the sensitivity of simple enzyme assays, by using antibodies or antigens coupled to an easily-assayed enzyme. ELISAs can provide a useful measurement of antigen or antibody concentration.

A capture antibody affixed to the solid phase is exposed to a test sample (as well as to positive- and negative-control samples)
After washing, the complex is exposed further to diluted detector antibody specific to the same antigen.

Finally, a conjugate antibody is added and the reaction is visualized. In this system, the antigen must have multiple epitope for antibody binding or a repeating, spatially distant, single epitope

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Enzyme-Linked Immunosorbent Assay (ELISA) - Multi-Lingual Captions

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Primarily a sexually transmitted disease that is most common in resource-poor countries. Rare in North America and Europe.

Caused by the fastidious, gram-negative coccobacillus Haemophilus ducreyi . Classically presents with the acute onset of a painful genital ulcer, and often associated with fluctuant lymphadenitis (bubo formation).

An important co-factor in HIV transmission. HIV status must be assessed.

Most cases resolve with antibiotic therapy; recurrence is rare.

Sexual partners within 10 days prior to onset of symptoms must be traced and treated, even if asymptomatic.

Several reports now describe non-genital cutaneous limb ulcerations due to H ducreyi in yaws-endemic countries.

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Visit us (http://www.khanacademy.org/science/healthcare-and-medicine) for health and medicine content or (http://www.khanacademy.org/test-prep/mcat) for MCAT related content. These videos do not provide medical advice and are for informational purposes only. The videos are not intended to be a substitute for professional medical advice, diagnosis or treatment.

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Gram stain of Haemophilus ducreyi

Adapted from G. Hammond, Public Health Image Library, CDC (1978)

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Buboes associated with Haemophilus ducreyi infection

Adapted from S. Lindsley, Public Health Image Library, CDC (1971)

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Chancroid pustule resembling syphilis

Adapted from Public Health Image Library, CDC (1971)

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Penile ulcers associated with chancroid

Adapted from J. Miller, Public Health Image Library, CDC (1974)

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*Pathophysiology*
-cytocidal toxin (HdCDT)
Haemophilus ducreyi penetrates into host through breaks in the mucosal barriers and microabrasionson the skin. It produces a cytocidal toxin (HdCDT) with swelling properties, which causes cell cycle arrest and apoptosis/necrosis of human cells and contributes to the aggravation of ulcers. Phagocytosis by macrophages is also impaired. Other virulence mechanisms:-
*LspA proteins- have antiphagocytic functions,
*DsrA map-facilitates adherence, and an
*influx transporter- protects pathogen from antimicrobial killing

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Chancroid is a sexually transmitted disease (STD) characterized by painful necrotizing genital ulcers that may be accompanied by inguinal lymphadenopathy. Chancroid was once endemic in many areas of the world, but social awareness of the disease and subsequent changes in characteristics of commercial sexual networks, along with improved diag...

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Mode of Transmission, Symptoms and Treatments

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Mode of Transmission, Symptoms and Treatments

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1) Mode of Transmission
Occurs through direct contact with the lesions. Sexual partners exposed by vaginal, oral or anal sex, without using a condom or dam, are at high risk of infection.

2) Symptoms
-Men may notice a small, red bump on their genitals that may change to an open sore within a day or two. The ulcer may form on any area of the genitals, including the penis and scrotum. The ulcers are frequently painful.
-Women may develop four or more red bumps on the labia, between the labia and anus, or on the thighs. The labia are the folds of skin that cover the female genitals. After the bumps become ulcerated, or open, women may experience a burning or painful sensation during urination or bowel movements.

3) Treatments
-Chancroid may be successfully treated with medication or surgery.
-Doctor will prescribe antibiotics to kill the bacteria that are causing ulcers. Antibiotics may also help decrease the chance of scarring as the ulcer heals.
-Doctor may drain a large and painful abscess in lymph nodes with a needle or through surgery. This reduces swelling and pain as the sore heals but might cause some light scarring at the site.

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Host–pathogen interplay of Haemophilus ducreyi

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Host–pathogen interplay of Haemophilus ducreyi

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How pathogen invade and what immmune response involves?

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How pathogen invade and what immmune response involves?

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1. How pathogen invade?

H. ducreyi infect  human skin.

The host responds with a robust infiltrate of polymorphonuclear leukocytes (PMNs) and macrophages.

This will leads to development of lesions which progress from papules to pustules to ulcers.

These bacteria are surrounded by PMNs and macrophages but remain extracellular.

2. What immmune response involves?

- A delayed-type (type IV) hypersensitivity reaction is response to H. ducreyi.Type IV hypersensitivity is a cell mediated immune response. This response will not effective against H. ducreyi infection. This is because cell mediated immune response only effective killing intracellular bacteria and viruses. H. ducreyi is extracellular in present to Chancroid lesions. Suggested that humoral immune response could be protective against infection. Protection does not 100% prevent from infection but reduced the viable H. ducreyi cells .

The bacteria induces rapid recruitment of innate and adaptive immune cells to infected sites. Then, dermal infiltrate of memory/effector CD4 and CD8 T cells, NK cells, myeloid DC, and macrophages. Only few B cells and no serum antibody induction during experimental infection. The cutaneous immune responses to H. ducreyi could promote phagocytosis and disease resolution.

Reference

1. Cole, L. E., Toffer, K. L., Fulcher, R. A., San Mateo, L. R., Orndorff, P. E., & Kawula, T. H. (2003). A Humoral Immune Response Confers Protection against Haemophilus ducreyi Infection. Infection and Immunity, 71(12), 6971–6977. http://doi.org/10.1128/IAI.71.12.6971-6977.2003.

2.  Janowicz, D. M., Li, W., & Bauer, M. E. (2010). Host-pathogen Interplay of Haemophilus ducreyi. Current Opinion in Infectious Diseases, 23(1), 64–69. http://doi.org/10.1097/QCO.0b013e328334c0cb

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A Humoral Immune Response Confers Protection against Haemophilus ducreyi Infection

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A Humoral Immune Response Confers Protection against Haemophilus ducreyi Infection