From August 15, 2015 to March 5, 2016, Tanzania reported 16,521 cholera cases and 251 deaths, with 4,596 cases and 44 deaths in its largest city, Dar es Salaam. To evaluate outbreak response efforts, we conducted a household survey with drinking water testing in the five most affected wards in Dar es Salaam. We interviewed 641 households 6 months after the beginning of the outbreak. Although most respondents knew that cholera causes diarrhea (90%) and would seek care if suspecting cholera (95%), only 45% were aware of the current outbreak in the area and only 5% would use oral rehydration salts (ORS) if ill. Of 200 (31%) respondents reporting no regular water treatment, 46% believed treatment was unnecessary and 18% believed treatment was too expensive. Fecal contamination was found in 45% of water samples and was associated with water availability (P = 0.047). Only 11% of samples had detectable free chlorine residual, which was associated with water availability (P = 0.025), reported current water treatment (P = 0.006), and observed free chlorine product in the household (P = 0.015). The provision of accessible, adequately chlorinated water supply, and implementation of social mobilization campaigns advocating household water treatment and use of ORS should be prioritized to address gaps in cholera prevention and treatment activities.

Introduction. Shigella sonnei, the cause of bacillary dysentery, belongs to Gram-negative enteropathogenic bacteria. S. sonnei contains a 210 kb virulence plasmid that encodes an O-antigen gene cluster of LPSs. However, this virulence plasmid is frequently lost during replication. It is well-documented that after losing the O-antigen and becoming rough strains, the Gram-negative bacteria may express an LPS core on its surface. Previous studies have suggested that by using the LPS core, Gram-negative bacteria can interact with several C-type lectin receptors that are expressed on antigen-presenting cells (APCs).Hypothesis/Gap Statement. S. sonnei by losing the virulence plasmid may hijack APCs via the interactions of LPS-CD209/CD207.Aim. This study aimed to investigate if the S. sonnei rough strain, by losing the virulence plasmid, interacted with APCs that express C-type lectins of human CD207, human CD209a and mouse CD209b.Methodology. SDS-PAGE silver staining was used to examine the O-antigen expression of S. sonnei WT and its rough strain. Invasion assays and inhibition assays were used to examine the ability of S. sonnei WT and its rough strain to invade APCs and investigate whether CD209 and CD207 are receptors for phagocytosis of rough S. sonnei. Animal assays were used to observe the dissemination of S. sonnei.Results. S. sonnei did not express O-antigens after losing the virulence plasmid. The S. sonnei rough strain invades with APCs, including human dendritic cells (DCs) and mouse macrophages. CD209 and CD207 are receptors for phagocytosis of rough S. sonnei. Expression of the O-antigen reduces the ability of the S. sonnei rough strain to be disseminated to mesenteric lymph nodes and spleens.Conclusion. This work demonstrated that S. sonnei rough strains - by losing the virulence plasmid - invaded APCs through interactions with CD209 and CD207 receptors.

Carbapenemase-producing carbapenem-resistant Enterobacteriaceae (CP-CRE) express plasmid-encoded carbapenemases, enzymes that inactivate carbapenem antibiotics. They have the potential for epidemic spread through person-to-person transmission and horizontal transfer of resistance mechanisms (1,2). Typically, CP-CRE are associated with health care exposure. Clinical CRE infections can have mortality rates as high as 50% (3); however, the majority of CRE patients are asymptomatic. These asymptomatic colonized patients can serve as a source for transmission to other patients (4).

Background: Histoplasmosis is a fungal infection associated with exposure to bat guano. An outbreak of an unknown severe febrile illness occurred among tunnel workers in the Dominican Republic (DR), and resulted in several deaths. We conducted an investigation to confirm etiology and recommend control measures. Methods: A case was defined as fever and ≥2 symptoms consistent with histoplasmosis in a tunnel worker, July-September, 2015. We interviewed workers and family members, reviewed medical records, tested serum and urine for Histoplasma antigen/antibody, and conducted a cohort study to identify risk factors for histoplasmosis and severe infection (intensive care). Results: A crew of 36 male workers removed large amounts of bat guano from tunnels without respiratory protection for a median of 24 days per worker (range: 1-25). Median age was 32 years (range: 18-62); none were immunocompromised. Thirty (83%) workers had illness that met the case definition of whom 28 (93%) were hospitalized, 9 (30%) required intensive care, 6 (20%) required intubation, and 3 (10%) died. The median time from symptom onset to antifungal treatment was 6 days (range: 1-11). Twenty-two of 34 (65%) workers had laboratory evidence of histoplasmosis infection. Conclusions: Severe illnesses and death likely resulted from exposure to large inocula of Histoplasma capsulatum spores in an enclosed space, lack of respiratory protection, and delay in recognition and treatment. Clinician education about histoplasmosis, improved laboratory capacity to diagnose fungal infections, and occupational health guidance to protect workers against endemic fungi are recommended in the DR to prevent future outbreaks.

On August 15, 2015, the Tanzanian Ministry of Health, Community Development, Gender, Elderly and Children (MOHCDGEC) was notified about a case of acute watery diarrhea with severe dehydration in a patient in Dar es Salaam. Vibrio cholerae O1, biotype El tor, serotype Ogawa, was isolated from the patient’s stool and an investigation was initiated. MOHCDGEC defined a suspected cholera case as the occurrence of severe dehydration or death from acute watery diarrhea in a person aged ≥5 years, or acute, profuse watery diarrhea with or without vomiting in a person aged ≥2 years in a region with an active cholera outbreak. A confirmed cholera case was defined as isolation of V. cholerae O1 from the stool of a person with suspected cholera. Tanzania’s first reported cholera epidemic was in 1974 with intermittent outbreaks since then; the largest epidemic occurred in 1997, with 40,249 cases and 2,231 deaths (case fatality rate [CFR] was 5.5%) (1). | As of November 26, 2016, the current epidemic continues, affecting 23 (92%) of 25 regions in mainland Tanzania (excluding the Zanzibar archipelago), with a cumulative reported case count of 23,258 and a cumulative CFR of 1.5%. The median number of reported cholera cases per week was 271 (range = 5–1,240) (Figure). Approximately half of all reported cases have been from four regions: Dar es Salaam (5,104; 22%), Morogoro (3,177; 14%), Mwanza (2,311; 10%), and Mara (2,299; 10%). Of 511 stool specimens tested during August 17, 2015–March 18, 2016 at the National Health Laboratory-Quality Assurance Training Center in Dar es Salaam, 268 (52%) were positive for V. cholerae; all specimens were serogroup O1, biotype El tor, serotype Ogawa. Antimicrobial resistance (AMR) testing revealed sensitivity to cotrimoxazole, ceftriaxone, tetracycline, ciprofloxacin, and chloramphenicol, and resistance to nalidixic acid and ampicillin.

BACKGROUND: Human cases of highly pathogenic avian influenza (HPAI) A (H5N1) have high mortality. Despite abundant data on seasonal patterns in influenza epidemics, it is unknown whether similar patterns exist for human HPAI H5N1 cases worldwide. Such knowledge could help decrease avian-to-human transmission through increased prevention and control activities during peak periods. METHODS: We performed a systematic search of published human HPAI H5N1 cases to date, collecting month, year, country, season, hemisphere, and climate data. We used negative binomial regression to predict changes in case incidence as a function of season. To investigate hemisphere as a potential moderator, we used AIC and the likelihood-ratio test to compare the season-only model to nested models including a main effect or interaction with hemisphere. Finally, we visually assessed replication of seasonal patterns across climate groups based on the Koppen-Geiger climate classification. FINDINGS: We identified 617 human cases (611 with complete seasonal data) occurring in 15 countries in Southeast Asia, Africa, and the Middle East. Case occurrence was much higher in winter (n = 285, p = 0.03) than summer (n = 64), and the winter peak occurred across diverse climate groups. There was no significant interaction between hemisphere and season. INTERPRETATION: Across diverse climates, HPAI H5N1 virus infection in humans increases significantly in winter. This is consistent with increased poultry outbreaks and HPAI H5N1 virus transmission during cold and dry conditions. Prioritizing prevention and control activities among poultry and focusing public health messaging to reduce poultry exposures during winter months may help to reduce zoonotic transmission of HPAI H5N1 virus in resource-limited settings.