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Communicable Diseases Surveillance Bulletin
May 2010
Volume 8, no. 2
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FOREWORD
The May Bulletin of 2010 includes surveillance reports for the bacterial and fungal diseases under surveillance in the GERMS-SA programme. The report includes a summary of the main findings from national surveillance including enhanced surveillance sites, at 25 hospitals in 9 provinces, for the year 2009.
These reports include updates on emerging antimicrobial resistance in several pathogens: several fluoroquinolone-resistant non-typhoidal Salmonella isolates; a single, fluoroquinolone-resistant Shigella isolate; and significantly increased penicillin and ceftriaxone resistance amongst Streptococcus pneumoniae isolates predominantly from young children between 2008 and 2009. The emergence of antimicrobial resistance may impact on the choice of empiric treatment of common disease syndromes such as meningitis. Consideration of these data will need to be included in updated clinical guidelines for the management of these syndromes.
The pneumococcal conjugate vaccine was introduced into the Expanded Programme on Immunisation in April 2009. Despite low, estimated coverage of PCV and a high HIV prevalence, GERMS-SA has already demonstrated a significant decrease in serotype-specific, invasive pneumococcal disease amongst South African infants. These early, direct effects are likely to be amplified as vaccine coverage increases. This also highlights the value of laboratory-based surveillance programmes in providing valuable information on the impact of new vaccine programmes.
The incidence of cryptococcosis, a useful, sentinel, HIV-associated opportunistic infection, has stabilised. This may be an indication that the antiretroviral treatment programme has reached sufficient people to prevent an escalation in the number of new cases year-on-year. However, the overall incidence of this life-threatening fungal disease still remains high and work needs to be done to ensure that more cases are prevented and new cases are managed optimally. Early in 2010 the late Deputy Minister of Health announced a new plan to scale up access to HIV prevention and treatment1. As South Africa prepares to enter a new era of enhanced access to HIV prevention and care, GERMS-SA is well positioned to monitor the impact of these new interventions on the burden of opportunistic infections in South Africa.
Reference
1. Cabinet gives thumbs-up to new Aids plan. http://www.mg.co.za/article/2010-03-11-cabinet-gives-thumbsup-to-new-aids-plan. Accessed 20 April 2010
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- GERMS-SA surveillance report for South Africa, 2009, including:-
- Enhanced surveillance site (ESS) project
- Salmonella enterica serotype Typhi and S. enterica serotypes Paratyphi A, Paratyphi B and Paratyphi C
- Non-typhoidal Salmonella enterica (NTS)
- Shigella species
- Diarrhoeagenic Escherichia coli (DEC)
- Vibrio cholerae O1
- Cryptococcus species
- Pneumocystis jirovecii
- Neisseria meningitidis
- Haemophilus influenzae
- Streptococcus pneumoniae
- Table 1: Provisional listing of laboratory-confirmed cases of diseases under surveillance : 01 January— 31 March 2010
- Table 2: Provisional laboratory indicators for NHLS and NICD: 01 January—31 March 2010
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THE GROUP FOR ENTERIC, RESPIRATORY & MENINGEAL DISEASE SURVEILLANCE IN SOUTH AFRICA (GERMS-SA)
INTRODUCTION
The Group for Enteric, Respiratory and Meningeal disease Surveillance in South Africa (GERMS-SA) has coordinated ongoing, national, population-based, laboratory-based, surveillance for several bacterial and fungal diseases since 2003. The system has been previously described(1). Further details are available in the GERMS-SA Annual Report 2009 (access at www.nicd.ac.za). In this edition of the Communicable Diseases Surveillance Bulletin, we report summarised results, by pathogen/disease under surveillance, for 2009. Incidence rates were calculated using mid-year population estimates for 2008 and 2009 from Statistics South Africa (Table 1)(2). Incidence rates in the HIV-infected and AIDS populations were calculated for 2008 and 2009, using estimated population denominators from the Actuarial Society of South Africa (ASSA) 2003 model (Table 1), assuming that the HIV/AIDS prevalence amongst cases with known status was similar to those with unknown status(3). All reported incidence rates are expressed as cases per 100,000 population, unless otherwise stated. Surveillance cases which were detected by audit of the NHLS Corporate Data Warehouse are included in this report.
Table 1: Population denominators used to calculate incidence rates, 2008 and 2009
| Province |
General population* |
HIV-infected population** |
AIDS population** |
2008 |
2009 |
2008 |
2009 |
2008 |
2009 |
| Eastern Cape |
6,579,245 |
6,648,601 |
728,915 |
757,818 |
75,300 |
79,705 |
| Free State |
2,877,694 |
2,902,518 |
393,863 |
395,344 |
49,656 |
50,111 |
| Gauteng |
10,447,246 |
10,531,308 |
1,446,094 |
1,454,006 |
165,632 |
166,078 |
| KwaZulu-Natal |
10,105,437 |
10,449,141 |
1,560,573 |
1,567,048 |
204,976 |
206,294 |
| Limpopo |
5,274,836 |
5,227,503 |
433,820 |
451,553 |
45,229 |
47,390 |
| Mpumalanga |
3,589,909 |
3,606,572 |
455,135 |
459,051 |
59,581 |
59,336 |
| Northern Cape |
1,125,881 |
1,147,137 |
67,330 |
69,595 |
6,787 |
7,458 |
| North West |
3,425,153 |
3,450,517 |
496,274 |
501,066 |
60,618 |
62,634 |
| Western Cape |
5,261,922 |
5,356,844 |
297,669 |
309,102 |
25,499 |
28,391 |
| South Africa |
48,687,323 |
49,320,141 |
5,879,673 |
5,964,583 |
693,278 |
707,397 |
Data source: *Statistics South Africa; **Actuarial Society of South Africa (ASSA)
References
- GERMS-SA Annual Report 2006. Available from: www.nicd.ac.za/units/germs 2006.
- Statistics South Africa. Mid-year population estimates, South Africa, 2009. P0302. 27 July 2009. Available from: http://www.statssa.gov.za/publications/P0302/P03022009.pdf. 2009. Accessed 15 April 2010.
- Actuarial Society of South Africa AIDS Committee. ASSA2003 AIDS and demographic model, 2005. Available from: http://www.actuarialsociety.org.za/Models-274.aspx. Accessed 15 April 2010
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ENHANCED SURVEILLANCE SITE (ESS) PROJECT
National Microbiology Surveillance Unit, National Institute for Communicable Diseases
In 2009, of 23199 surveillance case patients detected by GERMS-SA, 5854 (25%) were diagnosed at ESS. Of case patients with recorded HIV status, 85% (3368/3979) were HIV-infected (Table 1). The proportion of case patients with confirmed HIV infection varied by disease: unsurprisingly, a very high proportion of patients with AIDS-defining infections like cryptococcosis (98%) and PCP (88%) were HIV-infected; HIV infection in patients with invasive pneumococcal disease and non-typhoidal salmonellosis, for which HIV is a known risk factor, were 74% and 75% respectively; and just less than half (46%) of patients with invasive meningococcal disease were HIV-infected.
Table 1: Number and percentage* of patients, diagnosed with laboratory-confirmed disease at GERMS-SA enhanced surveillance sites, with confirmed HIV-1 infection**, South Africa, 2009, n=5,854.
| Pathogen |
Case patients, n |
Case patients with completed case report forms, n (%) |
Case patients with known HIV status, n (%) |
Case patients with confirmed HIV infection, n (%) |
| Cryptococcus species |
2,853 |
2371 (83) |
1927 (81) |
1887 (98) |
| Pneumocystis jirovecii |
149 |
138 (93) |
135 (98) |
119 (88) |
| Neisseria meningitidis |
170 |
156 (92) |
115 (74) |
53 (46) |
| Streptococcus pneumoniae |
2034 |
1755 (86) |
1363 (78) |
1012 (74) |
| Haemophilus influenzae |
177 |
145 (82) |
107 (74) |
53 (50) |
| Salmonella species |
430 |
356 (83) |
302 (85) |
226 (75) |
| Shigella species |
41 |
39 (95) |
30 (77) |
18 (60) |
| Total |
5,854 |
4,960 (85) |
3,979 (80) |
3,368 (85) |
*The percentage (in brackets) in each cell was calculated using the numerator from that cell and the corresponding denominator from the cell to the left; **HIV infection was confirmed by an age-appropriate, laboratory test and recorded by surveillance officers at enhanced surveillance sites.
Report compiled by (alphabetical order): Susan Meiring and Vanessa Quan
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SALMONELLA ENTERICA SEROTYPE TYPHI AND S. ENTERICA SEROTYPES PARATYPHI A, PARATYPHI B AND PARATYPHI C
Enteric Diseases Reference Unit, National Institute for Communicable Diseases
Results
Salmonella Typhi isolates from both invasive and non-invasive sites are reported in Table 1. Two isolates of Salmonella Paratyphi A were received from Western Cape and two from North West Province, all from adults; a single isolate of Salmonella Paratyphi B L (+) tartrate (+) (Salmonella Paratyphi B var. Java) was received from a 32 month-old child in the Free State. No isolates of Salmonella Paratyphi C were received. The number of isolates within each age group is reported in Table 2, indicating that most isolates were from children in the 5-14 year age group, although infection was also seen in older and younger age groups. Salmonella Typhi isolation by month suggested a seasonal pattern in 2009, although numbers are too low to be conclusive (Figure 1). No major outbreaks were detected in 2009. A single isolate of Salmonella Typhi was resistant to ciprofloxacin (1) (Table 3), the treatment of choice. Two Salmonella Paratyphi A isolates were available for susceptibility testing: both were resistant to nalidixic acid, but susceptible to ampicillin, cotrimoxazole and chloramphenicol. The Salmonella Paratyphi B isolate was resistant to ampicillin, chloramphenicol and nalidixic acid.
Discussion Salmonella Typhi isolates from both invasive and non-invasive sites were included in these analyses, as both added to the burden of infection in South Africa and thus represented a public health risk, although data may not reflect actual burden of disease. This is compounded by the challenges of alternative diagnostic methods for typhoid fever, including clinical and serological diagnosis. The number of reported Salmonella Typhi isolates was regarded as a substantial underestimate and thus incidence rates were not calculated. These results reflect culture-confirmed cases, and thus excluded those patients in whom a serological or clinical diagnosis was made without culture. Certain antimicrobials were tested for epidemiological purposes only, and should not be used for treatment of typhoid fever. Nalidixic acid resistance may be used as a marker for quinolone resistance; it is indicative of the potential for an organism to develop fluoroquinolone resistance (2). Response to ciprofloxacin may be poor in the presence of nalidixic acid resistance. Ceftriaxone would be regarded as the alternative therapy of choice in these cases, as well as those typhoid fever cases where the organism is fully resistant to ciprofloxacin. The ciprofloxacin E-test is recommended to guideantimicrobial management in such cases (2).
Table 1: Number of invasive and non-invasive Salmonella Typhi isolates reported to GERMS-SA, South Africa, 2009, n=66.
| Province |
Non-invasive Salmonella Typhi |
Invasive Salmonella Typhi |
| Eastern Cape |
2 |
10 |
| Free State |
1 |
2 |
| Gauteng |
1 |
25 |
| KwaZulu-Natal |
0 |
4 |
| Limpopo |
0 |
0 |
| Mpumalanga |
3 |
5 |
| Northern Cape |
0 |
1 |
| North West |
0 |
1 |
| Western Cape |
1 |
10 |
| South Africa |
8 |
58 |
Table 2: Number of Salmonella Typhi isolates reported to GERMS-SA by age category, South Africa, 2009, n=66.
| Age category (years) |
Salmonella Typhi |
| Neonate |
0 |
| < 1 |
0 |
| 1 - 4 |
7 |
| 5 - 14 |
22 |
| 15 - 24 |
12 |
| 25 - 34 |
5 |
| 35 - 44 |
10 |
| 45 - 54 |
2 |
| 55 - 64 |
3 |
| ≥ 65 |
3 |
| Unknown |
2 |
| Total |
66 |

Figure 1: Number of non-invasive and invasive cases of Salmonella Typhi and Paratyphi A and B, reported to GERMS-SA, by month of specimen collection, South Africa, 2009, n=71 (including audit reports).
Table 3: Antimicrobial susceptibility test results for all Salmonella Typhi isolates received by GERMS-SA, South Africa, 2009, n=65 (excluding audit reports).
| Antimicrobial agent |
Susceptible (%) |
Intermediate (%) |
Resistant (%) |
| Ampicillin |
50 |
(77) |
0 |
(0) |
15 |
(23) |
| Cotrimoxazole |
52 |
(80) |
0 |
(0) |
13 |
(20) |
| Chloramphenicol |
58 |
(89) |
0 |
(0) |
7 |
(11) |
| Nalidixic acid |
53 |
(82) |
0 |
(0) |
12 |
(18) |
| Ciprofloxacin |
64 |
(98) |
0 |
(0) |
1 |
(2) |
| Tetracycline |
56 |
(86) |
1 |
(2) |
8 |
(12) |
| Kanamycin |
65 |
(100) |
0 |
(0) |
0 |
(0) |
| Streptomycin |
53 |
(82) |
0 |
(0) |
12 |
(18) |
| Imipenem |
65 |
(100) |
0 |
(0) |
0 |
(0) |
| Ceftriaxone |
65 |
(100) |
0 |
(0) |
0 |
(0) |
References
- Keddy KH, Smith AM, Sooka A, Ismail H, Oliver S. Fluoroquinolone resistant typhoid fever, South Africa. Emerg.Infect Dis. 2010 May;16(5):879-80
- Crump JA, Barrett TJ, Nelson JT, Angulo FJ. Reevaluating fluoroquinolone breakpoints for Salmonella enterica serotype Typhi and for non-Typhi salmonellae. Clin Infect Dis 2003 Jul 1;37(1):75-81.
Report compiled by: Karen Keddy
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NON-TYPHOIDAL SALMONELLA ENTERICA (NTS)
Enteric Diseases Reference Unit, National Institute for Communicable Diseases
Results
Both invasive and non-invasive disease appeared to have a seasonal prevalence in the warmer months (Figure 1). The number of cases of invasive and non-invasive disease, by province, reported to GERMS-SA, is stated in Table 1. The number of cases of invasive and non-invasive disease, by age group, is shown in Table 2, but incidence rates were only calculated for invasive NTS, due to differences in stool-taking practices in adult and paediatric medical care. Most invasive isolates were identified from blood cultures, although isolates were frequently identified from both blood culture and another site, including stool and other normally-sterile sites (Table 3). Multi-drug resistance remained a challenge, including resistance to first-line antimicrobial agents and the quinolones (Table 4). Of 2094 NTS isolates tested, 149 (7%) were extended-spectrum beta-lactamase (ESBL) producers (Table 4). Multi-drug resistant serotypes included primarily Salmonella Typhimurium and Salmonella Isangi (Table 5).
Discussion
Non-typhoidal salmonellosis may be a food-borne disease, for which data are poorly captured in South Africa, and where the patients normally present with gastro-enteritis, or may be an AIDS-defining illness, in which case the organism frequently becomes invasive. No marked seasonal prevalence was noted in 2009 for invasive or non-invasive isolates. Salmonella Infantis appeared to gain importance as a common serotype in South Africa. Certain antimicrobial agents were tested for epidemiological reasons only, and should not be used for treatment. Antimicrobial resistance remained a cause for concern.

Figure 1: Number of non-invasive and invasive, non-typhoidal Salmonella cases, reported to GERMS-SA, by month of specimen collection, South Africa, 2009, n=2555 (including audit reports).
Table 1: Number* of invasive and non-invasive non-typhoidal Salmonella isolates reported to GERMS-SA, by province, South Africa, 2009, n=2555 (including audit reports).
| Province |
Non-invasive, non-typhoidal Salmonella |
Invasive, non-typhoidal Salmonella |
| Eastern Cape |
192 |
63 |
| Free State |
50 |
30 |
| Gauteng |
849 |
396 |
| KwaZulu-Natal |
156 |
93 |
| Limpopo |
37 |
9 |
| Mpumalanga |
161 |
45 |
| Northern Cape |
30 |
12 |
| North West |
78 |
36 |
| Western Cape |
239 |
79 |
| South Africa |
1792 |
763 |
Table 2: Number of cases and incidence rates for invasive* non-typhoidal Salmonella reported to GERMS-SA by age category, South Africa, 2009, n=2555 (including audit reports).
| Age Category (years) |
Cases |
Non-invasive |
Invasive |
Incidence rate for invasive disease ** |
| 0 - 4 |
711 |
215 |
4.24 |
| 5 - 14 |
172 |
35 |
0.34 |
| 15 - 24 |
116 |
58 |
0.57 |
| 25 - 34 |
213 |
142 |
1.71 |
| 35 - 44 |
196 |
154 |
2.69 |
| 45 - 54 |
136 |
85 |
1.98 |
| 55 - 64 |
90 |
32 |
1.09 |
| ≥ 65 |
93 |
18 |
0.75 |
| Unknown |
65 |
24 |
- |
| Total |
1792 |
763 |
1.55 |
*Incidence rates for non-invasive non-typhoidal Salmonella were not calculated because specimens may not have been submitted for culture from all patients, with gastroenteritis due to non-typhoidal Salmonella, in clinical practice; **Incidence rates are expressed as cases per 100,000 population.
Table 3: Number of non-typhoidal Salmonella isolates reported to GERMS-SA by primary anatomical site of isolation*, South Africa, 2009, n=2555 (including audit reports).
| Specimen |
n |
% |
| CSF |
33 |
1.29 |
| Blood culture |
643 |
25.17 |
| Stool |
1491 |
58.36 |
| Other |
388 |
15.19 |
| Total |
2555 |
100 |
Table 4: Antimicrobial susceptibility test results for all non-typhoidal Salmonella isolates received by GERMS-SA, South Africa, 2009, n=2094 (excluding audit reports).
| Antimicrobial agent |
Susceptible (%) |
Intermediate (%) |
Resistant (%) |
| Ampicillin |
1673 |
(80) |
0 |
(0) |
421 |
(20) |
| Cotrimoxazole |
1686 |
(81) |
0 |
(0) |
408 |
(19) |
| Chloramphenicol |
1710 |
(82) |
18 |
(1) |
366 |
(17) |
| Nalidixic acid |
1846 |
(88) |
0 |
(0) |
248 |
(12) |
| Ciprofloxacin |
2087 |
(99.7) |
4 |
(0.2) |
3 |
(0.1) |
| Tetracycline |
1365 |
(65) |
212 |
(10) |
517 |
(25) |
| Kanamycin |
1948 |
(93) |
47 |
(2) |
99 |
(5) |
| Streptomycin |
1592 |
(76) |
0 |
(0) |
502 |
(24) |
| Imipenem |
2094 |
(100) |
0 |
(0) |
0 |
(0) |
| Ceftriaxone |
1944 |
(93) |
1 |
(0.1) |
149 |
(6.9) |
Table 5: Commonest invasive and non-invasive non-typhoidal Salmonella serotypes reported to GERMS-SA by province, South Africa, 2009, n=1579 (excluding audit reports).
| Province |
Serotype |
Dublin |
Enteritidis |
Infantis |
Isangi |
Typhimurium |
| Eastern Cape |
4 |
15 |
7 |
18 |
118 |
| Free State |
2 |
8 |
7 |
0 |
32 |
| Gauteng |
19 |
223 |
182 |
28 |
326 |
| KwaZulu-Natal |
8 |
53 |
16 |
35 |
86 |
| Limpopo |
0 |
2 |
1 |
1 |
3 |
| Mpumalanga |
4 |
21 |
12 |
0 |
68 |
| Northern Cape |
1 |
6 |
0 |
0 |
13 |
| North West |
0 |
16 |
3 |
1 |
19 |
| Western Cape |
10 |
58 |
39 |
6 |
108 |
| South Africa |
48 |
402 |
267 |
89 |
773 |
Results
Both invasive and non-invasive disease appeared to have a seasonal prevalence in the warmer months (Figure 1). The number of cases of invasive and non-invasive disease, by province, reported to GERMS-SA, is stated in Table 1. The number of cases of invasive and non-invasive disease, by age group, is shown in Table 2, but incidence rates were only calculated for invasive NTS, due to differences in stool-taking practices in adult and paediatric medical care. Most invasive isolates were identified from blood cultures, although isolates were frequently identified from both blood culture and another site, including stool and other normally-sterile sites (Table 3). Multi-drug resistance remained a challenge, including resistance to first-line antimicrobial agents and the quinolones (Table 4). Of 2094 NTS isolates tested, 149 (7%) were extended-spectrum beta-lactamase (ESBL) producers (Table 4). Multi-drug resistant serotypes included primarily Salmonella Typhimurium and Salmonella Isangi (Table 5).
Discussion
Non-typhoidal salmonellosis may be a food-borne disease, for which data are poorly captured in South Africa, and where the patients normally present with gastro-enteritis, or may be an AIDS-defining illness, in which case the organism frequently becomes invasive. No marked seasonal prevalence was noted in 2009 for invasive or non-invasive isolates. Salmonella Infantis appeared to gain importance as a common serotype in South Africa. Certain antimicrobial agents were tested for epidemiological reasons only, and should not be used for treatment. Antimicrobial resistance remained a cause for concern.
Report compiled by: Karen Keddy
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SHIGELLA SPECIES
Enteric Diseases Reference Unit, National Institute for Communicable Diseases
Higher isolation rates in January to March and increasing numbers from October to December in 2009 suggested seasonality (Figure 1). Although the primary burden of disease due to Shigella is non-invasive dysentery or diarrhoea, invasive disease remained an important cause of morbidity in South Africa (Table 1). The predominant burden of disease, including both invasive and non-invasive shigellosis, was in the under-five-year age group (Table 2). Quinolone resistance remained low, but fluoroquinolone resistance appeared to be emerging (Table 3). Three of 1612 (0.2%) isolates tested were ESBL-producers. S. flexneri 2a remained the commonest cause of shigellosis in South Africa and S. dysenteriae type 1 was rarely isolated (Table 4).
Discussion
Shigella infection is largely due to water-borne outbreaks in South Africa, although person-to-person transmission may play a role. Certain antimicrobials were tested for surveillance purposes only, and should not be used for treatment. Resistance to the third generation cephalosporins and fluoroquinolones remains low, but should continue to be monitored.

Figure 1: Number of non-invasive and invasive Shigella isolates, reported to GERMS-SA, by month of specimen collection, South Africa, 2009, n=1812 (including audit reports).
Table 1: Number of invasive and non-invasive Shigella isolates reported to GERMS-SA by province, South Africa, 2009, n=1812 (including audit reports).
| Province |
Non-invasive Shigella |
Invasive Shigella |
| Eastern Cape |
277 |
3 |
| Free State |
80 |
4 |
| Gauteng |
664 |
21 |
| KwaZulu-Natal |
146 |
9 |
| Limpopo |
16 |
2 |
| Mpumalanga |
92 |
5 |
| Northern Cape |
20 |
0 |
| North West |
27 |
4 |
| Western Cape |
422 |
20 |
| South Africa |
1744 |
68 |
Table 2: Number of cases* and incidence rates for Shigella (invasive and non-invasive)** reported to GERMS-SA by age category, South Africa, 2009, n=1812.
| Age Category (years) |
Cases |
Non-invasive |
Invasive |
Incidence rate for invasive disease ** |
| 0 - 4 |
810 |
27 |
0.53 |
| 5 - 14 |
272 |
5 |
0.05 |
| 15 - 24 |
94 |
4 |
0.04 |
| 25 - 34 |
188 |
11 |
0.13 |
| 35 - 44 |
121 |
5 |
0.09 |
| 45 - 54 |
76 |
9 |
0.21 |
| 55 - 64 |
59 |
4 |
0.14 |
| ≥ 65 |
70 |
1 |
0.04 |
| Unknown |
54 |
2 |
- |
| Total |
1744 |
68 |
0.14 |
*Cases may be under-reported due to local clinical practices: no mixed infections were identified. **Incidence rates are expressed as cases per 100,000 population
Table 3: Antimicrobial susceptibility test results for Shigella isolates received by GERMS-SA, South Africa, 2009, n=1612.
| Antimicrobial agent |
Susceptible (%) |
Intermediate (%) |
Resistant (%) |
| Ampicillin |
866 |
(54) |
0 |
(0) |
746 |
(46) |
| Cotrimoxazole |
259 |
(16) |
0 |
(0) |
1353 |
(84) |
| Chloramphenicol |
1102 |
(68) |
8 |
(1) |
502 |
(31) |
| Nalidixic acid |
1594 |
(99) |
0 |
(0) |
18 |
(1) |
| Ciprofloxacin |
1611 |
(99.9) |
0 |
(0) |
1 |
(0.1) |
| Tetracycline |
679 |
(42) |
24 |
(2) |
909 |
(56) |
| Kanamycin |
1604 |
(99.5) |
1 |
(0.1) |
7 |
(0.4) |
| Streptomycin |
644 |
(40) |
0 |
(0) |
968 |
(60) |
| Imipenem |
1612 |
(100) |
0 |
(0) |
0 |
(0) |
| Ceftriaxone |
1609 |
(99.8) |
0 |
(0) |
3 |
(0.2) |
Table 4: Commonest* invasive and non-invasive Shigella serotypes reported to GERMS-SA by province, South Africa, 2009, n=1169 (excluding audit reports).
| Province |
S. dysenteriae type 1 |
S. flexneri type 1b |
S. flexneri type 2a |
S. flexneri type 6 |
S. sonnei phase I/II |
| Eastern Cape |
0 |
91 |
33 |
17 |
23 |
| Free State |
0 |
25 |
8 |
2 |
16 |
| Gauteng |
1 |
158 |
57 |
70 |
199 |
| KwaZulu-Natal |
0 |
38 |
16 |
13 |
20 |
| Limpopo |
0 |
2 |
0 |
2 |
1 |
| Mpumalanga |
1 |
14 |
5 |
11 |
21 |
| Northern Cape |
0 |
3 |
1 |
7 |
0 |
| North West |
0 |
2 |
1 |
1 |
8 |
| Western Cape |
0 |
175 |
64 |
25 |
38 |
| South Africa |
2 |
508 |
185 |
148 |
326 |
*Including Shigella dysenteriae type 1: Although these isolates are currently rare in South Africa, the potential for future epidemics remains while these strains are in circulation.
Report compiled by: Karen Keddy
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DIARRHOEAGENIC ESCHERICHIA COLI (DEC)
Enteric Diseases Reference Unit, National Institute for Communicable Diseases
Results
Enteropathogenic E. coli (EPEC) remained the commonest cause of diarrhoea, due to this pathogen, identified in South Africa (Table 1). The predominance of cases amongst younger children under five years of age may reflect, in part, specimen-taking practices, as well as the burden of diarrhoeal disease in this age group (Table 2). Three patients had mixed infections with three different DEC pathotypes and 23 patients had mixed infections with two different DEC pathotypes. A range of serotypes were associated with STEC/EHEC, including O157 (a single isolate), O26 and O111. Serotypes associated with EPEC included O55, O111, O119, O127, O142 and O157. Diverse serotypes were also noted for other enterovirulent E. coli isolates. Identification of both EHEC and STEC was incidental (1).
Discussion
Incidence rates were not calculated as numbers were not viewed as being fully representative. Actual burden of disease due to diarrhoeagenic E. coli was probably greatly underestimated in South Africa, as management is primarily syndromic and centres on rehydration. As a result, clinicians were unlikely to prioritise stool-submission in uncomplicated cases of diarrhoea. Disease in the past appears to have been primarily associated with water-borne outbreaks, due to high level of faecal contamination in water sources, and this trend appeared to continue. The predominance of isolates received in children under the age of one year may reflect culturing practices; infants are more likely to have stools taken for culture due to the devastating effects of diarrhoea in children of this age. Seasonality was not reflected as it is believed that the current specimen-taking and laboratory diagnostic practices may not be optimal to accurately reflect burden of illness in South Africa of disease due to diarrhoeagenic E. coli.
Table 1: Number of diarrhoeagenic Escherichia coli isolates reported to GERMS-SA by province, South Africa, 2009, n=549*.
| Province |
DAEC |
EAggEC |
STEC/ EHEC |
EIEC |
EPEC |
ETEC |
| Eastern Cape |
8 |
27 |
0 |
2 |
69 |
15 |
| Free State |
1 |
0 |
0 |
0 |
8 |
1 |
| Gauteng |
25 |
24 |
9 |
1 |
236 |
9 |
| Kwazulu-Natal |
1 |
4 |
1 |
0 |
4 |
0 |
| Limpopo |
1 |
1 |
0 |
0 |
0 |
0 |
| Mpumalanga |
31 |
16 |
0 |
0 |
15 |
16 |
| Northern Cape |
0 |
0 |
0 |
0 |
0 |
0 |
| North West |
1 |
3 |
0 |
0 |
7 |
0 |
| Western Cape |
9 |
0 |
0 |
1 |
3 |
0 |
| South Africa |
77 |
75 |
10 |
4 |
342 |
41 |
*Representing 520 infectious episodes, including those patients who had more than one pathotype; DAEC: diffusely-adherent E. coli; EAggEC: enteroaggregative E. coli; STEC/EHEC: Shiga-toxigenic E. coli or enterohaemorrhagic E. coli; EIEC: enteroinvasive E. coli; EPEC: enteropathogenic E. coli; ETEC: enterotoxigenic E. coli.
Table 2: Number of diarrhoeagenic E. coli isolates reported to GERMS-SA by age category, South Africa, 2009, n=549.
| Age category (years) |
DAEC |
EAggEC |
EHEC/ STEC |
EIEC |
EPEC |
ETEC |
| Neonate |
5 |
5 |
0 |
0 |
33 |
3 |
| < 1 |
19 |
31 |
3 |
0 |
144 |
15 |
| 1 - 4 |
21 |
27 |
5 |
2 |
150 |
15 |
| 5 - 14 |
5 |
0 |
0 |
0 |
2 |
0 |
| 15 - 24 |
3 |
0 |
0 |
0 |
2 |
2 |
| 25 - 34 |
8 |
4 |
1 |
1 |
1 |
3 |
| 35 - 44 |
4 |
3 |
0 |
1 |
2 |
1 |
| 45 - 54 |
6 |
2 |
0 |
0 |
1 |
0 |
| 55 - 64 |
2 |
1 |
0 |
0 |
1 |
1 |
| ≥ 65 |
4 |
0 |
0 |
0 |
1 |
0 |
| Unknown |
0 |
2 |
1 |
0 |
5 |
1 |
| Total |
77 |
75 |
10 |
4 |
342 |
41 |
Reference
1. Werber D, Frank C, Wadl M, Karch H, Fruth A, Stark K. Looking for tips to find icebergs - surveillance of haemolytic uraemic syndrome to detect outbreaks of Shiga toxin-producing E. coli infection. Website 2008 February13(9)Available from: URL: http://www.eurosurveillance.org/edition/v13n09/080228_4.asp |
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VIBRIO CHOLERAE O1
Enteric Diseases Reference Unit,, National Institute for Communicable Diseases
Results
The number of laboratory-confirmed cases reported to GERMS-SA in 2009 by province is shown in Table 1. This does not reflect the actual number of cases that were identified clinically and a large proportion was identified by audit. Where isolates were received contaminated or were missing, these have been included in the analysis, to improve estimates of duration of the outbreak and age distribution of cases. A number of cases may have been imported from Zimbabwe, but as these cases increase the burden on South African health care facilities as well as the public health risk to the local population, they have been included in the overall count. All age categories were affected (Table 2). Multidrug resistance was increasingly common and was noted with each outbreak cluster. Although resistance profiles differed amongst isolates from different clusters (data not shown), resistance to the quinolones was high (Table 3). Figure 1 shows the temporal clustering of the cholera outbreaks in South Africa in 2009. The case distribution highlights the epidemic that started in November 2008 (following an epidemic in Zimbabwe), and waned over the first half of 2009.
Table 1: Number of Vibrio cholerae O1 isolates reported to GERMS-SA by province, South Africa, 2009, n=575 (excluding audit reports).
| Province |
Vibrio cholerae O1 El Tor Inaba |
Vibrio cholerae O1 El Tor Ogawa |
| Eastern Cape |
0 |
0 |
| Free State |
0 |
0 |
| Gauteng |
0 |
37 |
| KwaZulu-Natal |
0 |
0 |
| Limpopo |
8 |
445 |
| Mpumalanga |
0 |
62 |
| Northern Cape |
0 |
0 |
| North West |
1 |
18 |
| Western Cape |
0 |
4 |
| South Africa |
9 |
566 |
Table 2: Number of V. cholerae O1 cases, reported to GERMS-SA, by age category, South Africa, 2009, n=1222 (including audit reports).
| Age category (years) |
V. cholerae O1 cases |
| < 1 |
14 |
| 1 - 4 |
82 |
| 5 - 14 |
119 |
| 15 - 24 |
202 |
| 25 - 34 |
224 |
| 35 - 44 |
150 |
| 45 - 54 |
105 |
| 55 - 64 |
103 |
| ≥ 65 |
130 |
| Unknown |
93 |
| Total |
1222 |
Discussion
Imported cases of cholera add to burden of infection in South Africa and thus represent a public health risk. The organism was multi-drug resistant, but as these resistant patterns were inconsistent, cumulative (for-the-year) resistance patterns could not be used to guide management of severely-dehydrated patients and could not be used to predict treatment for current or future outbreaks. Inappropriate usage of antimicrobials may have driven resistance. Antimicrobial treatment has not been shown to alter mortality rates(1). Certain antimicrobials were tested for epidemiological purposes only and are not suitable for treatment.
Table 3: Antimicrobial susceptibility test results for four outbreak clusters of V. cholerae O1 reported to GERMS-SA, South Africa, 2009, n=573.
Antimicrobial agent |
Susceptible (%) |
Intermediate (%) |
Resistant (%) |
Ampicillin |
556 |
(97) |
0 |
(0) |
17 |
(3) |
Cotrimoxazole |
1 |
(0.1) |
0 |
(0) |
572 |
(99.9) |
Chloramphenicol |
343 |
(60) |
222 |
(39) |
8 |
(1) |
Nalidixic acid |
1 |
(0.1) |
0 |
(0) |
572 |
(99.9) |
Ciprofloxacin |
573 |
(100) |
0 |
(0) |
0 |
(0) |
Tetracycline |
558 |
(97) |
10 |
(2) |
5 |
(1) |
Kanamycin |
557 |
(97) |
9 |
(2) |
7 |
(1) |
Streptomycin |
2 |
(0.3) |
0 |
(0) |
571 |
(99.7) |
Imipenem |
573 |
(100) |
0 |
(0) |
0 |
(0) |
Ceftriaxone |
566 |
(99) |
0 |
(0) |
7 |
(1) |
Erythromycin* |
391 |
(70) |
159 |
(29) |
5 |
(1) |
*Where standard CLSI breakpoints do not exist, susceptibility categories were determined according to the methods of Ng et al.(2) Not all viable isolates received were available for susceptibility testing and only 555 isolates were available for testing against erythromycin.

Figure 1: Number of V. cholerae O1 isolates, reported to GERMS-SA, by month of specimen collection, South Africa, 2009, n=1222 (including audit reports).
References
- Guerrant RL. Cholera--still teaching hard lessons. N Engl J Med 2006 Jun 8;354(23):2500-2.
- Ng L-K, Sawatsky P, Galas M, Dos Prazeres Rodrigues D, Heitmann I, Fernandez A, Bolstrom A. Can Etest be used to determine Vibrio cholerae susceptibility to erythromycin? Antimicrob.Agents Chemother 2003 Apr 1;47(4):1479-80
Report compiled by: Karen Keddy
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CRYPTOCOCCUS SPECIES
Mycology Reference Unit, National Institute for Communicable Diseases
Results During 2009, 7965 case patients, with laboratory-confirmed, incident cryptococcal episodes, were reported. The overall incidence for the general South African population remained stable: 15/100000 in 2008 and 16/100000 in 2009 (Table 1). Similarly, incidence amongst HIV-infected individuals (128/100000 in 2008 and 134/100000 in 2009) and people sick with AIDS (11/1000 in 2008 and 12/1000 in 2009) remained stable. Incidence remained fairly stable in all provinces, except Limpopo and Northern Cape where the incidence increased (Table 1). The absolute number of detected cases decreased in 3 provinces: Western Cape, North West and Free State. The peak incidence of cryptococcosis was recorded amongst patients aged 35-39 years (Figure 1). Two hundred and fifty four children, younger than 15 years, had laboratory-confirmed cryptococcosis; 66/254 (26%) were younger than 1 year-old. Where gender was known (7860/7965, 99%), 51% patients were female. Most patients (7347/7965; 92%) were diagnosed with meningitis (laboratory tests on cerebrospinal fluid positive for Cryptococcus species), and 545/7965 (7%) were diagnosed with fungaemia (Table 2). The remainder of case patients (n=73) were diagnosed by culture of urine, sputum, pleural fluid and other specimen types. At ESS, 2135 patients were diagnosed with cryptococcosis, with viable isolates received from 1537/2135 (72%) patients. Of 1533 isolates which were typed, 1470 (96%) were identified as Cryptococcus neoformans; the remaining 63 were identified as Cryptococcus gattii. C. gattii cases were diagnosed in 5 provinces: Gauteng (n=25), Mpumalanga (n=13), Limpopo (n=9), KwaZulu-Natal (n=7), North West (n=5), and Western Cape (n=4). The in-hospital case-fatality ratio for patients at enhanced surveillance sites did not significantly change between 2008 and 2009 (566/1841 (31%) vs. 591/1812 (33%); p=0.2).
Table 1: Number of cases and incidence rates of cryptococcal disease reported to GERMS-SA by province, South Africa, 2008 and 2009, n=15511.
| Province |
2008* † |
2009* |
n |
Incidence rate** |
n |
Incidence rate** |
| Eastern Cape |
1218 |
19 |
1329 |
20 |
| Free State |
497 |
17 |
467 |
16 |
| Gauteng |
2011 |
19 |
2049 |
19 |
| KwaZulu-Natal |
1242 |
12 |
1271 |
12 |
| Limpopo |
432 |
8 |
671 |
13 |
| Mpumalanga |
758 |
21 |
805 |
22 |
| Northern Cape |
57 |
5 |
87 |
8 |
| North West |
749 |
22 |
729 |
21 |
| Western Cape |
582 |
11 |
557 |
10 |
| South Africa |
7546 |
15 |
7965 |
16 |
*A similar surveillance audit was performed for NHLS laboratories in 8 provinces (excluding KwaZulu-Natal) in 2008 and 2009, detecting additional microscopy (India ink), cryptococcal antigen and culture-confirmed cases; **Incidence rates were calculated based on population denominators provided by Statistics South Africa, and are expressed as cases per 100,000 population; †The number of detected cases in 2008 was updated following data cleaning procedures.
| Site of specimen |
2008 |
2009 |
n |
% |
n |
% |
| CSF |
7079 |
94% |
7347 |
92% |
| Blood |
440 |
6% |
545 |
7% |
| Other |
27 |
<1% |
73 |
1% |
|
7546 |
7965 |

Figure 1: Age-specific incidence rates for laboratory-confirmed, cryptococcal cases, reported to GERMS-SA, South Africa, 2009, n=7965.
Reference
1. Wong ML, Back P, Candy G, Nelson G, Murray J. Cryptococcal pneumonia in African miners at autopsy. Int J Tuberc Lung Dis 2007 May;11(5):528-33.
Report compiled by Nelesh Govender
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PNEUMOCYSTIS JIROVECII
Parasitology Reference Unit, National Institute for Communicable Diseases
Results
In 2009, 371 cases of PCP were reported (Table 1). The number of P. jirovecii-positive specimens peaked amongst children less than one year of age and in the 20 to 59 year age group (Figure 1). Of cases with known gender, 62% (227/364) were female. Of all reported case patients, 153 (41%) were diagnosed at ESS and had available clinical data. During admission, 88% (125/142) of patients tested for HIV were HIV-infected. Where outcome was known, the in-hospital case-fatality ratio was 31% (44/144). In 18% (22/120) of patients, the diagnosis of PCP was associated with a second or later hospitalisation for PCP. Of patients who recovered, 96% (95/99) were discharged with a lower respiratory tract infection as a final diagnosis. Most of the case patients had concurrent infections, of which clinically-diagnosed candidiasis (49/153) and tuberculosis (23/153) were the most common (Figure 2).
PCP is often the first-diagnosed opportunistic infection (1). The number of cases reported here does not approximate the true burden of disease in South Africa. This is because PCP is usually clinically-diagnosed, and only laboratory confirmed cases of PCP are reported through GERMS-SA; there are only ten laboratories that offer PCP testing in four of the nine provinces in South Africa; PCP testing is expensive and needs well-trained personnel; and the quality of the specimens received by the testing laboratory is often poor which may affect the result. Since 2008, the Parasitology Reference Unit has taken steps to tackle some of these problems. Training was offered to all existing PCP-testing laboratories; five laboratories were trained in 2008 and 2009. In 2009, NHLS Grey’s Hospital (KwaZulu-Natal) became a testing site for PCP and was provided with a UV microscope and training. Set-up of PCP testing is now targeted for provinces where no such facilities exist: Eastern Cape, Northern Cape, North West, Limpopo and Mpumalanga. A proficiency testing scheme for the identification of P. jirovecii was launched in 2008; 9 laboratories participated in 2009.
Table 1: Number of Pneumocystisjirovecii pneumonia (PCP) cases reported to GERMS-SA by province, South Africa, 2008-2009, n=715.
| Province |
2008 |
2009 |
| Eastern Cape |
30 |
37 |
| Free State |
20 |
19 |
| Gauteng |
163 |
141 |
| KwaZulu-Natal |
23 |
19 |
| Limpopo |
1 |
0 |
| Mpumalanga |
14 |
6 |
| Northern Cape |
3 |
0 |
| North West |
25 |
44 |
| Western Cape |
65 |
105 |
| South Africa |
344 |
371 |

Figure 1: Number of laboratory-confirmed, Pneumocystis jirovecii pneumonia (PCP) cases reported to GERMS-SA, by age category, South Africa, 2008-2009, n=734.

Figure 2: Number of laboratory-confirmed Pneumocystis jirovecii pneumonia (PCP) cases with reported HIV-associated conditions, South Africa, 2009, n = 153*.
Discussion
PCP is often the first-diagnosed opportunistic infection (1). The number of cases reported here does not approximate the true burden of disease in South Africa. This is because PCP is usually clinically-diagnosed, and only laboratory confirmed cases of PCP are reported through GERMS-SA; there are only ten laboratories that offer PCP testing in four of the nine provinces in South Africa; PCP testing is expensive and needs well-trained personnel; and the quality of the specimens received by the testing laboratory is often poor which may affect the result. Since 2008, the Parasitology Reference Unit has taken steps to tackle some of these problems. Training was offered to all existing PCP-testing laboratories; five laboratories were trained in 2008 and 2009. In 2009, NHLS Grey’s Hospital (KwaZulu-Natal) became a testing site for PCP and was provided with a UV microscope and training. Set-up of PCP testing is now targeted for provinces where no such facilities exist: Eastern Cape, Northern Cape, North West, Limpopo and Mpumalanga. A proficiency testing scheme for the identification of P. jirovecii was launched in 2008; 9 laboratories participated in 2009.
Reference
- Morris A, Lundgren JD, Masur H, Walzer PD, Hanson DL, Frederick T, et al. Current epidemiology of Pneumocystis pneumonia. Emerg Infect Dis 2004 Oct;10(10):1713-20.
Report compiled by (in alphabetical order): Desiree du Plessis, John Frean and Bhavani Poonsamy
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NEISSERIA MENINGITIDIS
Respiratory & Meningeal Pathogens Reference Unit, National Institute for Communicable Diseases
Discussion
Overall incidence of disease did not change from 2008 and serogroup W135 disease remained stable. Increases of meningococcal disease incidence in Mpumalanga may reflect improved laboratory confirmation of disease and better reporting to the surveillance network, or may reflect a true increase in incidence. Case-fatality ratios decreased, and correspond more closely with the range 9% to 12% as reported from other settings (1)-(4). The prevalence of intermediate resistance to penicillin remained low in 2009, and was within the annual prevalence range (from 3% to 13%) previously reported from South Africa (5). The clinical relevance of increased MICs is unclear, and penicillin is, at present, still being recommended as the drug of choice for therapy for confirmed meningococcal disease.
Table 1: Number of cases and incidence rates of meningococcal disease reported to GERMS-SA by province, South Africa, 2008 and 2009, n=922 (including audit cases).
| Province |
2008 |
2009 |
n |
Incidence rate* |
n |
Incidence rate* |
| Eastern Cape |
29 |
0.44 |
36 |
0.54 |
| Free State |
21 |
0.73 |
18 |
0.62 |
| Gauteng |
224 |
2.14 |
203 |
1.93 |
| KwaZulu-Natal |
34 |
0.34 |
32 |
0.31 |
| Limpopo |
5 |
0.09 |
3 |
0.06 |
| Mpumalanga |
36 |
1.00 |
67 |
1.86 |
| Northern Cape |
8 |
0.71 |
9 |
0.78 |
| North West |
15 |
0.44 |
19 |
0.55 |
| Western Cape |
88 |
1.67 |
75 |
1.40 |
| South Africa |
460 |
0.94 |
462 |
0.94 |
*Incidence rates were calculated based on population denominators provided by Statistics South Africa, and are expressed as cases per 100,000 population. Figure 1: Number of laboratory-confirmed, invasive, meningococcal cases, reported to GERMS-SA, by month and year, South Africa, 2008-2009, n=922. Table 2: Number and percentage of cases of meningococcal disease reported to GERMS-SA by specimen type, South Africa, 2008 and 2009, n=922.
| Site of specimen |
2008 |
2009 |
n |
% |
n |
% |
| CSF |
318 |
69% |
336 |
73% |
| Blood |
136 |
30% |
124 |
27% |
| Other |
6 |
1% |
2 |
<1% |
|
460 |
462 |
Table 3: Number of cases of invasive meningococcal disease reported to GERMS-SA by serogroup and province, South Africa, 2009, n=462.*
| Province |
Serogroup |
Serogroup not available |
A |
B |
C |
W135 |
X |
Y |
Total |
| Eastern Cape |
6 |
0 |
8 |
3 |
16 |
1 |
2 |
36 |
| Free State |
3 |
0 |
3 |
6 |
4 |
0 |
2 |
18 |
| Gauteng |
30 |
2 |
32 |
13 |
111 |
0 |
14 |
203 |
| KwaZulu-Natal |
4 |
0 |
3 |
1 |
22 |
0 |
2 |
32 |
| Limpopo |
1 |
0 |
1 |
0 |
1 |
0 |
0 |
3 |
| Mpumalanga |
7 |
0 |
1 |
6 |
47 |
1 |
4 |
67 |
| Northern Cape |
1 |
0 |
3 |
0 |
4 |
0 |
1 |
9 |
| North West |
6 |
0 |
2 |
0 |
9 |
0 |
2 |
19 |
| Western Cape |
7 |
0 |
35 |
7 |
21 |
0 |
4 |
75 |
| South Africa |
65 |
2 |
88 |
36 |
235 |
2 |
31 |
462 |
*397 (86%) with specimens or viable isolates available for serogrouping.

Figure 2: Age-specific incidence rates for laboratory-confirmed, invasive, meningococcal cases, by serogroup, South Africa, 2009, n=462 (age unknown for n=12; specimens or viable isolates unavailable for serogrouping n=65).
References
- Stephens DS, Greenwood B, Brandtzaeg P. Epidemic meningitis, meningococcaemia, and Neisseria meningitidis. Lancet 2007 Jun 30;369(9580):2196-210.
- Pinner RW, Onyango F, Perkins BA, Mirza NB, Ngacha DM, Reeves M, et al. Epidemic meningococcal disease in Nairobi, Kenya, 1989. The Kenya/Centers for Disease Control (CDC) Meningitis Study Group. J Infect Dis 1992 Aug;166(2):359-64.
- Greenwood B. Manson Lecture. Meningococcal meningitis in Africa. Trans R Soc Trop Med Hyg 1999 Jul;93(4):341-53.
- Rosenstein NE, Perkins BA, Stephens DS, Popovic T, Hughes JM. Meningococcal disease. N Engl J Med 2001 May 3;344(18):1378-88.
- du Plessis M, von Gottberg A, Cohen C, de Gouveia L, Klugman KP. Neisseria meningitidis intermediately resistant to penicillin and causing invasive disease in South Africa in 2001 to 2005. J Clin Microbiol 2008 Oct;46(10):3208-14.
Report compiled by (in alphabetical order): Linda de Gouveia and Anne von Gottberg
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HAEMOPHILUS INFLUENZAE
Respiratory & Meningeal Pathogens Reference Unit, National Institute for Communicable Diseases
Results
The number of cases of Haemophilus influenzae invasive disease reported in 2009 was 292, while an additional 95 cases were identified during the surveillance audit (total number of cases available for analysis was 387). Of these, 264 (68%) had isolates or specimens available for serotyping, and 105/264 (40%) were confirmed as serotype b (Table 1). Serotype b isolates were more likely to be isolated from CSF than non-typeable H. influenzae (56/105, 53% vs. 9/112, 8%, p<0.001) (Table 2). In 2009, a total of 73 cases of H. influenzae serotype b (Hib) were reported in children <5 years (Figure 1). Of the non-viable isolates received or culture-negative cases reported, serotyping was identified by polymerase chain reaction (PCR) testing of transport media or specimens wherever possible. Serotype b was the more common H. influenzae causing disease in infants (Figure 2). Since 2002, rates of Hib disease as recorded by our surveillance network in infants <1 year of age have increased, and there seems to be a continued increase in 2009 (p<0.001, chi-squared test for trend, 2002 to 2009) (Figure 3). Small increases in numbers of Hib cases confirmed on viable isolates (methodology used since 2000) were seen for four provinces comparing 2008 to 2009 (Eastern Cape, Kwa-Zulu Natal, Northern Cape and Western Cape). Numbers were small for all provinces except Western Cape: increase from 13 viable isolates confirmed as Hib in 2008 to 24 in 2009. Nineteen percent of serotype b strains were resistant to ampicillin (MIC>1mg/L, all producing beta lactamase), 17 of 91 isolates tested, while 13% (12/96) of non-typeable strains were resistant (p=0.2).
Discussion
Since the introduction of the Hib conjugate vaccine into the Expanded Programme on Immunisation (EPI) for South Africa in 1999, there has been a reduction in cases reported due to this serotype (1). Population-based studies in South Africa before the introduction of the conjugate Hib vaccine had demonstrated annual rates of invasive Hib disease of 170 per 100 000 infants below one year of age (2),(3), and any increases noted recently are still small in comparison to the substantial decline in disease subsequent to the introduction of the vaccine. The biggest increase was seen for Western Cape, and this may have been linked to more aggressive laboratory protocols to maintain viability of bacterial isolates. Recognising that our surveillance system underestimates disease, the increases in reported cases of Hib disease in children <1 year are being monitored carefully. In April 2009, the updated infant vaccination programme in South Africa introduced a booster dose of conjugate Hib vaccine given at 18 months as part of a combination vaccine (Pentaxim: diphtheria-tetanus-acellular pertussis-inactivated poliovirus-Haemo-philus influenzae type-b conjugate). It is hoped that this booster will improve long-term protection against disease and impact on ongoing Hib transmission in the community. Table 1: Number of cases of invasive Haemophilus influenzae disease reported to GERMS-SA by serotype and province, South Africa, 2009, n=387*.
| Province |
Serotype |
Serotype not available |
a |
b |
c |
d |
e |
f |
Non-typeable |
Total |
| Eastern Cape |
22 |
0 |
13 |
0 |
0 |
1 |
0 |
3 |
39 |
| Free State |
8 |
1 |
8 |
0 |
1 |
0 |
0 |
4 |
22 |
| Gauteng |
54 |
9 |
26 |
2 |
3 |
2 |
11 |
52 |
159 |
| KwaZulu-Natal |
5 |
0 |
18 |
1 |
0 |
1 |
1 |
17 |
43 |
| Limpopo |
1 |
0 |
2 |
0 |
0 |
0 |
0 |
1 |
4 |
| Mpumalanga |
17 |
0 |
4 |
1 |
0 |
0 |
2 |
3 |
27 |
| Northern Cape |
3 |
0 |
4 |
0 |
0 |
0 |
0 |
1 |
8 |
| North West |
5 |
0 |
4 |
0 |
0 |
1 |
0 |
1 |
11 |
| Western Cape |
8 |
4 |
26 |
0 |
1 |
1 |
4 |
30 |
74 |
| South Africa |
123 |
14 |
105 |
4 |
5 |
6 |
18 |
112 |
387 |
*264 (68%) with specimens or viable isolates available for serotyping. Table 2: Number and percentage of cases of invasive Haemophilus influenzae disease reported to GERMS-SA by specimen type, South Africa, 2009, n=387.
| Site of specimen |
No serotype available |
Serotype b |
Serotypes a, c, d, e, f |
Non-typeable |
| |
n |
% |
n |
% |
n |
% |
n |
% |
| CSF |
24 |
20 |
56 |
53 |
19 |
40 |
9 |
8 |
| Blood |
68 |
55 |
46 |
44 |
27 |
57 |
90 |
80 |
| Other |
31 |
25 |
3 |
3 |
1 |
2 |
13 |
12 |
| Total |
123 |
105 |
47 |
112 |

Figure 1: Number of laboratory-confirmed, invasive, Haemophilus influenzae cases, reported to GERMS-SA, by serotype and age group, South Africa, 2009, n=387 (age unknown for n=10; specimens or viable isolates unavailable for serotyping for n=123).

Figure 2: Age-specific incidence rates for laboratory-confirmed, invasive Haemophilus influenzae disease, reported to GERMS-SA, by serotype, South Africa, 2009, n=387 (age unknown for n=10; viable isolates unavailable for serotyping for n=123).

Figure 3: Incidence rates of laboratory-confirmed, Haemophilus influenzae serotype b disease, reported to GERMS-SA, in children <5 years old, South Africa, 2000-2009 (excluding cases identified using polymerase chain reaction (PCR) on specimens which was only done 2007-2009).
References
- von Gottberg A, de Gouveia L., Madhi SA, du Plessis M., Quan V, Soma K, Huebner R, Flannery B, Schuchat A, Klugman K. Impact of conjugate Haemophilus influenzae type b (Hib) vaccine introduction in South Africa. Bull World Health Organ 2006;84:811-18.
- Hussey G, Hitchcock J, Schaaf H, Coetzee G, Hanslo D, van SE, et al. Epidemiology of invasive Haemophilus influenzae infections in Cape Town, South Africa. Ann Trop Paediatr 1994;14(2):97-103.
- Madhi SA, Petersen K, Khoosal M, Huebner RE, Mbelle N, Mothupi R, et al. Reduced effectiveness of Haemophilus influenzae type b conjugate vaccine in children with a high prevalence of human immunodeficiency virus type 1 infection. Pediatr Infect Dis J 2002 Apr;21(4):315-21.
Report compiled by (in alphabetical order): Linda de Gouveia and Anne von Gottberg |
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|
STREPTOCOCCUS PNEUMONIAE
Respiratory & Meningeal Pathogens Reference Unit, National Institute for Communicable Diseases
Results
Incidence of reported invasive pneumococcal disease (IPD) varied widely by province (Table 1). The age group at highest risk of disease in South Africa was infants <1 year of age, and there was a significant reduction in disease comparing 2008 to 2009, p<0.001(Figure 1). The majority of episodes reported to GERMS-SA were diagnosed from positive blood culture specimens (Table 2). Penicillin non-susceptible isolates (2009 CLSI breakpoints for penicillin [oral penicillin V], MIC>0.06mg/L) (1), have increased (1276/3326, 38% in 2008 compared to 1478/3387, 44% in 2009, p<0.0001). Prevalence of non-susceptible strains ranged from 32% to 52% in different provinces (Table 3). Penicillin non-susceptible isolates were common in children less than 5 years of age (Figure 2). A non-meningitis-causing pneumococcus with a penicillin MIC of ≤2mg/L, according to updated CLSI guidelines (penicillin parenteral, non-meningitis), can be considered susceptible (1). Using this breakpoint, only 3% (70/2141) of isolates cultured from specimens other than CSF were non-susceptible to penicillin. Ceftriaxone non-susceptibility was detected in 8% (276/3387) of all IPD cases, and in 8% (102/1246) of isolates detected from CSF specimens. Ceftriaxone-resistant pneumococci were more common in children <5 years (137/1007, 14% in children <5 years vs. 129/2267, 6% in individuals ≥5 years of age, p<0.001), and this remained significant if restricted to meningitis. The majority of cetriaxone-resistant isolates were serotypes contained in PCV7 (256/276, 93%). On preliminary univariate analysis, there were no differences by gender, province, enhanced surveillance site, syndrome or in mortality when comparing susceptible to non-susceptible isolates. Prevalence of ceftriaxone resistance as detected by the surveillance system from 2003 through 2008 ranged from 0.4% to 0.9% (data not shown). Prevenar® (7-valent conjugate pneumococcal vaccine, PCV7) was introduced into the EPI in South Africa from 1 April 2009. The number of cases in children less than 5 years of age due to common serotypes in 2009 (including the seven serotypes in PCV7: 4, 6B, 9V, 14, 18C, 19F and 23F) are compared with 2008 in Figure 3. The percentage of disease in 2009 in children <5 years due to PCV7 and newer valency vaccine formulations are shown in Table 4.
Discussion
Differences in IPD incidence by province have been documented for several years, and are partly due to differences in specimen-taking practices and laboratory reporting, however real differences in disease incidence cannot be excluded. The decrease in incidence of disease in children <1 year of age was mostly likely due to the introduction of PCV7 in South Africa. In a preliminary analysis performed within 6 months of PCV7 introduction, we noted a significant decrease of approximately 25% in serotype-specific disease among infants less than 1 year of age, and no changes in other age groups (2). Ongoing surveillance will be essential to document further reduction in disease in infants, and as vaccine coverage increases we hope to see declines in disease in older children. Our data for 2009 show an increase in pneumococcal resistance to penicillin and ceftriaxone. Although a true, sudden increase may be possible, we believe that this increase is due to a change in laboratory methodology that was introduced in 2009. For isolates that are screened non-susceptible by disk diffusion, we changed from using agar dilution or Etest® (AB bioMérieux, Solna, Sweden) methodology for MIC determination to broth microdilution methodology (the recommended CLSI method). The low levels of penicillin non-susceptibility from blood culture specimens still support the use of penicillin as first-line therapy for community-acquired pneumonia. Vancomycin, together with ceftriaxone, should be considered for the empiric treatment of suspected pneumococcal meningitis (CSF specimens positive for Gram-positive cocci or latex agglutination tests positive for S. pneumoniae), especially amongst unvaccinated children. As most of these ceftriaxone-resistant isolates were identified as serotypes contained in PCV7, we anticipate that the number of resistant isolates causing disease will decrease with wider use of the vaccine. Table 1: Number of cases and incidence rates of invasive pneumococcal disease reported to GERMS-SA by province, South Africa, 2008 and 2009, n=9605.
| Province |
2008 |
2009 |
| |
n |
Incidence rate* |
n |
Incidence rate* |
| Eastern Cape |
356 |
5.41 |
362 |
5.44 |
| Free State |
320 |
11.12 |
309 |
10.65 |
| Gauteng |
2356 |
22.55 |
2254 |
21.40 |
| KwaZulu-Natal |
573 |
5.67 |
528 |
5.05 |
| Limpopo |
112 |
2.12 |
111 |
2.12 |
| Mpumalanga |
257 |
7.16 |
302 |
8.37 |
| Northern Cape |
84 |
7.46 |
88 |
7.67 |
| North West |
193 |
5.63 |
175 |
5.07 |
| Western Cape |
586 |
11.14 |
639 |
11.93 |
| South Africa |
4837 |
9.93 |
4768 |
9.67 |
* Incidence rates were calculated based on population denominators provided by Statistics South Africa, and are expressed as cases per 100,000 population
Table 2: Number and percentage of cases of invasive pneumococcal disease reported to GERMS-SA by specimen type, South Africa, 2008 and 2009, n=9605.
| Site of specimen |
2008 |
2009 |
| |
n |
% |
n |
% |
| CSF |
1755 |
36% |
1805 |
38% |
| Blood |
2644 |
55% |
2513 |
53% |
| Other |
438 |
9% |
450 |
9% |
|
4837 |
4768 |
Table 3: Number and percentage of penicillin non-susceptible isolates from invasive pneumococcal disease cases reported to GERMS-SA by province, South Africa, 2009, n=4768.
| Province |
Isolate not available |
Susceptible* |
Intermediate* |
Resistant* |
n |
n |
% |
n |
% |
n |
% |
| Eastern Cape |
165 |
95 |
48 |
88 |
45 |
14 |
7 |
| Free State |
78 |
143 |
62 |
67 |
29 |
21 |
9 |
| Gauteng |
698 |
904 |
58 |
487 |
31 |
165 |
11 |
| KwaZulu-Natal |
69 |
233 |
51 |
196 |
43 |
30 |
7 |
| Limpopo |
48 |
43 |
68 |
18 |
29 |
2 |
3 |
| Mpumalanga |
141 |
98 |
61 |
49 |
30 |
14 |
9 |
| Northern Cape |
21 |
39 |
58 |
18 |
27 |
10 |
15 |
| North West |
83 |
56 |
61 |
31 |
34 |
5 |
5 |
| Western Cape |
78 |
298 |
53 |
217 |
39 |
46 |
8 |
| South Africa |
1381 |
1909 |
56 |
1171 |
35 |
307 |
9 |
*2009 CLSI breakpoints for penicillin (oral penicillin V) were used: susceptible, ≤0.06mg/L; intermediately resistant, 0.12-1mg/L; resistant, ≥2mg/L.

Figure 1: Age-specific incidence rates for laboratory-confirmed, invasive pneumococcal disease, reported to GERMS-SA, South Africa, 2008 and 2009 (2008: n=4837; age unknown for n=217; 2009: n=4768; age unknown for n=178). 2009 CLSI breakpoints for penicillin (oral penicillin V) were used: susceptible, ≤0.06mg/L; intermediately resistant, 0.12-1mg/L; resistant, ≥2mg/L.

Figure 2: Percentage of laboratory-confirmed, invasive pneumococcal disease cases, reported to GERMS-SA, by age group and penicillin susceptibility, South Africa, 2009, n=4768 (n=3387 with viable isolates). Figure 3: Pneumoccocal serotypes, in descending order, causing laboratory-confirmed, invasive pneumococcal disease, reported to GERMS-SA, in children <5 years, South Africa, 2008-2009 (2008: n=1464, n=1098 with viable isolates; 2009: n=1334; n=1007 with viable isolates).
Table 4: Number and percentage of invasive pneumococcal cases reported amongst children less than 5 years of age caused by the serotypes contained in the 7-valent, 10-valent and 13-valent pneumococcal, conjugate vaccines, South Africa, 2009, n=1007.
| Province |
Total isolates available for serotyping |
7-valent serotypes * |
Serotype 6A# |
10-valent serotypes* |
13-valent serotypes* |
| n |
% |
n |
% |
n |
% |
n |
% |
| Eastern Cape |
54 |
28 |
52 |
13 |
24 |
28 |
52 |
45 |
83 |
| Free State |
50 |
31 |
62 |
4 |
8 |
35 |
70 |
44 |
88 |
| Gauteng |
462 |
233 |
50 |
55 |
12 |
287 |
62 |
385 |
83 |
| KwaZulu-Natal |
145 |
83 |
57 |
15 |
10 |
90 |
62 |
122 |
84 |
| Limpopo |
12 |
8 |
67 |
2 |
17 |
8 |
67 |
10 |
83 |
| Mpumalanga |
47 |
18 |
38 |
6 |
13 |
27 |
57 |
37 |
79 |
| Northern Cape |
40 |
20 |
50 |
2 |
5 |
25 |
63 |
32 |
80 |
| North West |
11 |
6 |
55 |
2 |
18 |
7 |
64 |
11 |
100 |
| Western Cape |
186 |
115 |
62 |
24 |
13 |
121 |
65 |
166 |
89 |
| South Africa |
1007 |
542 |
54 |
123 |
12 |
628 |
62 |
852 |
85 |
* 7-valent serotypes: 4, 6B, 9V, 14, 18C, 19F, 23F; 10-valent serotypes: 4, 6B, 9V, 14, 18C, 19F, 23F, 1, 5, 7F; 13-valent serotypes: 4, 6B, 9V, 14, 18C, 19F, 23F, 1, 5, 7F, 19A, 3, 6A. # Cross-protection with 6B has been demonstrated (3)
References
- Clinical and Laboratory Standards Institute (CLSI) (Formerly NCCLS). Performance Standards for Antimicrobial Susceptibility Testing; Nineteenth Informational Supplement. CLSI document M100-S19 ed. Wayne, Pennsylvania: NCCLS; 2009.
- von Gottberg A, Cohen C, de Gouveia L, Dermaux-Msimang V, Quan V, Meiring S, et al. Early, direct effects of two doses of the 7-valent pneumococcal conjugate vaccine (PCV7) in South Africa, 2007-2009. Book of Abstracts, 7th International Symposium on Pneumococci and Pneumococcal Diseases, March 14-18, Tel Aviv, Israel. 2010.
- Whitney CG, Pilishvili T, Farley MM, Schaffner W, Craig AS, Lynfield R, et al. Effectiveness of seven-valent pneumococcal conjugate vaccine against invasive pneumococcal disease: a matched case-control study. Lancet 2006 Oct 28;368(9546):1495-502.
Report compiled by (in alphabetical order): Linda de Gouveia and Anne von Gottberg
|
Acknowledgements
GERMS-SA: Sandeep Vasaikar, Vivek Bhat (Eastern Cape); Gene Elliot (Free State); Anwar Hoosen, Kathy Lindeque, Olga Perovic, Trusha Nana, Charlotte Sriruttan, Charles Feldman, Alan Karstaedt, Jeannette Wadula, David Moore, Sharona Seetharam, Maphoshane Nchabeleng, Tlou Chephe (Gauteng); Nomonde Dlamini, Yacoob Coovadia, Halima Dawood, Sumayya Haffejee, Meera Chhagan (KwaZulu Natal); Ken Hamese (Limpopo); Greta Hoyland, Jacob Lebudi (Mpumalanga); Pieter Jooste, Eunice Weenink (Northern Cape), Andrew Rampe (North West); Elizabeth Wasserman, Siseko Martin, Andrew Whitelaw (Western Cape); Keshree Pillay (Lancet laboratories), Adrian Brink, Maria Botha, Peter Smith, Inge Zietsman, Suzy Budavari, Xoliswa Poswa (Ampath laboratories), Marthinus Senekal (PathCare); Anne Schuchat, Stephanie Schrag (CDC); Keith Klugman, Anne von Gottberg, Linda de Gouveia, Karen Keddy, Arvinda Sooka, John Frean, Desiree du Plessis, Jaymati Patel, Vanessa Quan, Susan Meiring, Penny Crowther, Cheryl Cohen and Nelesh Govender (NICD)
|
Erratum
March 2010;8:1:3.Table 1: Number and rate of suspected measles cases (SMC) with specimens submitted and measles and rubella IgM positive cases from suspected measles case-based surveillance, South Africa: 2009. The number of SMC/100 000 population for Gauteng province (GAP) presented in the table as 722 was incorrect. The correct figure is 72. This can be found in the corrected version of this publication available at: http://www.nicd.ac.za/pubs/survbull/2008/CommDisBullMar10_Vol0801.pdf
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|
Table 1: Provisional number of laboratory confirmed cases of diseases under surveillance reported to the NICD - South Africa, corresponding periods 1 January - 31 March 2009/2010*
| Disease/Organism |
Cumulative to 31 March, year |
EC |
FS |
GA |
KZ |
LP |
MP |
NC |
NW |
WC |
South Africa |
| Anthrax |
2009 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
| 2010 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
| Botulism |
2009 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
| 2010 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
| Cryptococcus spp. |
2009 |
415 |
145 |
671 |
399 |
157 |
254 |
22 |
221 |
178 |
2462 |
| 2010 |
355 |
136 |
597 |
296 |
143 |
228 |
17 |
189 |
138 |
2099 |
| Haemophilus influenzae, invasive disease, all serotypes |
2009 |
6 |
2 |
38 |
15 |
0 |
8 |
1 |
4 |
25 |
99 |
| 2010 |
7 |
5 |
38 |
12 |
1 |
0 |
2 |
2 |
20 |
87 |
| Haemophilus influenzae, invasive disease, < 5 years |
| |
Serotype b |
2009 |
1 |
1 |
5 |
6 |
0 |
0 |
1 |
0 |
7 |
21 |
| |
2010 |
0 |
1 |
4 |
1 |
0 |
0 |
1 |
1 |
3 |
11 |
| |
Serotypes a,c,d,e,f |
2009 |
0 |
1 |
7 |
0 |
0 |
1 |
0 |
0 |
4 |
13 |
| |
2010 |
0 |
0 |
1 |
3 |
0 |
0 |
0 |
0 |
3 |
7 |
| |
Non-typeable (unencapsulated) |
2009 |
0 |
0 |
5 |
4 |
0 |
0 |
0 |
0 |
4 |
13 |
| |
2010 |
0 |
0 |
13 |
3 |
0 |
0 |
0 |
0 |
5 |
21 |
| |
No isolate available for serotyping |
2009 |
1 |
0 |
4 |
3 |
0 |
3 |
0 |
2 |
1 |
14 |
| |
2010 |
3 |
1 |
3 |
0 |
1 |
0 |
1 |
0 |
1 |
10 |
| Measles |
2009 |
2 |
0 |
7 |
1 |
0 |
2 |
0 |
1 |
2 |
15 |
| 2010 |
888 |
253 |
574 |
1818 |
175 |
904 |
146 |
468 |
1069 |
6295 |
| Neisseria meningitidis, invasive disease |
2009 |
5 |
1 |
33 |
12 |
0 |
4 |
0 |
2 |
18 |
75 |
| 2010 |
7 |
4 |
24 |
4 |
1 |
3 |
5 |
2 |
13 |
63 |
| Novel Influenza A virus infections*** |
2009 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
| 2010 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
| Plague |
2009 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
| 2010 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
| Rabies |
2009 |
3 |
0 |
0 |
3 |
0 |
0 |
0 |
0 |
0 |
6 |
| 2010 |
1 |
0 |
0 |
1 |
3 |
1 |
0 |
0 |
0 |
6 |
| **Rubella |
2009 |
26 |
1 |
5 |
23 |
6 |
20 |
10 |
7 |
11 |
109 |
| 2010 |
139 |
32 |
43 |
116 |
13 |
57 |
13 |
56 |
106 |
575 |
| Salmonella spp. (not typhi), invasive disease |
2009 |
22 |
4 |
99 |
28 |
0 |
13 |
3 |
7 |
25 |
201 |
| 2010 |
11 |
3 |
74 |
15 |
3 |
5 |
2 |
1 |
20 |
134 |
| Salmonella spp. (not typhi), isolate from non-sterile site |
2009 |
53 |
16 |
144 |
19 |
10 |
37 |
16 |
19 |
56 |
370 |
| 2010 |
50 |
14 |
211 |
52 |
1 |
24 |
3 |
15 |
35 |
405 |
| Salmonella typhi |
2009 |
2 |
1 |
9 |
1 |
0 |
1 |
0 |
0 |
3 |
17 |
| 2010 |
2 |
0 |
11 |
5 |
0 |
4 |
0 |
0 |
2 |
24 |
| Shigella dysenteriae 1 |
2009 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
| 2010 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
| Shigella spp. (Non Sd1) |
2009 |
73 |
24 |
169 |
32 |
2 |
28 |
9 |
13 |
166 |
516 |
| 2010 |
68 |
15 |
219 |
23 |
0 |
9 |
5 |
8 |
110 |
457 |
| Streptococcus pneumoniae, invasive disease, all ages |
2009 |
85 |
64 |
425 |
106 |
13 |
42 |
17 |
29 |
153 |
934 |
| 2010 |
66 |
40 |
305 |
80 |
19 |
44 |
21 |
32 |
119 |
726 |
| Streptococcus pneumoniae, invasive disease, < 5 years |
2009 |
31 |
23 |
132 |
37 |
4 |
14 |
8 |
7 |
58 |
314 |
| 2010 |
15 |
9 |
87 |
22 |
2 |
11 |
12 |
8 |
32 |
198 |
| Vibrio cholerae O1 |
2009 |
1 |
1 |
45 |
0 |
639 |
396 |
0 |
55 |
5 |
1142 |
| 2010 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
| Viral Haemorrhagic Fever (VHF) |
|
|
|
|
|
|
|
|
|
|
|
| |
Crimean Congo Haemorrhagic Fever (CCHF) |
2009 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
| |
2010 |
0 |
1 |
0 |
0 |
0 |
0 |
1 |
0 |
0 |
2 |
| |
Other VHF (not CCHF)**** |
2009 |
0 |
0 |
0 |
4 |
0 |
0 |
0 |
0 |
0 |
4 |
| |
2010 |
7 |
69 |
0 |
0 |
0 |
0 |
11 |
0 |
0 |
87 |
| Footnotes |
| *Numbers are for cases of all ages unless otherwise specified. Data presented are provisional cases reported to date and are updated from figures reported in previous bulletins. |
| **Rubella cases are diagnosed from specimens submitted for suspected measles cases. |
| *** Confirmed cases. Excludes pandemic influenza H1N1. See weekly influenza reports on www.nicd.ac.za. |
| **** All Rift Valley fever |
| Provinces of South Africa: EC – Eastern Cape, FS – Free State, GA – Gauteng, KZ – KwaZulu-Natal, LP – Limpopo, MP – Mpumalanga, NC – Northern Cape, NW – North West, WC – Western Cape |
| U =unavailable, 0 = no cases reported |
|
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Table 2: Provisional laboratory indicators for NHLS and NICD, South Africa, corresponding periods 1 January - 31 March 2009/2010*
| Programme and Indicator |
Cumulative to 31 March, year |
EC |
FS |
GA |
KZ |
LP |
MP |
NC |
NW |
WC |
South Africa |
| Acute Flaccid Paralysis Surveillance |
| Cases < 15 years of age from whom specimens received |
2009 |
10 |
2 |
16 |
29 |
8 |
15 |
3 |
3 |
7 |
93 |
| 2010 |
14 |
3 |
18 |
26 |
9 |
10 |
0 |
9 |
5 |
94 |
| Laboratory Programme for the Comprehensive Care, Treatment and Management Programme for HIV and AIDS |
|
|
| CD4 count tests |
| Total CD4 count tests submitted |
2009 |
311,600 |
184,577 |
587,437 |
186,757 |
218,527 |
49,035 |
197,515 |
645,919 |
192,447 |
2,573,814 |
| 2010 |
367,052 |
227,070 |
696,976 |
242,671 |
273,181 |
55,592 |
226,253 |
784,075 |
222,064 |
3,094,934 |
| Tests with CD4 count < 200/ μ l |
2009 |
111,711 |
62,213 |
214,898 |
63,278 |
78,648 |
15,108 |
64,732 |
211,650 |
55,654 |
877,892 |
| 2010 |
113,916 |
69,426 |
227,469 |
74,775 |
81,882 |
17,994 |
68,290 |
227,664 |
55,643 |
937,059 |
| Viral load tests |
| Total viral load tests submitted |
2009 |
135,790 |
56,270 |
277,608 |
80,969 |
79,397 |
21,886 |
82,218 |
322,008 |
67,952 |
1,124,098 |
| 2010 |
138,894 |
59,191 |
313,523 |
93,412 |
89,811 |
22,232 |
90,636 |
411,531 |
94,397 |
1,313,627 |
| Tests with undetectable viral load |
2009 |
70,277 |
36,584 |
168,243 |
47,752 |
44,700 |
12,202 |
51,752 |
188,945 |
55,043 |
675,498 |
| 2010 |
90,417 |
42,913 |
226,849 |
62,299 |
65,713 |
14,467 |
64,970 |
298,673 |
76,350 |
942,651 |
| Diagnostic HIV-1 PCR tests |
| Total diagnostic HIV-1 PCR tests submitted |
2009 |
26,921 |
11,554 |
53,542 |
14,375 |
14,105 |
3,303 |
15,026 |
68,022 |
16,687 |
223,535 |
| 2010 |
28,574 |
12,523 |
57,092 |
19,555 |
21,738 |
3,884 |
16,883 |
78,627 |
16,654 |
255,530 |
| Diagnostic HIV-1 PCR tests positive for HIV |
2009 |
3,353 |
1,830 |
7,046 |
2,270 |
2,472 |
474 |
2,234 |
9,085 |
1,447 |
30,211 |
| 2010 |
2,583 |
1,352 |
5,971 |
2,372 |
2,510 |
431 |
1,781 |
6,629 |
1,238 |
24,867 |
| Footnotes |
| *Numbers are for all ages unless otherwise specified. Data presented are provisional numbers reported to date and are updated from figures reported in previous bulletins. |
| Provinces of South Africa: EC – Eastern Cape, FS – Free State, GA – Gauteng, KZ – KwaZulu-Natal, LP – Limpopo, MP – Mpumalanga, NC – Northern Cape, NW – North West, WC – Western Cape |
| U = unavailable, 0 = no cases reported |
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