STREPTOCOCCUS AND ENVIRONMENT (FIGURE )

The ubiquity of streptococci constitutes a continuous threat of infection. Herva (1979) reported on an outbreak of skin infection caused by streptococci (group A,β-hemolytic) in hunters from a wild moose.

Group L streptococci were isolated from meat handlers (processing chickens and pigs) together with Staphylococcus aureus (Barnham and Neilson, 1987). Feng et al. (2010), following two severe large scale outbreaks in China of S. suis originating from swine industry, described a new disease form of streptococcal toxic shock syndrome (STSS). The Chinese variant ofS. suisexhibited strong invasiveness and high pathogenicity. Epidemiological data showed thatS. suiscases occurred mainly in South China, from summer to autumn, a period characterized by high moisture and high temperature.

Cockroaches isolated from public hospitals, were also reported to carry streptococci internally and externally, consequently constituting a continuous source of human infections (Salehzadehet al., 2007).

Water is also a source of fecalStreptococci(Enterococci) as reported during Nile flood season (Saleh, 1980), Apalachicola River, Florida (Elder, 1987) and in New Zealand where the main source of enterococci in river waters was most likely runoff from dairy farms located on the flood plains (Deely

Table 2.22.1 ZoonoticStreptococcusspp. classified according to their Lancefield group antigen.

A, C, G and L S. dysgalactiae β Bacteremia yes

E, P, U, V, none

S. agalactiaebeing suspected as the cause of this fatal infection (Jafaret al., 2009). The authors, using random amplification of polymorphic DNA (RAPD) analyses, found nearly identical RAPD banding patterns between S. agalactiae from fish and sewage sources and deduct that sewage may be the principal fish contamination source. Unfortunately, they did not report on human cases related to fish handling or consumption. An additional relationship between fish and human streptococcal disease was presented by Miller and Neely (2004) who successfully used zebra fish (Danio rerio) as a model to study these infections, presenting similar pathologies.

In connection to sea environment,Streptococcus equisubsp.zooepidemicusstrain was isolated from two remote seals (harbor and grey types) in the North Sea, Germany. According to authors, grey seals were probably the vectors of this strain (Akinedenet al., 2007).

Some environmental parameters (temperature, pH and osmolarity) were found to modulate some genes (multifunctional adhesions) inS. gordonii. SomeS. gordoniistrains are harmless and commensals of the human oral cavity, however some are strongly connected to severe disease (infective endocarditis) (El-Sabaeny et al., 2000). The main question remaining is whether these environmental conditions are the only prerequisite for virulence direction change.

Harmeetet al.(2009) reported on the better capability of group B streptococci (GBS) strains isolated from asymptomatic carriers (pregnant women) to form biofilms compared to those from symptomatic Figure 2.22.1. Streptococcispp. and various environmental aspects connected to their infection

Environmental Aspects of Zoonotic Diseases 142

animal organs are less exposed to these stresses and, owing to their defense mechanism against immunological cascade and affable environment, do not require biofilm formation but dispersal in order to succeed.

Bishop et al.(2007) reported on a necrotizing fasciitis outbreak caused byS. agalactiaein a captive crocodile species. There were several speculative suggestions on this infection’s origin such as: a) high stocking density that may increase the bite wounds and captivity stress; b) infected mice used as feed;

and c) inhabitation of mucous membranes by these microorganisms. However, none of these suggestions was clear cut evidence.

The in vitro optimal atmosphere (aerobic vs. anaerobic) for the isolation and growth of group A β-hemolytic streptococci is still under considerable debate. Schwartzet al. (1985) found that this group isolated from throat, grew better under anaerobic atmosphere; however, other studies did not support this conclusion (Roddeyet al., 1995).

An interesting finding on the facultative anaerobe group B Streptococcus (GBS) (an opportunistic pathogen of pregnant women, newborns, and elderly persons) revealed that its invasiveness [using the dynamicin vitroattachment and invasion system (DIVAS) in neonatal mice] is significantly enhanced in the presence of ≥5% oxygen. The invasiveness of this group was described as linked to enhanced polysaccharide production especially under aerobic atmosphere (von Hunolsteinet al., 1993).

A study of risk factors of increased carrier potential of group B streptococcus in southern Israel was performed on different human populations. Women, particularly immigrants from the former USSR, were significantly more prone to carry the pathogen than native Israeli women (comprised of ethnical groups such as Bedouins and Jews) with expected transmission rate of neonatal disease populations at low incidence.

Lam et al. (2007) described the identification of S. canis from dog owners associated with ulcer infections. It should be pointed out that the described cases were linked to preceding diseases such as diabetes mellitus that by itself causes permanent wounds and ulcers.

Finally, air flow was also suggested as a possible route of contamination. Thompsonet al.(1978), in relation to cows infected with S. agalactiae, found that rapid airflow toward teats as a result of sudden vacuum loss characterized vacuum abnormalities associated with increased risk of mastitis infection in these animals.

2.22.2 REFERENCES

Akineden, O., Alber, J., Lammler, C., Weiss, R., Siebert, U., Foster, G.,et al.(2007) Relatedness ofStreptococcus equi subsp.zooepidemicusstrains isolated from harbour seals (Phoca vitulina) and grey seals (Halichoerus grypus) of various origins of the North Sea during 1988-2005.Vet. Microbiol.121, 158–162.

Barnham, M. & Neilson, D.J. (1987) Group L β-haemolytic streptococcal infection in meat handlers: another streptococcal zoonosis?.Epidemiol. Infect.99, 257–64.

Bishop, E.J., Shilton, C., Benedict, S., Kong, F., Gilbert, G.L., Gal, D.et al.(2007) Necrotizing fasciitis in captive juvenileCrocodylus porosus caused byStreptococcus agalactiae: an outbreak and review of the animal and human literature.Epidemiol. Infect.135, 1248–1255.

Deely, J., Hodges, S., Mcintosh, J. & Bassett, D. (1997) Enterococcal numbers measured in waters of marine, lake, and river swimming sites of the Bay of Plenty, New Zealand.N. Z. J. Mar. Freshwater Res.31, 89–101.

Elder, J.F. (1987) Indicator bacteria concentrations as affected by hydrologic variables in the Apalachicola River, Florida.Water Air Soil Pollut32, 407–416.

El-Sabaeny, A., Donald R. Demuth, D.R., Yoonsuk Parka, Y. & Lamont, R.J. (2000) Environmental conditions modulate the expression of thesspAandsspBgenes inStreptococcus gordonii. Microb. Pathog.29, 101–113.

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Feng, Y., Zhang, H., Ma, Y. & Gao, G.F. (2010) Uncovering newly emerging variants ofStreptococcus suis, an important zoonotic agent.Trends Microbiol.18, 124–131.

Harmeet, K., Praveen, K., Pallab, R., Jaswinder, K. & Anuradha, C. (2009) Biofilm formation in clinical isolates of group B streptococci from north India.Microb. Pathog.46, 321–327.

Herva, E. (1979) An outbreak of skin infections caused by group Aβ-hemolytic streptococci probably originating from wild moose.Scand. J. Infect. Dis.11, 125–127.

Jafar, Q.A., Al-Zinki, S., Al-Mouqati, S., Al-Amad, S., Al-Marzouk, A. & Al-Sharifi, F. (2009) Molecular investigation ofStreptococcus agalactiaeisolates from environmental samples and fish specimens during a massive fish kill in Kuwait Bay.Afr J Microbiol Res3, 022–026.

Johri, A.K., Padilla, J., Malin, G. & Paoletti, L.C. (2003) Oxygen regulates invasiveness and virulence of group B streptococcus.Infect. Immun.71, 6707–6711.

Lam, M.M., Clarridge III, J.E., Young, E.J. & Mizuki, S. (2007) The other group G streptococcus: increased detection ofStreptococcus canisulcer infections in dog owners.J. Clin. Microbiol.45, 2327–2329.

Marchaim, D., Hallak, M., Gortzak-Uzan, L., Peled, N., Riesenberg, K. & Schlaeffer, F. (2003) Risk factors for carriage of group B streptococcus in southern Israel.Isr. Med. Assoc. J.5, 646–648.

Martel, A., Decostere, A., De Leener, E., Marien, M., De Graef, E.et al.(2005) Comparison and transferability of theerm(B) genes between human and farm animalStreptococci. Microb. Drug Resist.11, 295–302.

Miller, J.D. & Neely, M.N. (2004) Zebrafish as a model host for streptococcal pathogenesis.Acta Trop.91, 53–68.

Roddey, O.F.Jr., Clegg, H.W., Martin, E.S., Swetenburg, R.L. & Koonce, E.W. (1995) Comparison of throat culture methods for the recovery of group A streptococci in a pediatric office setting.JAMA274, 1863–1865.

Saleh, F.A. (1980) Bacteriological quality of Nile water before and after impoundment (1963–1973): a review.Zentralbl Bakteriol Naturwiss135, 123–129.

Salehzadeh, A., Tavacol, P. & Mahjub, H. (2007) Bacterial, fungal and parasitic contamination of cockroaches in public hospitals of Hamadan, Iran.J Vector Borne Dis44, 105–110.

Schwartz, R.H., Gerber, M.A. & McCoy, P. (1985) Effect of atmosphere of incubation on the isolation of group A streptococci from throat cultures.J. Lab. Clin. Med.106, 88–92.

Smith, K.L., Todhunter, D.A. & P. S. Schoenberger, P.S. (1985) Environmental Mastitis: Cause, Prevalence, Prevention.J Dairy Sci68, 1531–1553.

Stock, I. (2009) Streptococcus pyogenes-much more than the aetiological agent of scarlet fever.Med Monatsschr Pharm 32, 408–416.

Thompson, P.D., Schultze, W.D., Sauls, J.N. & Arapis, S.C. (1978) Mastitis infection from abrupt loss of milking vacuum.J. Dairy Sci.61, 344–351.

von Hunolstein, C., Nicolini, L., D’Ascenzi, S., Volpe, C., Alfarone, G. & Orefici, G. (1993) Sialic acid and biomass production by Streptococcus agalactiae under different growth conditions. Appl Microbiol Biotechnol 38, 458–462.

Weinstein, M.R., Litt, M., Kertesz, D.A., Wyper, P., Rose, D.et al.(1997) Invasive infections due to a fish pathogen, Streptococcus iniae. N. Engl. J. Med.337, 589–594.

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Chapter 2.23 Tularemia

[FRANCISELLA TULARENSIS]

Francisella is a genus of gram-negative, strict aerobic, small non-motile rod-shaped or coccobacillary bacteria that are also facultative intracellular parasites of macrophages. The genusFrancisellacontains at the moment five species:F. tularensis, F. hispaniensis,F. noatunensis,F. philomiragiaandF. piscicida.

F. tularensisis the most infective and virulent zoonotic species for humans. The speciesF. tularensishas four subspecies (or serovars):1) F. tularensis subsp. tularensis(Type A) (found in North America and the most virulent to humans and domestic rabbits; 2)F. tularensissubsp.palaearcticaorholarctica(Type B) (found in North America in aquatic rodents such as beavers and muskrats, and in other small rodents in northern Eurasia); 3)F.tularensis subsp. novicida(formerly classified as a species) a relative non-virulent strain found in North America; and 4)F.tularensis subsp. mediasiatica(primarily found in central Asia, isolated from human, gerbil and tick) at the moment without information on its pathogenicity for humans (Petersen and Schrifer, 2005). A large variety of animals (.125 species) has been found to host F. tularensis(Avashiaet al., 2004; Parket al., 2009), among which rodents are the main reservoir with ticks, fleas, lice and flies as vectors (Hubalek et al., 1998; Meka-Mechenkoet al., 2003; Eliasson and Back, 2003; Aldea-Mansilla et al., 2010). Direct contact with rodents’ excreta is also known as a transmission route in addition to inhalation of contaminated dust (the ID is 10 to 50 organisms), consequently making it a possible bioterrorism weapon (Denniset al., 2001). Water was also implicated as a reservoir of F. tularensisspp. foci, associated to protozoa and water related arthropods (Tikhenko et al., 2001; Ul’ianova et al., 1982). The disease is also called Francis disease, marketmen’s disease, rabbit fever, deer fly fever, Pahvant valley plague (in USA), yato-byo, Ohara’s disease (in Japan) and lemming fever (in Norway). The clinical manifestation is related to the entry portal: from skin purulent ulcerate papule to pharyngitis, cervical lympadenitis, stomatitis, pneumonia, gastrointestinal bleeding, meningitis, diarrhea, renal failure and hepatosplenomegaly and death (∼30% without treatment).