Kitten Season Is Upon Us and sadly some kittens will not survive the first days and weeks of life A likely culprit – Streptococcus G One of the greatest pleasures of cat breeding is celebrating the safe arrival of a litter of healthy kittens. Watching an unfussed queen have an easy labour, deliver her kittens competently and happily, and go on to rear a litter of bright-eyed, bouncy, happy, friendly little cats is the “best it can get” experience. Unfortunately it is not always like that. UNEXPLAINED KITTEN DEATHS Sometimes things go wrong. Kittens get sick, sometimes very sick, and deteriorate rapidly. Onset of illness can be hours, days or a few weeks after birth, and progression of the infection is characteristically rapid – well in the morning, dead by nightfall or the next day or two. You rush to the vet, come home with antibiotics, kitten milk replacer, subcutaneous fluids, and watch as the tiny kittens struggle to live. Standard URTI treatments are usually prescribed, but they aren’t very successful. Some kittens do recover if they are treated early in the course of the infection, but there are litters where, despite best efforts, some kittens succumb to intractable upper respiratory disease, losing weight and losing strength, and within hours or a few days, dying. Sometimes none survive. Does this scenario sound familiar? It’s a mystery bug that is rapid and lethal for kittens. This is the profile of Streptococcus G infection. STREP G Strep G is a bacterium that can live on the queen’s vulva and vagina, causing her no problem. It is introduced to the kitten’s respiratory tract during birth, and rapidly becomes rampant. A bacterial weed – growing like mad in the wrong place. The surviving female kittens are almost certainly carriers from this early age, as the queen already is. Strep G cocci which find their way into the female kittens’ vaginas are ready for the next generation of kittens to be infected. Unless Strep G is eradicated, the pattern will likely reoccur in infected females in subsequent generations. HOW INFECTION HAPPENS Cats pass Strep G around because of the friendly mutual grooming habits, licking the genital areas of friends and themselves. Queens grooming their kittens infect the kittens. Infected “aunties” can do the same thing. HOW CAN I TELL IF MY CATS MIGHT HAVE STREP G? Here’s how to go about it. Go back through the breeding records of all of your breeding stock, and list the following. Yes, write the information down; you can use it in discussions with your vet later. Seeing the information written down makes it easier to see the overall picture. The pattern in your cattery over time is the evidence you need to make your case for treating your cats. For every queen, note the following: 1. Is she a survivor of a litter where one or more kittens died of respiratory illness? 2. Has she had aborted or absorbed litters? 3. Has she delivered any dead kittens early or full term? 4. Has she, at full term, been in labour that was half-hearted, sporadic, and eventually needed veterinary intervention? Has she evidenced uterine inertia? 5. Has she had kittens where one or more became very ill, and even died in the period from 24 hours to 2 months after delivery? 6. Has that pattern repeated in subsequent litters? 7. With different studs? 8. What treatment was prescribed? 9. How well did it work? 10. What was the survival rate, and how long did the kittens live? 11. Did you have any tests done and what were the findings? 12. Any autopsies? What were the findings? 13. Have any of her daughters been bred, and what are their relevant histories? Create this list for each of them. 14. What about her mother? Create this list for her too. Look for patterns, clusters of these events occurring over time and involving some or all of your queens. Include females you may have sold for breeding. The pattern is the clue that there is a persisting underlying problem that has not been correctly treated, probably because it has never been accurately diagnosed. If your own research reveals some or all of these 14 issues in your own cattery, take one or more of your affected queens to your vet for a vaginal swab to test for Strep G. SPECIAL TEST FOR STREP G available at Gribbles Veterinary Pathology Laboratory (some path labs don’t test for Strep G). Tell your vet to order GVPL to (1) determine if Strep G is present in the cat’s vagina, and (2) to culture and do drug sensitivities. Your vet will have the details for GVPL. ERADICATION Clindamycin kills Strep G. Treat with Clindamycin (Antirobe) daily for 21 days. This is safe for pregnant cats. Treat all your cats as described above. Routinely weigh kittens daily, and if there is no weight gain, or a loss, and the queen has milk, start treatment immediately. The sooner treatment is begun the better the outcome. Don’t wait until tomorrow; it may be too late, and the kitten may already be too sick to recover. Control requires treating every cat in your cattery, male, female, entire, desexed, with clindamycin for 21 days. If you house your cats in separate colonies, treat every member of each colony at the same time, and do not allow any intermixing between members of treated and untreated colonies, or you will reinfect the treated cats. Read below how Strep G was identified as the cause of unexplained kitten deaths, and what medical interventions and cattery practices worked to manage this distressing problem. Source: Appendix 11, Breeding Cats: A Practical Guide (rev). Truda M Straede. Self published, 1997. Streptococcus G THAT ELUSIVE BACTERIUM A Study in the Pursuit of an Australia Wide Feline Health Problem in the Early 1990’s This article combines elements from articles and letters published in the RAS Cat Control Journal from August 1993 to February 1995. The problem described in the very first article ‘It’s easy to see the Pattern - In Retrospect’, struck a chord with readers throughout Australia, and contacts were made with me from as far away as Darwin - and New Zealand. At the time of publication of the second part of the first edition of Breeding Cats…. a practical guide, I still had occasional requests from breeders to help them to solve similar problems. Some of those who were helped in the past requested that the salient articles be included as an appendix in that second volume. After a break of 10 years or so, where Streptococcus G appeared to have somewhat faded into the background, there was a new wave of problems of a similar nature reported in Australia, but in the meantime there had been a ripple affect worldwide, with similar problems in far flung places being treated as recommended here. Emails1 from all over the world have come to me asking for help, which is why I consider that it is worthwhile reprinting this saga as an example of what we as breeders can do with co-operation amongst ourselves, friendly vets and pathologists…. Big pharmaceutical companies and universities have their own research agendas, not always interested in responding to the concerns of breeders, but we should not ‘lie down and take it’, but attempt to move the agenda onto our concerns. In August 1993 I first reported on the RASCC Journal a rash of problems, which had been occurring amongst my cats for the previous 12 months. As I had by this stage a wholly Leukaemia free cattery, with all breeding stock Leucogen vaccinated, I was becoming very dispirited with a cattery wide rash of late abortions, and fading kittens. My cattery was free of Leukaemia so why was I having these problems, so indicative of a Leukaemia outbreak? In addition to the kittens which were fading from a few days old, the longer lasting ones on autopsy showed massive involvement of the lungs. They were totally unresponsive to Chloramphenicol, Amoxil, Clavulox, Tylan and Penstrep, where could this apparent flu infection have come from? Several of these same queens had had healthy normal kittens in the past. In January 1993 I was losing a litter of 7 one by one - the first died within 48 hours after a sudden weight loss, this is how I described what happened: 10-12-92 Quassia has seven beautiful robust kittens to Jolyf. Quassia herself initially a bit off colour - Penstrep shots, yoghurt for her and all her kittens, all settled down by 15 Dec. Suddenly on 23-12 one of the two boys lost weight, supplemented this one, and others with yoghurt/Energel cream and iron supplement. 10-1-93 this male suddenly took a nose dive in weight and other male also suddenly lost weight. Autopsy first male - some lung congestion - all kittens onto Clavulox and Mucodine. 12-1 all starting to go down hill rapidly - assessed chances as: one definitely dying, two with only days to go, one sickening, and one normal weight. Why not try Antirobe? There was nothing to lose. (Antirobe was very new at this time).Within an hour the dying one was dead, the two really ill ones were running around looking bright eyed - though it took me a lot of careful feeding and it wasn’t till the 16th that these two started to eat by themselves, the litter never looked back - but please note, I did not treat Mum. This was only the beginning - I had further problems with later litters from queens where only the kittens were treated, and even when I also treated the queens I still had residual problems. I came to the conclusion that the causative/ bacterial agent/s can be carried in a latent state. While I managed to destroy the internal manifestation so that kittens were carried to term, it looked very much as though it lodged in the respiratory passages, and could be shed over the kittens by the mother. As kittens fell prey to the infection at about the same time as they would if it were viral (ie about 5 weeks on, when maternally derived antibodies are wearing off), it was hardly surprising that it was lumped with ’cat flu’ in the mind of vet and breeder alike. Gathering up my personal experiences and those relayed to me by many other breeders, this is how I summed up my thoughts on this problem: ? MICRO-AEROPHILIC BACTERIA in CATS Truda M Straede 15-6-94 What did we know? 1 An Antirobe (Clindamycin) sensitive organism was involved with cases of early abortion, premature birth, low birth weight weak kittens, reluctance to go into labour, perinatal deaths and some concurrent congenital defects. 2 An Antirobe sensitive organism was involved with some kitten deaths, which may start as soon as a few days old, and may continue sporadically till all the kittens die, as old as 8-9 weeks, or until a couple of weeks after the kittens are removed from their mothers. Kittens typically looked normal, gained weight normally, till a sudden weight drop occurred over night, after which they withered away in 4-5 days, apparently unresponsive to any antibiotics, unless Antirobe was used. These kittens usually, but not always appeared to be dying from an acute upper respiratory tract infection, and on autopsy showed lung changes which confirmed this. Even kittens which showed no external signs, eg sneezing, stuffy noses and inflamed and stuck up eyes, on autopsy showed extreme changes consonant with pneumonia. Mother cats often also looked a bit off colour when this happened to their kittens, with depressed appetites and lack of interest in their kittens.(eg my queens Zouiidi, Quassia) 3 A queen treated with Antirobe, quite aggressively ie 14 day course, at the time of an episode such as 2, may have a perfectly normal litter next mating. (eg my queen Kit'n'Caboodle was treated with litter number 3, number 4,5,6 all OK.) 4 A queen (Quassi) not treated with Antirobe at the same time as her kittens were (the 4 week old kittens had responded like magic when they had been dying one by one), had a litter one week premature next time, all of which died (one was also deformed) at birth. After this she was treated with Antirobe. Her next litter was full term, but had some problems at about 4 weeks old, both they and Mum were treated with Antirobe. Her next litter was without problems throughout, in these last three litters, the sire was the same. 5 A queen treated with Antirobe both from the start of a call and throughout mating, (at least 10 days) and from week 5-6 of the pregnancy has an excellent chance of having a perfectly healthy litter, which grows very well and is remarkably trouble free. This treatment is equally successful whether the queen has been only in contact with queens affected in the past, or has herself lost a litter in one of the ways described above. 6 Young queens with their first litter may have some of the problems outlined in 1, if their mother was affected, whether she, or they were treated or untreated at the time of the first occurrence of symptoms in either. These young queens respond to treatment 0-1, 5-6 weeks of their next pregnancy, rearing strapping healthy babies. 7 A queen (Bisquit) who lost her first litter apparently because she failed to go into labour in time (only 2 kittens) appeared to be healthy. She became pregnant again, but in the last 10 days of pregnancy succumbed to an upper respiratory bug, for which sensitivity testing indicated a penicillin group treatment. She failed to respond adequately - so was treated with Antirobe, and was definitely on the mend within 24 hours. Quite unaided she produced an on time litter of one very large, healthy kitten, which thrived. 8 An only survivor kitten from a case such as 2, grew into a perfectly healthy brood queen (Bella). Called, mated, carried litter - till almost (62 days) term. Two apparently fat healthy kittens, and one dead at birth because labour was also protracted as well as early. Kittens lived for 8-10 days - apparently died of acute pneumonia. I then realised that mother was only survivor of the first litter of a queen whose only other litter was treated aggressively with Antirobe. Bella had never been treated with Antirobe till this kitten loss. HYPOTHESIS By drawing a parallel with what Kim Kendall had told me about Contagious Equine Metritis,1 caused by a micro-aerophilic bacterium, carried on the mare's vulva, which causes no symptoms or disease in the mare, but when it is enabled to pass into the uterus during mating, causes early abortions, premature births and neonatal losses, (it is thought to be transmitted by the stallion from mare to mare) I surmised that our losses could be caused the same way by a similar type of organism. Firstly, though many samples were sent off to pathology labs by my vet (Karen Hedberg) who was quite concerned about the apparent epidemic amongst many breeders, the results had been either no growth, or a range of other organisms, including most frequently, Pasteurella multicida which were unlikely to be the main cause. Such a result would not be surprising, if the causal agent was indeed a microaerophilic bacterium, which would elude all the routine tests, because of its very specialised environmental requirements. Secondly, causes other than bacterial were fairly clearly ruled out because of the very dramatic response to one specific antibiotic, Clindamycin, used generally for anaerobic bacteria, including some pretty nasty ones! Some concern was felt, not only by me, that this antibiotic, so important in treating very refractory and serious conditions, should not be indiscriminately used - a good reason why actually tracking down the cause, studying it specifically, developing a lab test for queens, and working out an effective treatment that doesn't encourage the growth of drug resistance is very important. Thirdly, queens appeared to be able, like mares, to carry this organism with no adverse effect to themselves - the trouble only started with mating. This once again suggested the inside/outside type location, such as the vulva as the preferred site for the bug, allowing ready entry through the cervix at mating. Fourthly, unlike mares, cats behave in such a way that transmission horizontally, from queen to queen is very probable (I have no evidence implicating studs) - queens live in colonies, and it is the height of feline good manners for them to lick each other's bums - and then their own. Fifthly, the constant grooming of neonates by their mothers, who are also assiduously grooming themselves, particularly, after birth, their rear ends, gives abundant opportunities for vertical transmission, the bug to be liberally smeared all over kitten bums and mouths, for it to enter the lungs, giving a set of symptoms which are absent in the mare/foal interface because of differences in behaviour, but also creating a new generation of carrier queens. 1 B.Rogerson, Contagious Equine Metritis Bacteriology Vic IInst of Animal Science, Dept of Ag Equine Veterinary Science 8(1), 1988 SOME NIFTY BUG As an ecologist I was full of admiration for its exploitation of an obscure niche; one where it was so ‘safe’!! By the time that I had come to this conclusion, I had begun to have confirmation from breeders all around Australia and as far away as New Zealand that I was not alone. They came as timid calls, guarded calls, anonymous calls and letters for the RASCC Journal where the name was to be withheld. I invoked the wrath of one vet, who wrote a letter very critical of my whole hypothesis, but equally, I had many calls from vets who had clients who wanted to use the treatment we had worked out. I talked to them, I passed them on to my vet (Karen Hedberg BVSc), they were, if not convinced, at least prepared to try the treatment regime. One Australian Mist breeder, who had also suffered the same kind of problems, was, by chance, an outstanding Microbiologist. She prepared an answer for a critical vet, which was printed in the RASCC Journal in May 1994. Her letter is reprinted here in full as it provides not only a measured answer to the specific criticisms made by the vet, but also presents a well reasoned view of the balance between vet, hobbyist and professional, and is of interest in its own right. The Editor As an experienced microbiologist (virology and epidemiology), cat breeder and Victorian reader of the RASCC Journal, I have read with interest the series of articles (Aug and Nov 93) and arising correspondence (Feb 94) concerning diagnosis and treatment of infectious diseases in cats and litters of kittens. In particular I would like to draw attention to comments made by Nicholas Jonsson (Feb 94). He quite correctly states that Pasteurella multocida may be a normal inhabitant (flora) of the mouth and respiratory tract of most normal cats. BUT WHAT IS A NORMAL CAT? I believe a ‘normal cat’ to be your everyday domestic cat that is free to roam (only during daylight hours of course!), sharing an area and being in contact with many other cats and therefore in contact with a variety of pathogenic (disease producing) and non-pathogenic microorganisms (bacteria, viruses, protozoans, fungi, yeast ). Consequently, these cats are continually challenged (infected) by the local population of microorganisms and therefore have well developed, mature immune systems (immunocompetance). Vaccinations are helpful but do not protect cats from all infectious diseases. On the other hand, I believe that ‘cattery cats’ (pedigree), although vaccinated and given lots of love and care, are maintained in isolated environments on a long term basis are no longer ‘normal cats’. I believe there are two main reasons for this: 1. The maintenance of pedigree cats in isolated colonies (catteries) around Australia (or any country) allows for each colony of cats to establish their own microflora (‘normal flora’). Consequently, each colony of cats (cattery) will establish its own epidemiological pattern. This trend also occurs in the human population. For instance, overseas or even interstate travellers often succumb to mild to severe gastrointestinal upsets upon relocation. These upsets are often caused by encountering a new set of normally non-pathogenic (friendly) microorganisms that are different from the ones at home. Cat breeders often encounter this same phenomena when a new cat is introduced to their colony, even from a colony that is ‘just down the road’. 2. With our efforts to protect our precious and most-loved pedigree cats, I feel we have unknowingly done them a disservice, as such isolation, not only during the lifespan of one cat but over many generations has lead to the inability of our cats to deal adequately with some infectious agents, including the friendly ones. They have become immunocompromised. Again one can cite the same phenomena occurring in the human population where a simple cold virus can have a devastating effect on a geographically isolated group of humans eg. island populations. In fact, it is well documented that during the colonisation of the USA, Europeans almost wiped out entire tribes of Native Americans by introducing the measles virus. So, where there is diminished immunocompetance associated with altered normal microflora and/or isolation from a wide variety of pathogens, there is the potential for altered or unusual immune responses. For instance, a microorganism that is regarded as normal flora may now become a potential pathogen. Therefore it may be unwise to immediately dismiss Pastuerella multocida as a possible cause of disease in some catteries. Potentially it may be as fatal to our much loved but isolated cats as measles was to the Native Americans!! On the question of antibiotic use raised by the various authors, I agree with Nicholas Jonsson that swapping from one antibiotic to another leads to the evolution of drug resistant strains. However, it seems he failed to understand that where there is a failure to respond to a broad spectrum antibiotic of first choice (eg penicillin derivatives) within an acceptable time frame (and that may only be a matter of hours in a neonatal kitten) then either the addition of (if compatible) or replacement with (if incompatible) another antibiotic to further broaden the spectrum covered is acceptable. This may mean introducing an antibiotic such as Antirobe to cover the possibilities that certain bacteria regarded as ‘normal flora in normal cats’ DO produce clinical syndromes in some ‘cattery cats’ or unusual bacteria and microorganisms that are yet to be detected and identified (isolation, culture etc) are involved. As a microbiologist, I quote my personal experience in this very area, where rotaviruses (now regarded as the main cause of epidemics of gastroenteritis in humans and animals) may still have remained undetected if we had stuck to what was regarded as conventional thinking in the early to mid 1970's (1,2,3,4) 2. Whether we may be research scientists, veterinarians, breeders or whatever, we MUST remain openminded when a ‘non-text book’ incident arises. It is indeed unfortunate that research funding for small animals is so limited .... cats are only regarded as ‘economically important’ by the people who pay their veterinary bills!! A large portion of information on infectious disease in cats is based on what is normal for the ‘domestic cat’, but when it comes to unusual ‘cattery cat’ problems, much of the information is anecdotal, coming from experienced breeders. The nature of the problem may also vary from cattery to cattery. Thus I recommend that breeders keep detailed records of problems, symptoms, observations, living arrangements (of the cats!!!) and even ‘gut-feelings’, as in the absence of scientific proof, these records may be gold mines of information that avert future disasters for themselves and other breeders. Regards Dr.Sue Roger-Withers, B.Sc., Ph.D.(Melb). The personal success one breeder had had using our advised course of treatment was neatly summed up in her letter in the same issue of the Journal: Dear Truda, 2 References: 1. Rodger, S.M. Biochemical and biophysical characterisation of rotaviruses. 1977. Ph.D. thesis. University of Melbourne. 2. Rodger, S.M. J.A.Craven and I.Williams. 1975. Demonstration of reovirus-like particles in the intestinal contents of piglets with diarrhoea. Aust. Vet. J.51:536. 3. Rodger, S.M. M.J.Studdert and I.H.Holmes. 1980. Characteristics of the genomes of equine rotaviruses. Vet.Microbiol. 5:243-248. 4. Rodger, S.M. R.F.Bishop, C.Birch, B.McLean and I.H.Holmes.1981. Molecular epidemiology of human rotaviruses in Melbourne, Australia, from 1973-1979, as determined by electrophoresis of genome ribonucleic acid. J.Clin. Micro. 19:272278 I hope I'm not too late for the next RAS Journal. I have just read the Feb one at a friends house, and I feel I simply must write and say how angry I was when I read that vets letter about your ‘Bacteria’ series in the last two journals. I am one of your anonymous callers, who asked you for help at the end of last year. I had lost litters early, had mixed live and dead births, and had lost kittens early in their lives, I was in despair. My vet had helped me a lot, but after clearing all my cats for AIDS and leukaemia (a somewhat expensive exercise in itself), he couldn't make any more suggestions, though in one case he did suggest that progesterone might help during pregnancy. After reading your first articles, I was so excited that here might be a possible solution, that I rang my vet, and read him chunks of it over the phone. As you can imagine, he wasn't wildly enthusiastic, but agreed to read the article, and suggested I also talk to you. As a cautious vet, he suggested that we try the girl whose last litter had contained one dead kitten at birth, and two more who died separately at 10 days and 3 weeks. We used the Antirobe and Clavulox combination for 10 days from the start of the call, and over the mating, then the repeat of 7 days Antirobe from week 5 to week 6. Five beautiful kittens, who all lived to be sold to satisfied customers. I am now just finishing a round of litters from my other 3 Queens, all of whom had also had some problems. While not all are yet grown to sale age, all were born live and have thrived. That vet's letter really angered me because the narrow attitude it displayed seemed to suggest that no one but a vet knows anything about rearing kittens, and cat health, and that breeders observations are worthless. He made criticisms of both you, and implicitly your vet, and the other one who contributed, as though you were all dimwits who needed taking down a peg. I know that there are a lot of much happier breeders up here after this kitten season, because you seem to have put your finger on something that has been going on - that all are reporting 100% survivorship where they were doing poorer than 50% last season. I think that the time has come for some research effort to be put into discovering whether you are really onto some new problem - as far as I can see, the fact that Antirobe works to clear up my problem, is only a clue. My vet is also of the opinion that your observations, and the huge response other breeders obviously made, suggest that there is some ‘epidemic’ type problem which needs investigating. I hope I am in time for the next journal, but I would like to remain anonymous - the Fancy up here is very small, and not very cooperative! Indeed we had put considerable effort into trying to isolate a causative bug, with the co-operation of some of Sue’s colleagues, pathology tests were carried out on a selection of kittens which had died of the apparent syndrome, using culture systems not generally available in Veterinary Pathology labs. The final result was published in the RASCC Journal, February 1995, and is reprinted here. THAT BACTERIUM - ON THE TRACK AT LAST The lsolation of Group G Streptococcus from Aborted Kittens As promised in the November 1994 issue of the RAS Cat Control of NSW Journal, we are able to announce that the elusive Clindamycin (Antirobe) sensitive micro-organism that has cleverly evaded repeated attempts at isolation and identification appears to be a Group G Streptococcus (Straede et.al. 1995). For those owners, breeders, veterinarians and other interested persons who have experienced or followed the saga of kitten losses due to abortion, stillbirths, foetal abnormalities and sudden death from apparent rapid onset bronchopneumonia etc. (RASCC journals August 1993 to November 1994, National Cat 1994) this isolation provides relief and reassurance for all concerned. Although we had gained an insight into treatment and control of these problems we had no idea what micro-organism(s) were responsible for the apparent Australia-wide epidemic affecting almost all breeds of cat. Attempts to isolate and identify a Clindamycin-sensitive micro-organism have been hampered by a number of factors related to the nature of the Group G Streptococci and the pattern of disease. The nature of the bacterium is such that it can easily remain undetected by routine Laboratory testing. In relation to the pattern of disease, problems experienced by breeders resemble patterns that are consistent with other diseases such as feline leukaemia, feline immunodeficiency virus (cat AIDS), Chlamydia or mycoplasma. Frustration among breeders arose when extensive laboratory testing and retesting as well as aggressive antibiotic treatment programs for such micro-organisms proved unsuccessful. Following successful treatment of the symptoms and pattern of disease with Clindamycin, the authors began searching for another cause. With the help of the Victorian Department of Agriculture as well as frustrated breeders and veterinarians from all over Australia who were willing to provide specimens, Group G Streptococci were first isolated from stillborn kittens obtained from a Western Australian breeder. After following a treatment program outlined by the authors, there has been no recurrence of the problem in this cattery. It is interesting to note that while group G Streptococci have been associated with sinusitis, septicaemia and endocarditis in humans (Review Medical Microbiology 18thEd), the only recorded isolation of Group G Streptococci in cats was in association with infectious lymphadenitis (Swindle et al. 1980). Also, in humans, Clindamycin is indicated for serious infections of the respiratory tract and infections of the female pelvis and genital tract (endometritis, ovarian abscesses, pelvic cellulitis, vaginal cuff infections) that are caused by Streptococci able to survive with little oxygen (including Group G) (Mims Annual 1994). It appears that the patterns of disease in humans closely resemble those patterns observed by cat breeders. It is now necessary to conduct further research to establish the role of the Group G Streptococci in breeding losses in cats. During routine laboratory testing for possible causative agents, a number of other bacteria have also been occasionally isolated. These include Pastuerella multocida some untyped Streptococci (which may have included Group G) and a * Gram positive bacillus that to date is unable to be identified. The significance of such isolates is yet to be established, but supports the authors’ view that well conducted research now be performed to resolve a potentially complex issue regarding feline reproductive disorders. The possibility that a number of other causative agents may exist is further supported by the observation that the described pattern of reproductive and/or respiratory problems can sometimes be resolved with antibiotics other than Clindamycin. These include lincomycin (related to Clindamycin) and tetracyclines. Although these observations may be explained by variations in drug sensitivity, it does raise another very important aspect to problem management: the choice of antibiotic must be based on bacterial drug sensitivity testing. Until recently, Antirobe (Clindamycin) was not scheduled for use in cats. However, due to its increasing widespread use throughout Australia by cat breeders it has now been scheduled. While many breeders have successfully eliminated their breeding and/or kitten problems with Clindamycin, it is very important that Clindamycin does not become the ‘magic bullet’ and be used indiscriminately for everything. It has been reported that some bacteria rapidly develop resistance to Clindamycin (Mims Annual 1994) and as responsible breeders, the last thing we need is to create Clindamycin *Gram= Gram stain - a basic laboratory test used in preliminary identification of bacteria. resistant bacteria through misuse and abuse of the antibiotic!!! It is now more important than ever that, where possible, antibiotic selection be based on the results of drug sensitivity testing. Now that we are progressing with the detection of causative agents, veterinary diagnostic laboratories will be able to perform tests to help select the correct antibiotic. If antibiotics are used incorrectly or inappropriately, then a breeder in distress may risk further disasters eg. queens becoming carriers and at times of stress (during pregnancy, travel etc) shedding the organisms to other queens or perhaps experiencing a recurrence of the problem themselves. Anyone who may be experiencing repeated breeding and/or kitten losses similar to the described pattern, and even if only trouble-some, is encouraged to have samples tested. Once the correct bacterial sensitivity has been determined, the results have been spectacular. There is improved reproductive success, minimal kitten losses (abortions, deformities, respiratory infections) and consequently, reduced veterinary costs, not to mention reduced stress for the owners!!!! Breeders are encouraged to contact the authors before launching into testing and/or treatment programs blindfold. Advice is available regarding testing (now relatively simple and inexpensive) and treatment strategies. Should you so wish, your confidentiality will be respected. In summary, the isolation of Group G Streptococci associated with breeding problems in cats is a major step forward (and a relief to many) in understanding and controlling what appears to be a nation wide epidemic. There is still a way to go in obtaining ‘the real story’ but with the help of willing and responsible breeders and the co-operation of veterinarians and veterinary laboratories, we can jointly put the puzzle together. The Authors: Dr T M Straede B.Sc. Ph.D. Nintu Cattery NSW (02)4575 0227 Dr S M Rodger-Withers BSc DAc PhD Member Australian Society of Microbiology, Member Victorian Society of Venereology FCCV Qihai Cattery Victoria (03)9391 5028 Dr Karen Hedberg B.V.Sc North Richmond Veterinary Hospital NSW (02) 4571 2042 Jeanette Perkins B.S.W ,C.O.A.WA. Satu Cattery Western Australia (08) 9821 2171 The authors wish to thank breeders, veterinarians and all interested persons who have provided specimens, encouragement help and support in getting this project off the ground. References Swindle M M and Norayan 0 1980. Contagious Streptococcal lymphadenitis in cats. J.A.V.M.A. 177 829-830 In conclusion I would like to say that whether or not there is indeed a complete syndrome as suggested in my original hypothesis, the value of the use of Clindamycin (Antirobe) has been further investigated, particularly by Dr Richard Malik (Veterinary Science, Sydney University), in relation to its use in treating upper respiratory infections in cats. This appendix is very much a ‘work in progress’. Even if it never again provides a specific answer to a breeder’s problem, it may demonstrate that breeders are able to pursue their own elusive feline health problem, ‘with a little help from their vets, and ‘friends’.