Abstract
This study summarizes the diagnostic findings from all anemic cats diagnosed with hemotropic mycoplasma (HM) infections at the Western College of Veterinary Medicine — Veterinary Teaching Hospital between 1996 and 2005. The objectives were to determine the frequency of HM-induced anemia among all cats presented with anemia during this period, the clinical findings and risk factors associated with clinical HM infection, and factors affecting or predicting survival. Medical records were examined from 23 cats with HM-induced anemia from the total of 170 cats diagnosed with anemia during this period. The frequency of HM-induced anemia was 14% (23/170) among all anemic cats. Cats with HM-induced anemia were less likely to be purebred (P = 0.04) than other cats with anemia. Of the cats with HM-induced anemia, those with positive retroviral status (P = 0.01), concurrent illness (P < 0.01), or lack of erythroid regeneration (P = 0.01) were most likely to die. The 1-year survival of HM-infected cats was 65% (13/20).
Résumé
Anémie chez les chats atteints d’une infection aux mycoplasmes hémotropes : Évaluation rétrospective de 23 cas (de 1996 à 2005). Cette étude résume les résultats diagnostiques de tous les chats anémiques diagnostiqués avec des infections aux mycoplasmes hémotropes (MH) à l’hôpital d’enseignement vétérinaire du Western College of Veterinary Medicine de 1996 à 2005. Les objectifs consistaient à déterminer la fréquence de l’anémie induite par les MH parmi tous les chats présentés avec de l’anémie durant cette période, les résultats cliniques et les facteurs de risque associés à l’infection clinique aux MH ainsi que les facteurs affectant ou prédisant la survie. Les dossiers médicaux de 23 chats atteints d’anémie induite par MH ont été examinés parmi un total de 170 chats diagnostiqués avec l’anémie durant cette période. La fréquence de l’anémie induite par MH était de 14 % (23/170) parmi tous les chats anémiques. Il était moins probable que les chats avec de l’anémie induite par MH étaient des chats de race (P = 0,04) que les autres chats anémiques. Parmi les chats atteints de l’anémie induite par MH, la mort était plus probable chez ceux avec un statut rétroviral positif (P = 0,01), une maladie concomitante (P < 0,01) ou l’absence de régénération érythrocytaire (P = 0,01). Le taux de survie après 1 an des chats infectés par MH était de 65 % (13/20).
(Traduit par Isabelle Vallières)
Introduction
Hemotropic mycoplasmas (HM), also called hemoplasmas, are gram-negative epierythrocytic parasites that can induce hemolytic anemia in infected hosts (1). Hemotropic mycoplasmas have recently been reclassified from the Hemobartonella genus of the order Rickettsiales to the order Mycoplasmatales, family Mycoplasmataceae, genus Mycoplasma on the basis of 16S rRNA gene sequence analysis (2,3). There are 4 species of HM known to infect cats: Mycoplasma haemofelis, “Candidatus Mycoplasma haemominutum”, “Candidatus Mycoplasma turicensis”, and “Candidatus Mycoplasma haematoparvum” (2,3). The latter 2 species have only recently been documented, and testing for these species is not commercially available. Host factors, HM species, and strain-associated virulence factors may affect the clinical outcome of HM infection (1,4–6).
Mycoplasmas are not free-living, and require a host cell for survival making them extremely difficult to culture; indeed, feline HM species have never been successfully cultured. Polymerase chain reaction (PCR) has improved our ability to detect subclinical and clinical HM infections in cats and has also been useful in documenting the global distribution of HM infections in domestic and wild felids (4–10).
The most likely route of infection for feline HM is via arthropod vectors (fleas or ticks) and though DNA has been detected in cat saliva and feces, direct transmission has not been demonstrated (11–13). Retroviral co-infection may increase the risk of hemoplasma infection and may be associated with more severe clinical disease (14,15). Administration of tetracycline, doxycycline, enrofloxacin, marbofloxacin, or pradofloxacin has decreased the bacterial burden and clinical signs, but no antibiotic protocol has consistently eliminated infection (15–19).
The primary objectives of this retrospective study were to describe the relative frequency of HM infection as a cause of anemia in cats at the Western College of Veterinary Medicine — Veterinary Teaching Hospital (WCVM-VTH) from 1996 to 2005 inclusive, and to describe the clinical findings and risk factors associated with clinical HM infection. The secondary objective was to identify factors affecting or predicting 1-year survival in cats with HM infection.
Materials and methods
Medical records were reviewed from all cats with a diagnosis of HM-induced anemia that had been examined at the WCVM-VTH between January 1, 1996 and December 31, 2005. A definitive diagnosis of HM-induced anemia was determined by either blood smear evaluation (exhibiting epicellular red blood cell parasites) or by a positive validated PCR test (20). Signalment of the cats with HM-induced anemia (age, sex, breed) was recorded and compared with signalment of cats examined for other causes of anemia at the WCVM-VTH during the same period. Medical records from the cats with HM-induced anemia were examined for details regarding the presenting complaint, housing (indoors only versus access to the outdoors), a history of or presence of wounds consistent with a recent cat fight, evidence of external parasites, retroviral status, hematology results, therapy, and disease outcome. The cats with HM-induced anemia were divided into 2 categories based on presenting complaints: those with signs typically associated with anemia (one or more of anorexia, lethargy, and weakness) and those with signs not typically associated with anemia. Anemia was considered regenerative if reticulocytosis was evident (reticulocytes > 1%) and blood smear evaluation was supportive (polychromasia on Wright-Giemsa-stained smears) (21). Cases with multiple admissions for either HM or other causes of anemia were included once. Owners were contacted to determine 1-year survival when this information was not available in the medical record.
All cats diagnosed with anemia from any potential cause (except HM) during the same time period were identified and the medical records reviewed. The etiology of the anemia did not need to be identified for the case to be included in the study.
The associations between age (< 2 y or ≥ 2 y), sex (male or female), spay or neuter status, breed (domestic breeds such as domestic short hair, domestic medium hair, and domestic long hair versus purebred cats), and HM as a cause for anemia were examined. The associations between survival of cats with HM-induced anemia for 1 y and retroviral infection, erythroid response, administration of blood transfusion, and existence of concurrent illness were also examined. All associations were evaluated using chi-squared (χ2) analysis (Statistix version 8 2003; Analytical Software, Tallahasse, Florida, USA) with P < 0.05 considered significant. If an expected cell value was < 5, a 2-tailed Fisher exact test was used.
Results
During the 10-year period, 23 cats with HM-induced anemia met the criteria for inclusion in the study. During the same time period, a total of 170 cats were identified with anemia (HM-induced and other causes). Hemotropic mycoplasma infection was responsible for the anemia in 14% (23/170) of the cats.
Signalment was compared between cats with HM-induced anemia and the total anemic population (Table 1). Young cats (< 2 y) were no more likely to be infected with HM than older cats (< 2 y) (P = 0.44). Gender did not achieve statistical significance (P = 0.05) though males were 2.9 times more likely to be infected with HM than were females [95% confidence interval (CI): 0.95 to 8.93]. Neuter status was not associated with a diagnosis of anemia due to HM (P = 0.29). Domestic breeds of cats were more likely to be diagnosed with HM-induced anemia than were purebred cats (P = 0.04).
Table 1.
Signalment-associated risk factors for hemotropic mycoplasma-induced anemic cats and cats with anemia due to all causes
| Hemotropic mycoplasma- induced anemia (n =23) | Anemia due to all causes (n =170) | |
|---|---|---|
| Median age (range) | 2.5 y (0.7–18 y) | 7.5 y (0.1–21 y) |
| Cases < 2 y of age (%) | 6 (27%) | 32 (20%) |
| Male (%) | 19 (83%) | 102 (60%) |
| Neutered males (%) | 12 (52%) | 79 (77%) |
| Female (%) | 4 (17%) | 64 (38%) |
| Neutered females (%) | 3 (13%) | 48 (75%) |
| Domestic breed (%)a | 23 (100%) | 120 (82%) |
Significant difference between cats with hemotropic mycoplasma and cats with anemia from all causes (P < 0.05).
Of the 23 cats with HM-induced anemia, 18/19 (95%) had known outdoor access and 4/23 (17%) had a history of a recent cat fight. The most common presenting complaints for 17/23 (74%) of the cats with HM-induced anemia were lethargy, weakness, and anorexia. Cats were also presented for problems not directly attributable to HM infection including cat bite abscess (n = 1), and dystocia (n = 1). Two cats were presented with generalized seizures and another cat for acute collapse. Based on response to therapy for anemia, the seizures and collapse in these 3 cats were considered to be manifestations of hypoxia secondary to severe anemia.
Concurrent illnesses or stressors identified in the cats diagnosed with HM-induced anemia included retroviral infection (n = 4), dystocia (n = 1), hepatic lipidosis (n = 1), pancreatitis (n = 1), diabetes mellitus (n = 1), recent surgery (n = 1), hypertrophic cardiomyopathy (n = 1), obstipation (n = 1), recurrent cat bite abscess (n = 1), pancytopenia (n = 1), and myelofibrosis (n = 1). The cat with hepatic lipidosis initially became anemic as a result of hypophosphatemia associated with refeeding syndrome and required a blood transfusion. The donor cat was later found to be a subclinical carrier of HM (M. haemofelis as determined by PCR). The recipient of the transfusion was presented to the WCVM-VTH in a collapsed state from anemia 1 wk following the transfusion. Of the 19 cats with HM-induced anemia tested for retroviral infection, 1 was positive for both FeLV and FIV (5%), 1 for FIV (5%), and 2 for FeLV (10%). External parasites, in particular fleas and ticks, were not noted on any of the cats, although 2 cats did have ear mite (Otodectes cyanotis) infestations. Ear mites were not considered a concurrent illness.
Where a complete blood (cell) count was available, erythroid regeneration was noted in 59% (10/17) of cases with HM-induced anemia. In 1 case, there was an insufficient quantity of blood to generate a reticulocyte count. However, the blood smear evaluation was supportive of a regenerative response with polychromasia, nucleated red blood cells, and nuclear remnants.
Definitive diagnosis of HM infection was made by PCR in 13% (3/23) of cases and was based on blood smear evaluation in the remaining 20 cases. Blood smear evaluation was performed in 74% (17/23) of cases by a veterinary clinical pathologist and in 13% (3/23) of cases by a practicing veterinarian. Of the 3 cats that had positive PCR assays, 2 cats tested positive for “Candidatus M. haemominutum” and 1 cat tested positive for M. haemofelis. Blood smear evaluation was negative for HM parasites in 1 of these 3 cats (“Candidatus M. haemominutum”) and positive in the other 2 (1 each of M. haemofelis and “Candidatus M. haemominutum”). The M. haemofelis positive case was the cat with hepatic lipidosis that was infected via a blood transfusion. Both of the “Candidatus M. haemominutum” infected cats had concurrent illnesses: pancreatitis determined antemortem in 1 cat and myelofibrosis found at postmortem in the other cat. The primary disease leading to myelofibrosis was not identified.
Treatment was initiated in 87% (20/23) of the HM cats. All of these cats were treated with doxycycline (19/20) or tetracycline (1/20) at previously published dosages, dosage intervals and durations of therapy. Antibiotic therapy was the sole treatment administered in 20% (4/20) of HM cases. Oral prednisone therapy (immunomodulatory doses of > 2 mg/kg q24h) was administered in addition to doxycycline in 75% (15/20) of HM cases. At least 1 blood transfusion was administered to 55% (11/20) of HM cases. Fifty percent (10/20) of HM cases received all 3 therapies (antibiotics, prednisone, and blood transfusion). The average packed cell volume (PCV) of HM infected cats that received a blood transfusion was 9.8% (range: 7% to 20%) which was significantly lower (P < 0.01) when compared with 13% (range: 7% to 27%) for all the HM cats. Blood type was determined in 10 HM cases requiring transfusions, with 80% (8/10) being type A and 20% (2/10) being type AB.
The outcome was known in 83% (19/23) of cats with HM-induced anemia. One-year survival occurred in 63% (12/19) of HM cats. All but 1 cat surviving the first month after diagnosis survived at least 1 y. Five cats were euthanized at the time of diagnosis (2/6; both of which had positive retroviral status) or within a few wk of starting therapy (3/6; 1 with positive retroviral status and 2 that were apparently nonresponsive to therapy), and 1 cat died during initial treatment. This latter cat was the cat with hepatic lipidosis that contracted HM infection from a blood transfusion. One diabetic cat was euthanized 2 mo after apparent recovery from HM-induced anemia and concurrent pancreatitis. There was no indication in the medical record as to why elective euthanasia was performed. Recurrence of HM-induced anemia was reported in 1 cat (1/19; 5%) 9 mo after initial diagnosis and treatment. This cat responded to repeat treatment and subsequently had a 1-year disease-free interval.
Factors examined in this study that were not associated with 1-year survival included: sex (P = 0.54), spay/neuter status (P = 0.36), access to the outdoors (P = 0.14), evidence of a recent cat fight (P = 0.36), typical presenting complaint (P = 0.86), blood type (P = 0.15), treatment with a blood transfusion (P = 0.51), and treatment with prednisone (P = 0.42). Concurrent disease (P < 0.01), retroviral infection (P = 0.01), and lack of an erythroid response (P = 0.01) all decreased the likelihood of survival in cats with HM-induced anemia (Table 2). An erythroid response was present in 90% (9/10) of cats with no concurrent illness and absent in 86% (6/7) of cats with concurrent illness (P < 0.01).
Table 2.
Clinical factors significantly associated with a poor 1-year survival in 23 cats with hemotropic mycoplasma-induced anemia
| Number of cats affected | Number of cats that survived (%) | P-value | |
|---|---|---|---|
| Concurrent disease | 9 | 2 (22%) | < 0.01 |
| Retroviral infection | 3 | 0 (0%) | 0.01 |
| No erythroid response | 6 | 3 (50%) | 0.01 |
Discussion
The 14% relative frequency of HM as a cause of anemia in cats in this study is similar to previous reports of 8.7% to 20.2% (4,5,22). Comparison among different studies is challenging as population definitions are variable. Variability in infection rates may reflect differences in both the geographic distribution of HM and the population sampled.
The finding that purebred cats were less likely to be affected with HM-induced anemia is similar to data from other recent prevalence studies (5,23). All but 1 of the cats with HM-induced anemia in this study had outdoor access. Outdoor activities increase exposure to HM-infected cats and to potential arthropod vectors. Tick or flea infestation was not reported for any cats in this study; however, ectoparasite infestation may not have been thoroughly evaluated in all cases. In this geographic area, with low flea prevalence, direct transmission of disease through interaction with other cats may play a more important role.
In other recently reported prevalence studies, male cats were reported to be more likely to be infected than were female cats (5,23). Though males in the present study were not more likely to be infected with HM, the P-value approached significance (P = 0.05) and the odds ratio indicated that male cats were 2.9 times more likely to be affected with HM-induced anemia than female cats.
Age was not associated with the risk of infection, but this may have been related to the use of 2 y of age as a break-point in the population. The average age of cats with HM-induced anemia in this study (median 2.5 y: range 0.7–18 y) was younger than that for cats diagnosed with anemia from all causes (median 7.5 y: range 0.1–21 y). This is also younger than reported ages in other studies where cats with an average age of 10 y are reported to be at highest risk for clinical HM infection (4,6).
Similar to other reports, concurrent disease was a negative prognostic indicator for cats with HM infection in this study (6). In a retrospective study of clinically ill cats testing positive for “Candidatus M. haemominutum” by PCR, 7 of 21 cats did not have good long-term survival, and of these, 5 had concurrent disease (6). These findings may indicate that response to therapy for hemoplasma infection may be impacted by concurrent disorders. Comparison of treatment and outcome was not possible given the small number of cases and heterogenous concurrent diseases.
Limitations to this retrospective study include the lack of standardization regarding diagnoses and treatments as well as the method used to determine the total number of anemic cats. Diagnostic workup was limited in many of the HM-induced anemia cases. Few cats were tested using PCR, since this test was not routinely available during the early years of the study. A PCR assay was used in only 3 of the 170 anemia cases and was positive in all 3 cases. Blood smear evaluation was positive for HM in 2 of the 3 cases that were positive by PCR assay. Smear evaluation is not as sensitive as PCR assay for diagnosis of HM and may also be prone to false positive results due to stain artifact (18). It is not known if there were any false positives based on smear evaluation in this study. Blood smear evaluation by veterinary clinical pathologists would decrease the likelihood of false positive results. Also, the species of HM can not be determined on smear evaluation and knowing the species of HM may have an impact on the prognosis (1). The infecting HM species was unknown for many cases and subsequently, prognosis could not be related to HM species.
It is difficult to be certain that HM infection was the definitive cause of the anemia in all 23 of the HM cases in this study. Hemotropic mycoplasma infection may have been incidental or one of many factors contributing to anemia in some of the cats. Studies show that HM infections (including M. haemofelis) in cats are not always associated with anemia and hemoplasma blood loads, as determined by real time PCR, are not highly correlated with PCV (5). Some of the cats with anemia from other causes could have had concurrent HM infection that might have been detected using the more sensitive PCR assay.
The total number of anemic cats seen at the WCVM-VTH during the study period is suspected to be underestimated, as anemia had to be recorded as a major problem in the medical record. An alternative approach would have been to determine the total number of anemic cats based on clinical hematology submissions to Prairie Diagnostic Services, which processed all the samples during the study period. It was not possible to use this approach as the hematology submissions from the teaching hospital to this laboratory could not be separated from submissions from private veterinary clinics.
We conclude that cats with anemia, whether regenerative or nonregenerative, should be evaluated for HM infection. The possibility of concurrent disease, including retroviral infection, should be explored in cats with HM infection (determined by blood smear evaluation and/or PCR assay). Cats with HM-induced anemia that do not have concurrent disease have an excellent prognosis for clinical recovery and survival, even when they present in a severe hemolytic crisis due to HM infection. CVJ
Footnotes
Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office (hbroughton@cvma-acmv.org) for additional copies or permission to use this material elsewhere.
References
- 1.Messick JB. New perspectives about Hemotrophic mycoplasma (formerly, Haemobartonella and Eperythrozoon species) infections in dogs and cats. Vet Clin North Am Small Anim Pract. 2003;33:1453–1465. doi: 10.1016/j.cvsm.2003.08.002. [DOI] [PubMed] [Google Scholar]
- 2.Neimark H, Johansson KE, Rikihisa Y, Tully JG. Revision of hae-motrophic Mycoplasma species names. Int J Syst Evol Microbiol. 2002;52(Pt 2):683. doi: 10.1099/00207713-52-2-683. [DOI] [PubMed] [Google Scholar]
- 3.Neimark H, Johansson KE, Rikihisa Y, Tully JG. Proposal to transfer some members of the genera Haemobartonella and Eperythrozoon to the genus Mycoplasma with descriptions of ‘Candidatus Mycoplasma haemofelis’, ‘Candidatus Mycoplasma haemomuris’, ‘Candidatus Mycoplasma haemosuis’ and ‘Candidatus Mycoplasma wenyonii’. Int J Syst Evol Microbiol. 2001;51(Pt 3):891–899. doi: 10.1099/00207713-51-3-891. [DOI] [PubMed] [Google Scholar]
- 4.Sykes JE, Drazenovich NL, Ball LM, Leutenegger CM. Use of conventional and real-time polymerase chain reaction to determine the epidemiology of hemoplasma infections in anemic and nonanemic cats. J Vet Intern Med. 2007;21:685–693. doi: 10.1892/0891-6640(2007)21[685:uocarp]2.0.co;2. [DOI] [PubMed] [Google Scholar]
- 5.Willi B, Boretti FS, Baumgartner C, et al. Prevalence, risk factor analysis, and follow-up of infections caused by three feline hemoplasma species in cats in Switzerland. J Clin Microbiol. 2006;44:961–969. doi: 10.1128/JCM.44.3.961-969.2006. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Reynolds CA, Lappin MR. “Candidatus Mycoplasma haemominutum” infections in 21 client-owned cats. J Am Anim Hosp Assoc. 2007;43:249–257. doi: 10.5326/0430249. [DOI] [PubMed] [Google Scholar]
- 7.Fujihara M, Watanabe M, Yamada T, Harasawa R. Occurrence of “Candidatus Mycoplasma turicensis” infection in domestic cats in Japan. J Vet Med Sci. 2007;69:1061–1063. doi: 10.1292/jvms.69.1061. [DOI] [PubMed] [Google Scholar]
- 8.Macieira DB, de Menezes RD, Damico CB, et al. Prevalence and risk factors for hemoplasmas in domestic cats naturally infected with feline immunodeficiency virus and/or feline leukemia virus in Rio de Janeiro — Brazil. J Feline Med Surg. 2008;10:120–129. doi: 10.1016/j.jfms.2007.08.002. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9.Willi B, Tasker S, Boretti FS, et al. Phylogenetic analysis of “Candidatus Mycoplasma turicensis” isolates from pet cats in the United Kingdom, Australia, and South Africa, with analysis of risk factors for infection. J Clin Microbiol. 2006;44:4430–4435. doi: 10.1128/JCM.00987-06. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10.Willi B, Filoni C, Catão-Dias JL, et al. Worldwide occurrence of feline hemoplasma infections in wild felid species. J Clin Microbiol. 2007;45:1159–1166. doi: 10.1128/JCM.02005-06. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Willi B, Boretti FS, Meli ML, et al. Real-time PCR investigation of potential vectors, reservoirs, and shedding patterns of feline hemotropic mycoplasmas. Appl Environ Microbiol. 2007;73:3798–3802. doi: 10.1128/AEM.02977-06. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Woods J, Brewer M, Hawley J. Evaluation of experimental transmission of Candidatus Mycoplasma haemominutum and Mycoplasma haemofelis by Ctenocephalides felis to cats. Am J Vet Res. 2005;66:1008–1012. doi: 10.2460/ajvr.2005.66.1008. [DOI] [PubMed] [Google Scholar]
- 13.Woods JE, Wisnewski N, Lappin MR. Attempted transmission of Candidatus Mycoplasma haemominutum and Mycoplasma haemofelis by feeding cats infected Ctenocephalides felis. Am J Vet Res. 2006;67:494–497. doi: 10.2460/ajvr.67.3.494. [DOI] [PubMed] [Google Scholar]
- 14.George JW, Rideout BA, Griffey SM, Pedersen NC. Effect of preexisting FeLV infection or FeLV and feline immunodeficiency virus coinfection on pathogenicity of the small variant of Haemobartonella felis in cats. Am J Vet Res. 2002;63:1172–1178. doi: 10.2460/ajvr.2002.63.1172. [DOI] [PubMed] [Google Scholar]
- 15.Tasker S, Caney SM, Day MJ, et al. Effect of chronic FIV infection, and efficacy of marbofloxacin treatment, on Mycoplasma haemofelis infection. Vet Microbiol. 2006;117:169–179. doi: 10.1016/j.vetmic.2006.06.015. [DOI] [PubMed] [Google Scholar]
- 16.Tasker S, Caney SM, Day MJ, et al. Effect of chronic feline immuno-deficiency infection, and efficacy of marbofloxacin treatment, on ‘Candidatus Mycoplasma haemominutum’ infection. Microbes Infect. 2006;8:653–661. doi: 10.1016/j.micinf.2005.08.015. [DOI] [PubMed] [Google Scholar]
- 17.Tasker S, Helps CR, Day MJ, Harbour DA, Gruffydd-Jones TJ, Lappin MR. Use of a Taqman PCR to determine the response of Mycoplasma haemofelis infection to antibiotic treatment. J Microbiol Methods. 2004;56:63–71. doi: 10.1016/j.mimet.2003.09.017. [DOI] [PubMed] [Google Scholar]
- 18.Westfall DS, Jensen WA, Reagan WJ, Radecki SV, Lappin MR. Innoculation of two genotypes of Hemobartonella felis (California and Ohio variants) to induce infection in cats and the response to treatment with azithromycin. Am J Vet Res. 2001;62:687–691. doi: 10.2460/ajvr.2001.62.687. [DOI] [PubMed] [Google Scholar]
- 19.Dowers KL, Tasker S, Lappin MR. Use of pradofloxacin to treat experimentally induced Mycoplasma haemofelis infection in cats. J Vet Intern Med. 2007;21:629. [Google Scholar]
- 20.Kewish KE, Appleyard GD, Myers SL, Kidney BA, Jackson ML. Mycoplasma haemofelis and Mycoplasma haemominutum detection by polymerase chain reaction in cats from Saskatchewan and Alberta. Can Vet J. 2004;45:749–752. [PMC free article] [PubMed] [Google Scholar]
- 21.Latimer KS, Mahaffey EA, Prasse KW. Duncan and Prasse’s Veterinary Laboratory Medicine: Clinical Pathology. 4th ed. Ames, Iowa: Blackwell Publ; 2003. p. 22. [Google Scholar]
- 22.Ishak A, Radecki S, Lappin M. Prevalence of Mycoplasma haemofelis, “Candidatus Mycoplasma haemominutum”, Bartonella species, Ehrlichia species, and Anaplasma phagocytophilum DNA in the blood of cats with anemia. J Fel Med and Surg. 2007;9:1–7. doi: 10.1016/j.jfms.2006.05.003. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Tasker S, Binns SH, Day MJ, Gruffydd-Jones TJ, et al. Use of a PCR assay to assess the prevalence and risk factors for Mycoplasma haemofelis and ‘Candidatus Mycoplasma haemominutum’ in cats in the United Kingdom. Vet Rec. 2003;152:193–198. doi: 10.1136/vr.152.7.193. [DOI] [PubMed] [Google Scholar]