DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on November 18, 2025 has been entered.
Claims 2, 4, 5, 7, 9, 10, 16 and 18-21 remain pending wherein claims 18-21 remain withdrawn. No claims were amended.
Response to Arguments
Applicant's arguments with respect to the patentability of the claims have been fully considered but they are not persuasive.
Applicant argues that the claimed invention is patentable over the disclosure of Walshe because Walshe does not “distinguish infectious from non-infectious inflammatory conditions”. Remarks 6. According to Applicant, the method taught by Walshe merely determines the extent or severity of inflammation without actually determining whether the inflammation is caused by an infection. Id.
The argument is not persuasive because Applicant’s argument is not commensurate with the scope of the claims. Contrary to the implication of Applicant’s remarks, the claimed method simply requires correlating SAA concentration of a mammal to an infectious status without confirming whether the claimed mammal is in fact infectious (e.g. using another methodology). That said, Walshe explicitly discloses diagnosing an infection based on measured concentration of SAA (see [0034] disclosing “diagnosing a condition in a human or animal…the condition comprises…infection”; see also [0048] that explicitly teaches diagnosing an infection), which is sufficient to reject the limitations in question.
As for whether it would have been obvious to administer antibiotics in Walshe without confirming the infection, based on Walshe’s disclosure of consulting a medical practitioner and administering antibiotics after the consultation (see [0129]), the examiner maintains that it would have been obvious to consult a medical practitioner to confirm the SAA test diagnosis prior to administering antibiotics to the mammal. This additional step of consulting a medical practitioner was not discussed in the rejection because the claims do not actually recite/require such step.
Regarding Applicant’s remarks that Walshe conflates the distinction between “inflammation” and “infection” (Remarks 6), the fact that Walshe “diagnoses” infection based on SAA concentration does not mean that the disclosure of Walshe equates inflammation and infection. Rather, Walshe presumes (i.e. diagnoses) infection based on evidence of inflammation (elevated SAA concentration), which is not equating infection and inflammation. In fact, diagnosing infection based on sign of inflammation is evidence that Walshe considers infection and inflammation to be distinct (i.e. Walshe is establishing a correlation between two different biological processes, inflammation and infection). This is further evidenced by Walshe disclosing a step of consulting a medical practitioner to confirm infection the following day (see [0129]). Based on the disclosure of Walshe, the examiner maintains that Walshe properly delineates inflammation from infection, contrary to Applicant’s remarks.
Applicant also argues that the claims are patentable over the disclosure of Walshe because Walshe does not teach or suggest using 30 µg/ml as a threshold for diagnosing infection (Remarks 7). According to Applicant, the claimed 30 µg/ml threshold “achieves unexpectedly accurate discrimination, representing a new property of SAA measurement not suggested in Walshe”. Remarks 7. The argument is not persuasive because Applicant’s assertion of unexpected results is a conclusory statement not supported by evidence. Absent evidence, the examiner maintains that it would have been obvious to one of ordinary skill in the art to select any value within the range of 10-50 µg/ml taught by Walshe for the purpose of identifying clinically significant inflammation (i.e. inflammation that can be diagnosed as infection).
As for Applicant’s remarks that the 10-50 µg/ml taught by Walshe does not even represent a diagnostic cut-off (Remarks 7), Walshe explicitly discloses that the range corresponds to “mild inflammation” (see [0077]-[0078]), which is considered clinically significant (less than 10 µg/ml is “normal”, meaning values above 10 µg/ml are abnormal and thus clinically significant).
Regarding Applicant’s argument that Walshe does not “teach, suggest or enable any diagnostic linked treatment process based on distinguishing infectious diseases from non-infectious aetiologies in a mammal exhibiting an inflammatory response” (Remarks 8), Walshe explicitly teaches measuring the SAA concentration of a blood sample of a human, and upon determining that the SAA concentration exceeds a threshold, diagnosing the human with an infection and prescribing antibiotics (see [0129]).
For the foregoing reasons, the claims remain rejected based on the disclosure of Walshe.
Regarding Applicant’s remarks directed to Satue et al. (Remarks 9-10), the disclosure of Satue et al. is not relied upon in the outstanding rejection. Consequently, response to Applicant’s remarks regarding Satue et al. is deemed moot at this moment. Consequently, they will not be addressed.
Claim Rejections - 35 USC § 103
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
Claims 2, 4, 5, 7, 9, 10 and 16 are rejected under 35 U.S.C. 103 as being unpatentable over Walshe (US 2014/0322724 A1).
With respect to claim 2, Walshe discloses a method of distinguishing infectious diseases from non-infectious aetiologies in a mammal (e.g. a horse) exhibiting an inflammatory response by determining whether the concentration of Serum Amyloid A (SAA) in a body fluid sample of said mammal is above a specified level (see [0117] and [0120]), and prescribing treatment based on the determination (see [0129]), the method comprising:
determining that the inflammatory response results from an infectious aetiology (see [0034]) based on a concentration of SAA in the body fluid sample of said mammal being 32.9 µg/ml (see Table 1, [0120]).
The method disclosed by Walshe differs from the claimed invention in that Walshe does not explicitly disclose that the determination is based on whether the SAA concentration is above 30 µg/ml. In addition, Walshe does not explicitly disclose a step of treating the mammal with antibiotics.
Regarding the use of 30 µg/m as a benchmark, given that Walshe discloses that SAA concentration of 32.9 µg/ml corresponds to a mild inflammatory response in horses (see Table 1, [0120]), it would have been obvious to one of ordinary skill in the art to use 30 µg/ml as a benchmark for determining whether a horse is exhibiting an inflammatory response (see also [0077]-[0078] of Walshe disclosing that SAA levels of 10-50 µg/ml corresponds to a test line of the disclosed lateral flow device that denotes “mild inflammation”, meaning based on size, gender, age, species of the mammal, it would have been obvious to use any value within the range, for example 30 µg/ml, as the benchmark for denoting “mild inflammation”).
Regarding the step of administering antibiotics to the mammal, Walshe discloses an analogous method in which humans are prescribed antibiotics if they exhibit SAA concentrations corresponding to an inflammatory response and later confirmed to be infectious (see [0129]). Based on the disclosure, it would have been obvious to one of ordinary skill in the art to treat the horses exhibiting an inflammatory response and subsequently confirmed to be infectious by administering antibiotics.
With respect to claims 4 and 5, as discussed above, horses comprising SAA levels above 30 µg/ml would be diagnosed with the infectious disease, and horses comprising SAA levels below 30 µg/ml would be deemed normal.
With respect to claim 7, Walshe discloses that the method can be a useful prognostic tool to assess horses recovering from respiratory infections (see [0014]). Based on the disclosure, it would have been obvious to one of ordinary skill in the art to use the method to monitor the progress of a bacterial lung infection and diagnose a sick horse accordingly (e.g. mild, moderate, severe infection; early stage, peak stage, recovery stage) based on measured SAA levels of the horse.
With respect to claim 9, the body fluid sample is a blood sample (see [0118]).
With respect to claim 10, it would have been obvious to one of ordinary skill in the art to apply the method to a mammal (e.g. a horse) of any stage of a life cycle, including a neonate. In fact, Walshe discloses that one application of the invention is to determine a pregnant mare’s ability to rear new born foals (see [0064]), suggesting that the method is applicable for determining the viability of neonates.
With respect to claim 16, Walshe discloses that the determination of the inflammatory response is made using a lateral flow device (LFD) for quantifying SAA (see [0053]-[0054]), wherein the LFD comprises a housing and a flow path heading from a sample well to a viewing window through which a bodily fluid sample can flow by capillary action, wherein the viewing window provides a signal indicative of the results of the test within minutes (see Fig. 2, [0112] and [0134]). The viewing window indicates whether the SAA falls within various concentration ranges (see [0077]-[0078]). If the LFD is modified to use 30 µg/ml as the benchmark as discussed above, then the viewing window of the LFD would indicate whether the SAA is below or above the specified level of 30 µg/ml.
Conclusion
The following prior art is made of record because it is considered pertinent to Applicant's disclosure:
-Satue et al. “Factors Influencing Serum Amyloid Type A (SAA) Concentrations in Horses” (see IDS) discloses that SAA concentrations in normal horses range from 0.5 to 20 µg/ml (see left column, p. 59), and it can reach 4 to 40 times higher experiencing inflammation as a result of an infection (see section 3.3, p. 60). The claimed threshold concentration of 30 µg/ml for determining whether a mammal is exhibiting inflammation as a result of an infection falls within the range taught by Satue et al.
Conclusion
All claims are identical to or patentably indistinct from, or have unity of invention with claims in the application prior to the entry of the submission under 37 CFR 1.114 (that is, restriction (including a lack of unity of invention) would not be proper) and all claims could have been finally rejected on the grounds and art of record in the next Office action if they had been entered in the application prior to entry under 37 CFR 1.114. Accordingly, THIS ACTION IS MADE FINAL even though it is a first action after the filing of a request for continued examination and the submission under 37 CFR 1.114. See MPEP § 706.07(b). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to PAUL S HYUN whose telephone number is (571)272-8559. The examiner can normally be reached M-F 8:30-5:00.
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/PAUL S HYUN/Primary Examiner, Art Unit 1796